A Comparasion of Laboratory and Cardiopulmonary Effects of Desflurane, Detomidine and Medetomidine Anaesthetic Combinations in Horses

Background: Equine anesthesia morbidity and mortality rates are greater than in other domestic animals because of hypotension and hypoventilation. The important features desired in general anesthesia for horses are a rapid effect, rapid emergence and balanced anesthesia. The long duration of action of currently used anesthetic agents cause various complications in horses. The aim of the present study was to compare the clinical effects of combination of the anesthetics desflurane, detomidine and medetomidine in horses.Materials, Methods & Results: Eight healthy mixed-breed horses (four males and four females) with weighing 275 ± 56 kg [mean ± standard deviation (SD)] and aged 6.8 ± 5 years [(mean ± SD)] were used for this study. The horses were placed into one of four groups: group I (detomidine-desflurane), group II (detomidine-desflurane-atipamezole), group III (medetomidinedesflurane), or group IV (medetomidine-desflurane-atipamezole). Horses were rested for 15 days before each group starts to study. Intravenous detomidine (25 µg/kg) was used for premedication in groups I and II, and intravenous medetomidine (7 µg/ kg) was used for premedication in groups III and IV. Ketamine hydrocholoride (2 mg/kg) and midazolam (0.03 mg/kg) were intravenously administered in the same syringe to induce anesthesia. After induction of anesthesia, horses were placed in the left lateral re

A comparasion of laboratory and cardiopulmonary effects of desflurane, detomidine and medetomidine anaesthetic combinations in horses

Background: Equine anesthesia morbidity and mortality rates are greater than in other domestic animals because of hypotension and hypoventilation. The important features desired in general anesthesia for horses are a rapid effect, rapid emergence and balanced anesthesia. The long duration of action of currently used anesthetic agents cause various complications in horses. The aim of the present study was to compare the clinical effects of combination of the anesthetics desflurane, detomidine and medetomidine in horses.Materials, Methods & Results: Eight healthy mixed-breed horses (four males and four females) with weighing 275 ± 56 kg [mean ± standard deviation (SD)] and aged 6.8 ± 5 years [(mean ± SD)] were used for this study. The horses were placed into one of four groups: group I (detomidine-desflurane), group II (detomidine-desflurane-atipamezole), group III (medetomidine- desflurane), or group IV (medetomidine-desflurane-atipamezole). Horses were rested for 15 days before each group starts to study. Intravenous detomidine (25 μg/kg) was used for premedication in groups I and II, and intravenous medetomidine (7 μg/kg) was used for premedication in groups III and IV. Ketamine hydrocholoride (2 mg/kg) and midazolam (0.03 mg/kg) were intravenously administered in the same syringe to induce anesthesia. After induction of anesthesia, horses were placed in the left lateral recumbent position, and the trachea was intubated with a cuffed endotracheal tube with an internal diameter of 28 mm. The endotracheal tube was attached to a large animal circle breathing system anesthesia machine, and anesthesia was maintained with desflurane for 90 min. The initial dosage of desflurane was 14% + 4 L O2/min, and was reduced by 2% every 10 min over the first 30 min of anesthesia. After 30 min, the desflurane dose was changed to 8% + 4 L, which was maintained until the end of anesthesia (90 min).[...]

A comparasion of laboratory and cardiopulmonary effects of desflurane, detomidine and medetomidine anaesthetic combinations in horses

Background: Equine anesthesia morbidity and mortality rates are greater than in other domestic animals because of hypotension and hypoventilation. The important features desired in general anesthesia for horses are a rapid effect, rapid emergence and balanced anesthesia. The long duration of action of currently used anesthetic agents cause various complications in horses. The aim of the present study was to compare the clinical effects of combination of the anesthetics desflurane, detomidine and medetomidine in horses.Materials, Methods & Results: Eight healthy mixed-breed horses (four males and four females) with weighing 275 ± 56 kg [mean ± standard deviation (SD)] and aged 6.8 ± 5 years [(mean ± SD)] were used for this study. The horses were placed into one of four groups: group I (detomidine-desflurane), group II (detomidine-desflurane-atipamezole), group III (medetomidine- desflurane), or group IV (medetomidine-desflurane-atipamezole). Horses were rested for 15 days before each group starts to study. Intravenous detomidine (25 μg/kg) was used for premedication in groups I and II, and intravenous medetomidine (7 μg/kg) was used for premedication in groups III and IV. Ketamine hydrocholoride (2 mg/kg) and midazolam (0.03 mg/kg) were intravenously administered in the same syringe to induce anesthesia. After induction of anesthesia, horses were placed in the left lateral recumbent position, and the trachea was intubated with a cuffed endotracheal tube with an internal diameter of 28 mm. The endotracheal tube was attached to a large animal circle breathing system anesthesia machine, and anesthesia was maintained with desflurane for 90 min. The initial dosage of desflurane was 14% + 4 L O2/min, and was reduced by 2% every 10 min over the first 30 min of anesthesia. After 30 min, the desflurane dose was changed to 8% + 4 L, which was maintained until the end of anesthesia (90 min).[...](AU)

Early postoperative recovery after intracranial surgical procedures. Comparison of the effects of sevoflurane and desflurane

PURPOSE: To compared the effects of sevoflurane and desflurane on early anesthesia recovery in patients undergoing to craniotomy for intracranial lesions. METHODS: After IRB approval, the study included 50 patients aged 18-70 years who had ASA physical statuses of I-II and were scheduled for intracranial surgery. Patients were randomly divided into two groups: sevoflurane and desflurane. Anaesthesia was routinely induced in all patients followed by desflurane 5%-6% or sevoflurane 1%-2%. Moreover remifentanil infusion (0.05-0.2 mcg/kg/min) was adjusted to maintain mean arterial pressure (MAP) within 20% baseline and heart rate 90 bpm. Postoperatively, patients were evaluated over time for responses to painful stimulus, eye opening, hand squeezing, extubation, orientation and time required to achieve a Modified Aldrete Score of 9-10. Parametric and non-parametric data were assessed using Student's t- and Mann-Whitney U tests, respectively. A p 0.05 was taken as statistically significant. RESULTS: The times to responses to painful stimuli (7.7±2.7 vs. 4.8±1.7 min.; p 0.001), emergence (9.5±2.81 vs. 6.3±2.2 min.; p 0.001), hand-squeezing (12.1±2.9 vs. 8.2±2.3 min.; p 0.001), extubation (10.1±2.87 vs. 7.1±1.6 min.; p 0.001), orientation (15.3±3.2 vs. 10.3±2.7 min.; p 0.001) and Aldrete score of 9-10 (23.3±6.1 vs. 15.8±3.8 min.; p 0.001) were significantly lower with desflurane-based anaesthesia vs. sevoflurane-based anaesthesia. CONCLUSION: Desflurane yields early recovery functions and facilitates early postoperative neurologic examinations of intracranial surgery patients.(AU)

Can thiamine pyrophosphate prevent desflurane induced hepatotoxicity in rats?

PURPOSE: To investigate the effects of thiamine pyrophosphate (TPP) against desflurane induced hepatotoxicity.METHODS: Thirty experimental animals were divided into groups as healthy (HG), desflurane control (DCG) , TPP and desflurane group (TDG). 20 mg/kg TPP was injected to intraperitoneally TDG. After one hour of TPP administration, desflurane was applied for two hours. After 24 hours, liver tissues of the animals killed with decapitation were removed. The oxidant/antioxidant levels and ALT, AST and LDH activities were measured. The histopathological examinations were performed in the liver tissues for all rats.RESULTS: Notwithstanding the levels of oxidants and liver enzymes were significantly increased (p<0.0001), antioxidant levels were significantly decreased in DCG (p<0.0001). On contrary to the antioxidant parameters were increased (p<0.05) the oxidant parameters and liver enzymes were decreased in TDG (p<0.0001). Whereas multiple prominent, congestion, hemorrhage and dilatation were observed in sinusoids and lymphocyte-rich inflammation results in the centrilobular and portal areas of liver tissue in DCG, these findings were observed less frequently in TDG.CONCLUSİON: Thiamine pyrophosphate prevented liver oxidative damage induced with desflurane and may be useful in prophylaxis of desflurane induced hepatotoxicity.(AU)

Infusão contínua de lidocaína e/ou de cetamina como adjuntes durante anestesia inalatória em cães: revisão de literatura / Constant rate infusion of lidocaine and/or ketamine as adjuvants during inhalation anesthesia in dogs: literature review

A anestesia geral é uma prática rotineira na medicina veterinária para realização de procedimentos cirúrgicosnos animais. Tal prática pode ser realizada com fármacos inalatórios ou injetáveis. Atualmente,a anestesia inalatória é a modalidade de manutenção mais empregada em cães devido a algumas vantagenscomo o fácil ajuste na profundidade anestésica, o fornecimento obrigatório de oxigênio, recuperaçãoanestésica rápida e biotransformação hepática mínima para os anestésicos contemporâneos isoflurano,sevoflurano e desflurano. Apesar das características favoráveis dos anestésicos inalatórios, estes nãoapresentam propriedade analgésica específica e altas concentrações são necessárias quando usados isoladamentena manutenção da anestesia, desencadeando efeitos adversos cardiovasculares e respiratórios.A anestesia balanceada consiste na associação de fármacos com propriedade analgésica e/ou sedativaaos anestésicos gerais, com o objetivo de melhorar a analgesia e reduzir os efeitos adversos individuaisde cada fármaco. O uso da cetamina e da lidocaína nessa técnica anestésica vem crescendo em cães.Esses fármacos reduzem a concentração alveolar mínima (CAM) dos agentes voláteis de maneira dose--dependente, resultando em maior estabilidade cardiovascular. Além disso, atuam em pontos distintosda via nociceptiva promovendo analgesia eficaz, a qual pode se estender ao período pós-operatório. Comesta revisão, objetivou-se realizar uma atualização sobre o uso da cetamina e da lidocaína na anestesiabalanceada em cães.(AU)

General anesthesia is a routine practice in veterinary medicine for surgical procedures in animals. It canbe performed with injectable or inhaled drugs. Currently, inhalation anesthesia is the most used technirevisão que for maintenance of anesthesia in dogs due to some advantages such as fast and easy adjustment inanesthetic depth, mandatory supply of oxygen, rapid recovery from anesthesia and minimal hepatic biotransformationfor the contemporary anesthetics (isoflurane, sevoflurane and desflurane). Despite thesefavorable characteristics, inhaled anesthetics have no specific analgesic properties and high concentrationsare required when used alone for maintenance of anesthesia, resulting in adverse effects within thecardiovascular and respiratory systems. Balanced anesthesia consists in the combination of drugs withanalgesic and/or sedating properties with general anesthetics, aiming to improve analgesia and to reducethe adverse effects of each individual drug. The use of ketamine and lidocaine in balanced anesthesiais increasing in dogs. These drugs reduce the minimum alveolar concentration (MAC) of volatile anestheticin a dose-dependent manner, resulting in increased cardiovascular stability. Moreover, ketamine andlidocaine act at different points of the nociceptive pathway providing effective analgesia, which can beextended to the postoperative period. The objective of this review was to update on the use of ketamineand lidocaine in balanced anesthesia in dogs.(AU)

Infusão contínua de lidocaína e/ou de cetamina como adjuntes durante anestesia inalatória em cães: revisão de literatura / Constant rate infusion of lidocaine and/or ketamine as adjuvants during inhalation anesthesia in dogs: literature review

A anestesia geral é uma prática rotineira na medicina veterinária para realização de procedimentos cirúrgicosnos animais. Tal prática pode ser realizada com fármacos inalatórios ou injetáveis. Atualmente,a anestesia inalatória é a modalidade de manutenção mais empregada em cães devido a algumas vantagenscomo o fácil ajuste na profundidade anestésica, o fornecimento obrigatório de oxigênio, recuperaçãoanestésica rápida e biotransformação hepática mínima para os anestésicos contemporâneos isoflurano,sevoflurano e desflurano. Apesar das características favoráveis dos anestésicos inalatórios, estes nãoapresentam propriedade analgésica específica e altas concentrações são necessárias quando usados isoladamentena manutenção da anestesia, desencadeando efeitos adversos cardiovasculares e respiratórios.A anestesia balanceada consiste na associação de fármacos com propriedade analgésica e/ou sedativaaos anestésicos gerais, com o objetivo de melhorar a analgesia e reduzir os efeitos adversos individuaisde cada fármaco. O uso da cetamina e da lidocaína nessa técnica anestésica vem crescendo em cães.Esses fármacos reduzem a concentração alveolar mínima (CAM) dos agentes voláteis de maneira dose--dependente, resultando em maior estabilidade cardiovascular. Além disso, atuam em pontos distintosda via nociceptiva promovendo analgesia eficaz, a qual pode se estender ao período pós-operatório. Comesta revisão, objetivou-se realizar uma atualização sobre o uso da cetamina e da lidocaína na anestesiabalanceada em cães.

General anesthesia is a routine practice in veterinary medicine for surgical procedures in animals. It canbe performed with injectable or inhaled drugs. Currently, inhalation anesthesia is the most used technirevisão que for maintenance of anesthesia in dogs due to some advantages such as fast and easy adjustment inanesthetic depth, mandatory supply of oxygen, rapid recovery from anesthesia and minimal hepatic biotransformationfor the contemporary anesthetics (isoflurane, sevoflurane and desflurane). Despite thesefavorable characteristics, inhaled anesthetics have no specific analgesic properties and high concentrationsare required when used alone for maintenance of anesthesia, resulting in adverse effects within thecardiovascular and respiratory systems. Balanced anesthesia consists in the combination of drugs withanalgesic and/or sedating properties with general anesthetics, aiming to improve analgesia and to reducethe adverse effects of each individual drug. The use of ketamine and lidocaine in balanced anesthesiais increasing in dogs. These drugs reduce the minimum alveolar concentration (MAC) of volatile anestheticin a dose-dependent manner, resulting in increased cardiovascular stability. Moreover, ketamine andlidocaine act at different points of the nociceptive pathway providing effective analgesia, which can beextended to the postoperative period. The objective of this review was to update on the use of ketamineand lidocaine in balanced anesthesia in dogs.

Effects of nitrous oxide on minimum alveolar concentration of desflurane in dogs / Efeitos do óxido nitroso sobre a concentração alveolar mínima do desfluorano, em cães

Effects of nitrous oxide (N2O) on minimum alveolar concentration (MAC) of desflurane were studied. For that purpose, 30 dogs were randomly allocated into two groups: desflurane group (GD) and N2O and desflurane group (GDN). GD animals received propofol to intubation, and 11.5V% of desflurane diluted in 100% O2. After 30 minutes, they received electric stimulus and if the animal did not react to stimulus, desflurane concentration was reduced by 1.5V%. This protocol was repeated at each 15 minutes, and stimulus was interrupted when voluntary reaction was observed. GDN dogs were submitted to diluent flow 30% O2 and 70% N2O. Desflurane's MAC; heart (HR) and respiratory (RR) rates; systolic, diastolic and mean arterial pressures (SAP, DAP, and MAP, respectively); end tidal carbon dioxide (ETCO2); oxyhemoglobin saturation (SpO2) and body temperature (T) were evaluated. In both groups increase in HR and ETCO2, and decrease in RR and T were associated with administration of the highest dose of desflurane. Blood pressures decreased 30 minutes after desflurane administration in GDN, and after this measurement the values increased. Reduction in desflurane's MAC was observed as well. It is concluded that N2O associated with desflurane reduced desflurane's MAC by 16% with increase in HR and respiratory depression.(AU)

Estudaram-se os efeitos do óxido nitroso (N2O) sobre a concentração alveolar mínima (CAM) do desfluorano. Trinta cães foram distribuídos em dois grupos: desfluorano (GD) e N2O e desfluorano (GDN). Os do GD receberam propofol (8,9±1,65mg/kg) para intubação orotraqueal e após, 11,5V% de desfluorano em 100% de O2. Após 30 minutos, os animais receberam estímulo elétrico e não havendo reação do animal, reduziu-se a concentração em 1,5V%. Repetiu-se o protocolo a cada 15 minutos, cessando-se os estímulos quando observada reação voluntária. Os GDN foram submetidos ao mesmo protocolo, substituindo-se o fluxo diluente por 30% O2 e 70% N2O. Mensuraram-se freqüências cardíaca (FC) e respiratória (FR), pressões arteriais sistólica, diastólica e média (PAS, PAD e PAM), concentração de dióxido de carbono ao final da expiração (ETCO2), saturação de oxihemoglobina (SpO2), temperatura corpórea (TC) e a CAM do desfluorano. Observou-se aumento da FC, ETCO2 e SpO2, e redução da FR e da TC concomitantemente à administração da maior dose de desfluorano, além de redução da CAM do desfluorano. As pressões arteriais diminuíram em M30 aumentando posteriormente. Concluiu-se que o N2O associado ao desfluorano reduz em 16% a CAM do anestésico volátil. Além disso, essa associação promoveu aumento da FC e depressão respiratória.(AU)

Hemogasometria e variáveis cardiopulmonares após administração do butorfanol em cães anestesiados pelo desfluorano sob ventilação espontânea

The cardiopulmonary and acid-base effects of butorphanol in desflurane anesthetized dogs breathing spontaneously were evaluated. Twenty adult healthy, male and female dogs were used. They were separated into two groups of 10 animals each (GS and GB). Anesthesia was induced with propofol (8.4±0.8mg kg-1 IV) and maintained with desflurane (10V%). After 40 minutes of induction, the animals from GS received saline solution at 0.9% (0.05mL kg-1) and from GB received butorphanol (0.4mg kg-1), both applied intramuscularly. Heart (HR) and respiratory (RR) rates; systolic (SAP), diastolic (DAP) and mean (MAP) arterial pressures; arterial blood pH (pH), arterial partial pressure of O2 (PaO2) and arterial partial pressure of CO2 (PaCO2); base deficit (BD), arterial oxygen saturation (SaO2) and bicarbonate ion concentration (HCO3) were measured. The measurements were taken immediately before the application of the agents (M0). Serial measurements were carried out at 15 minutes intervals after the administration of butorphanol or saline up to 75 minutes (M15, M30, M45, M60 and M75). Data were submitted to Profile Analysis (P 0.05). After butorphanol administration HR, SAP, DAP and MAP decreased significantly. PaO2 had discreet alterations, however without clinical meaning. RR and pH decreased after butorphanol administration while PaCO2 increased significantly. It was possible to conclude that butorphanol administration in desflurane anesthetized dogs produced reduction in the averages of heart rate and arterial pressure and relatively to the respiratory parameters, the opioid produced hypoventilation in spontaneously breathing dogs.

Este experimento teve por objetivos avaliar as possíveis alterações cardiopulmonares e hemogasométricas decorrentes do uso do butorfanol em cães submetidos à anestesia pelo desfluorano sob ventilação espontânea. Para tal, foram utilizados vinte cães adultos, clinicamente saudáveis, pesando 12±3kg. Os animais foram distribuídos igualmente em dois grupos, GS e GB, e induzidos à anestesia com propofol (8,4±0,8mg kg-1, IV), intubados e submetidos à anestesia inalatória pelo desfluorano (10V%). Decorridos 40 minutos da indução, foi administrado aos animais do GS 0,05mL kg-1 de solução fisiológica a 0,9% (salina), enquanto que, no GB, foi aplicado butorfanol na dose de 0,4mg kg-1, ambos pela via intramuscular. As observações das variáveis freqüências cardíaca (FC) e respiratória (f), pressões arteriais sistólica (PAS), diastólica (PAD) e média (PAM), pH arterial (pH), pressão parcial de oxigênio no sangue arterial (PaO2), pressão parcial de dióxido de carbono no sangue arterial (PaCO2), déficit de base (DB), bicarbonato (HCO3) e saturação de oxigênio na hemoglobina (SatO2) tiveram início imediatamente antes da aplicação do opióide ou salina (M0). Novas mensurações foram realizadas 15 minutos após a administração do butorfanol ou salina (M15) e as demais colheitas foram realizadas a intervalos de 15 minutos, por um período de 60 minutos (M30, M45, M60 e M75). Os dados numéricos dessas variáveis foram submetidos à Análise de Perfil (P 0,05). A freqüência cardíaca apresentou alteração no GB, com média de M0 maior que as demais. As PAS, PAD e PAM, assim como a f e o pH, apresentaram valores menores após a administração do opióide no GB, em comparação ao GS. A PaO2 apresentou discretas alterações, entretanto sem significado clínico, enquanto que a PaCO2 e o DB apresentaram valores de M0 menores que os demais após a aplicação do butorfanol. Os resultados obtidos permitem concluir que a administração do butorfanol em cães submetidos à anestesia pelo desfluorano, sob ventilação espontânea, reduz a freqüência cardíaca e a pressão arterial e promove certo grau de hipoventilação.

Hemogasometria e variáveis cardiopulmonares após administração do butorfanol em cães anestesiados pelo desfluorano sob ventilação espontânea

The cardiopulmonary and acid-base effects of butorphanol in desflurane anesthetized dogs breathing spontaneously were evaluated. Twenty adult healthy, male and female dogs were used. They were separated into two groups of 10 animals each (GS and GB). Anesthesia was induced with propofol (8.4±0.8mg kg-1 IV) and maintained with desflurane (10V%). After 40 minutes of induction, the animals from GS received saline solution at 0.9% (0.05mL kg-1) and from GB received butorphanol (0.4mg kg-1), both applied intramuscularly. Heart (HR) and respiratory (RR) rates; systolic (SAP), diastolic (DAP) and mean (MAP) arterial pressures; arterial blood pH (pH), arterial partial pressure of O2 (PaO2) and arterial partial pressure of CO2 (PaCO2); base deficit (BD), arterial oxygen saturation (SaO2) and bicarbonate ion concentration (HCO3) were measured. The measurements were taken immediately before the application of the agents (M0). Serial measurements were carried out at 15 minutes intervals after the administration of butorphanol or saline up to 75 minutes (M15, M30, M45, M60 and M75). Data were submitted to Profile Analysis (P 0.05). After butorphanol administration HR, SAP, DAP and MAP decreased significantly. PaO2 had discreet alterations, however without clinical meaning. RR and pH decreased after butorphanol administration while PaCO2 increased significantly. It was possible to conclude that butorphanol administration in desflurane anesthetized dogs produced reduction in the averages of heart rate and arterial pressure and relatively to the respiratory parameters, the opioid produced hypoventilation in spontaneously breathing dogs.

Este experimento teve por objetivos avaliar as possíveis alterações cardiopulmonares e hemogasométricas decorrentes do uso do butorfanol em cães submetidos à anestesia pelo desfluorano sob ventilação espontânea. Para tal, foram utilizados vinte cães adultos, clinicamente saudáveis, pesando 12±3kg. Os animais foram distribuídos igualmente em dois grupos, GS e GB, e induzidos à anestesia com propofol (8,4±0,8mg kg-1, IV), intubados e submetidos à anestesia inalatória pelo desfluorano (10V%). Decorridos 40 minutos da indução, foi administrado aos animais do GS 0,05mL kg-1 de solução fisiológica a 0,9% (salina), enquanto que, no GB, foi aplicado butorfanol na dose de 0,4mg kg-1, ambos pela via intramuscular. As observações das variáveis freqüências cardíaca (FC) e respiratória (f), pressões arteriais sistólica (PAS), diastólica (PAD) e média (PAM), pH arterial (pH), pressão parcial de oxigênio no sangue arterial (PaO2), pressão parcial de dióxido de carbono no sangue arterial (PaCO2), déficit de base (DB), bicarbonato (HCO3) e saturação de oxigênio na hemoglobina (SatO2) tiveram início imediatamente antes da aplicação do opióide ou salina (M0). Novas mensurações foram realizadas 15 minutos após a administração do butorfanol ou salina (M15) e as demais colheitas foram realizadas a intervalos de 15 minutos, por um período de 60 minutos (M30, M45, M60 e M75). Os dados numéricos dessas variáveis foram submetidos à Análise de Perfil (P 0,05). A freqüência cardíaca apresentou alteração no GB, com média de M0 maior que as demais. As PAS, PAD e PAM, assim como a f e o pH, apresentaram valores menores após a administração do opióide no GB, em comparação ao GS. A PaO2 apresentou discretas alterações, entretanto sem significado clínico, enquanto que a PaCO2 e o DB apresentaram valores de M0 menores que os demais após a aplicação do butorfanol. Os resultados obtidos permitem concluir que a administração do butorfanol em cães submetidos à anestesia pelo desfluorano, sob ventilação espontânea, reduz a freqüência cardíaca e a pressão arterial e promove certo grau de hipoventilação.

Efeitos cardiovasculares e neuroendócrinos do butorfanol e da buprenorfina em cães anestesiados pelo desfluorano / Cardiovascular and neuroendocrine effects of butorphanol and buprenorphine in dogs anesthetized with desflurane

Avaliaram-se os efeitos do butorfanol e da buprenorfina sobre variáveis cardiovasculares e neuroendócrinas em cães anestesiados com desfluorano, utilizando-se 30 cães adultos, machos e fêmeas, distribuídos em três grupos denominados grupo butorfanol (GBT), grupo buprenorfina (GBP) e grupo-controle (GCO). A anestesia foi induzida com propofol (8mg/kgIV) e nos animais intubados administrou-se desfluorano (1,5CAM). Após 30 minutos, nos cães do GBT, aplicou-se butorfanol (0,4mg/kgIM); nos do GBP, buprenorfina (0,02mg/kgIM); e nos do GCO, solução de NaCl a 0,9 por cento (0,05ml/kgIM). Avaliaram-se: freqüência cardíaca; pressões arteriais sistólica, diastólica e média; débito cardíaco; pressão venosa central; cortisol; hormônio adrenocorticotrópico; noradrenalina; e glicose. As colheitas dos dados foram feitas aos 30 minutos após o início da administração do desfluorano (M0), 15 minutos após a administração do opióide ou placebo (M15), e a cada 15 minutos após M15 (M30, M45, M60 e M75). Para a avaliação neuroendócrina utilizaram-se os momentos M-30 (antes da administração dos fármacos), M0, M15 e M45. Na freqüência cardíaca houve diferença entre M0 e M15 (129 e 111bat/min) em GBT, e entre M0 e M30 (131 e 112bat/min) em GBP. Na pressão arterial média, a diferença foi entre M0 (86mmHg) e todos os momentos que se seguiram (todos os valores foram menores que 72mmHg), em GBT. A pressão arterial diastólica foi menor em todos os momentos (<53mmHg) quando comparada com a do M0 (67mmHg), em GBT. Na pressão arterial sistólica, a diferença foi entre M0 e M15 e M30 (112 versus 93 e 94mmHg, respectivamente) em GBT. A inclusão dos opióides determinou discreta redução nos parâmetros cardiovasculares, enquanto o desfluorano interferiu na função neuroendócrina elevando os níveis plasmáticos de glicose.(AU)

The effects of butorphanol and buprenorphine on cardiovascular and neuroendocrine variables in dogs anesthetized with desflurane were studied. Thirty adult healthy, males and females, mongrel dogs were distributed in three groups denominated butorphanol group (BTG), buprenorphine group (BPG) and control group (COG). The anesthetic induction was done using propofol (8mg/kg, IV), and immediately, the dogs were intubated and submited to desflurane anaesthesia (1.5 MAC). After 30 minutes, the BTG animals received butorphanol (0.4mg/kg IM), the BPG animals buprenorphine (0.02mg/kg IM) and the COG animals saline solution at 0.9 percent (0.05 ml/kg IM). Heart rate; systolic, diastolic and mean arterial blood pressures; cardiac output; venous central pressure; cortisol; ACTH; noradrenalin; and glucose were measured. The measurements were recorded at 30 minutes after beginning the inhalatory anaesthesia (M0) and at 15 minutes after opioid or saline administration (M15). Also a serial measurements were carried out in 15-minute intervals after M15 (M30, M45, M60 and M75). For neuroendocrine evaluation measurements were recorded before desflurane administration (M-30), and at M0, M15 AND m45. For heart rate there were differences between M0 and M15 (129 and 111 beats/min) in BTG, and between M0 and M30 (131 and 112 beats/min), in BPG. For mean arterial blood pressure there were differences between M0 (86mmHg) and all the recorded measurements (all measurements were lower than 72mmHg), in BTG. All recorded diastolic arterial blood pressures were lower than 53mmHg and different of the recorded measure M0 (67mmHg), in BTG. For systolic arterial blood pressure there were differences between M0 and M15 and M30 (112 vs 93 and 94mmHg, respectively), in BTG. Opioids administration determined discrete reduction in cardiovascular parameters while desflurane caused alterations in neuroendocrine function, increasing plasmatic levels of glucose.(AU)

Electrocardiography in dogs anesthetized with desflurane diluted in either intermediate or low flow oxygen / Eletrocardiografia em cães submetidos à anestesia pelo desfluorano com fluxo baixo ou intermediário de oxigênio

Desflurane anesthesia in low or intermediate oxygen flow rates were compared in dogs regarding its effects on heart rate (HR) and electrocardiography (ECG). In this experiment, 26 adult healthy mongrel dogs, males and females, weighing 32.04 ± 4.0 kg, were used. Dogs were randomly assigned to two equal groups (G1 and G2). In both groups, general anesthesia was induced with propofol (8.0 ± 2.0 mg/kg IV), followed by inhalation anesthesia with desflurane (7.2V% expired), diluted in oxygen (O2) at a flow rate of 50 mL/kg/min, using a semi-closed anesthetic system. After 15 35 minutes, O2 flow was decreased to 7 mL/kg/min and 30 mL/kg/min for G1 and G2 animals, respectively. After reducing O2 flow rate, the pop-off valve was closed for G1 animals, resulting in a closed anesthetic circuit. Parameters were measured immediately before the drugs were given (M0) and 15 minutes after anesthetic induction (M15), with repeated data collection at 15-minute intervals (M30 to M60). Statistical analysis was performed by Profile Analysis (p£0.05). We concluded that low flow anesthesia does not cause threatening changes in heart rate or in electrocardiographic parameters. KEY-WORDS: Anesthesia. Dogs. Desflurane. Low flow. Electrocardiography.

Efeitos cardiorrespiratórios da buprenorfina em cães anestesiados pelo desfluorano

The aim of this study was to evaluate the effects of buprenorphine on cardiovascular and respiratory variables in dogs anesthetized with desflurane. Twenty adult healthy male and female mongrel dogs were randomly distributed in two groups of ten animals each (GB and GC). The anesthetic induction was done using propofol (8mg kg-1, IV), and immediately, the dogs were intubated and submited to desflurane anesthesia administrated at 1.5 MAC. After 30 minutes of induction, animals from GB received buprenorphine (0.02mg kg-1) and GC saline solution at 0.9% (0.05ml kg-1), both applied intramuscularly. Heart Rate (HR); Systolic, Diastolic and Mean Arterial Blood Pressure (SAP, DAP and MAP); Cardiac Output (CO); Venous Central Pressure (VCP); Respiratory Rate (RR); Corporal Temperature (CT) and hemogasometrics variables. The measurement were realized 30 minutes after beginning the inhalatory anesthesia (MO); 15 minutes after opioid or saline administration (M15). Serial measurements were carried out in 15-minute intervals after M15 (M30, M45, M60 and M75). The numerical data were submited to ANOVA (P 0.05). The HR, RR and pH decreased after opioid administration, while for PaCO2 increased. The results allow us to conclude that buprenorphine determine discreet reduction in the cardiovascular parameters and promotes potentially hypoventilation in dogs anesthetized with desflurane.

Objetivou-se, com este estudo, avaliar os efeitos da buprenorfina sobre variáveis cardiovasculares e respiratórias em cães durante anestesia com desfluorano. Para tanto, foram utilizados 20 cães adultos, distribuídos em dois grupos (GB e GC). A anestesia foi induzida com propofol (8mg kg-1 IV) e em seguida os animais foram intubados com sonda de Magill, a qual foi conectada ao aparelho de anestesia para administração de desfluorano (1,5 CAM). Após 30 minutos, foi aplicado no GB buprenorfina (0,02mg kg-1) e no GC solução de NaCl à 0,9% (0,05ml kg-1). Avaliaram-se: freqüências cardíaca e respiratória (FC e FONT FACE=Symbol>¦ /FONT>); pressões arteriais sistólica, diastólica e média (PAS, PAD e PAM); débito cardíaco (DC); pressão venosa central (PVC); e as variáveis hemogasométricas pH, PaCO2, PaO2, HCO3, SatO2 e DB. As colheitas dos dados foram feitas aos 30 minutos após o início da administração do desfluorano (MO), 15 minutos após a administração do opióide ou placebo (M15), e a cada 15 minutos após Ml5 (M30, M45, M60 e M75). A avaliação estatística dos dados foi efetuada por meio de Análise de Perfil (P 0,05). Houve discreta redução da FC no GB, enquanto as outras variáveis cardiovasculares não tiveram redução significativa. A FONT FACE=Symbol>¦ /FONT> e o pH tiveram reduções no GB, enquanto a PaCO2 esteve aumentada. Concluiu-se que a inclusão da buprenorfina durante anestesia inalatória pelo desfluorano determina discretas alterações cardiovasculares, bem-como potencializa a hipoventilação promovida pelo desfluorano, com a manifestação de hipercapnia, o que não contra-indica o seu uso em pacientes estáveis.

Efeitos cardiorrespiratórios da buprenorfina em cães anestesiados pelo desfluorano

The aim of this study was to evaluate the effects of buprenorphine on cardiovascular and respiratory variables in dogs anesthetized with desflurane. Twenty adult healthy male and female mongrel dogs were randomly distributed in two groups of ten animals each (GB and GC). The anesthetic induction was done using propofol (8mg kg-1, IV), and immediately, the dogs were intubated and submited to desflurane anesthesia administrated at 1.5 MAC. After 30 minutes of induction, animals from GB received buprenorphine (0.02mg kg-1) and GC saline solution at 0.9% (0.05ml kg-1), both applied intramuscularly. Heart Rate (HR); Systolic, Diastolic and Mean Arterial Blood Pressure (SAP, DAP and MAP); Cardiac Output (CO); Venous Central Pressure (VCP); Respiratory Rate (RR); Corporal Temperature (CT) and hemogasometrics variables. The measurement were realized 30 minutes after beginning the inhalatory anesthesia (MO); 15 minutes after opioid or saline administration (M15). Serial measurements were carried out in 15-minute intervals after M15 (M30, M45, M60 and M75). The numerical data were submited to ANOVA (P 0.05). The HR, RR and pH decreased after opioid administration, while for PaCO2 increased. The results allow us to conclude that buprenorphine determine discreet reduction in the cardiovascular parameters and promotes potentially hypoventilation in dogs anesthetized with desflurane.

Objetivou-se, com este estudo, avaliar os efeitos da buprenorfina sobre variáveis cardiovasculares e respiratórias em cães durante anestesia com desfluorano. Para tanto, foram utilizados 20 cães adultos, distribuídos em dois grupos (GB e GC). A anestesia foi induzida com propofol (8mg kg-1 IV) e em seguida os animais foram intubados com sonda de Magill, a qual foi conectada ao aparelho de anestesia para administração de desfluorano (1,5 CAM). Após 30 minutos, foi aplicado no GB buprenorfina (0,02mg kg-1) e no GC solução de NaCl à 0,9% (0,05ml kg-1). Avaliaram-se: freqüências cardíaca e respiratória (FC e FONT FACE=Symbol>¦ /FONT>); pressões arteriais sistólica, diastólica e média (PAS, PAD e PAM); débito cardíaco (DC); pressão venosa central (PVC); e as variáveis hemogasométricas pH, PaCO2, PaO2, HCO3, SatO2 e DB. As colheitas dos dados foram feitas aos 30 minutos após o início da administração do desfluorano (MO), 15 minutos após a administração do opióide ou placebo (M15), e a cada 15 minutos após Ml5 (M30, M45, M60 e M75). A avaliação estatística dos dados foi efetuada por meio de Análise de Perfil (P 0,05). Houve discreta redução da FC no GB, enquanto as outras variáveis cardiovasculares não tiveram redução significativa. A FONT FACE=Symbol>¦ /FONT> e o pH tiveram reduções no GB, enquanto a PaCO2 esteve aumentada. Concluiu-se que a inclusão da buprenorfina durante anestesia inalatória pelo desfluorano determina discretas alterações cardiovasculares, bem-como potencializa a hipoventilação promovida pelo desfluorano, com a manifestação de hipercapnia, o que não contra-indica o seu uso em pacientes estáveis.

Sevoflurano e desflurano sobre o ritmo cardíaco de cães tratados com infusão contínua de doses crescentes de adrenalina

The volatile anesthetics increase the sensibility of the myocardium or its conduction system to the action of endogenous and/or exogenous epinephrine, predisposing the animal to cardiac arrhythmias. Among the volatile anesthetics, sevoflurane and desflurane are quite recent drugs and even though they have antiarrhythmogenic characteristics, there arent studies comparing these properties. The aim of this work was to study comparatively the cardiac rhythm and observe occasional atrioventricular blockages in dogs anesthetized with desflurane and sevoflurane, receiving increasing doses of epinephrine. 20 healthy adult male and female mongrel dogs were used. The animals were separated in two groups (G1 and G2). In G1, anesthesia was induced with propofol (10mmg-1.kg-1IV) and maintained with sevoflurane (1.5 MAC). Thirty minutes after the begin of volatile anesthetic administration, the epinephrine infusion was initiated at a dose of 1mmg.kg-1.min-1. At each 10 minutes the dose was increased in 1mmg.kg-1.min-1 until 6mmg.kg-1.min-1. For G2, the same methodology was used, except that sevoflurane was replaced by desflurane (1.5 MAC). At each epinephrine dose, the non-sinusal cardiac beats were counted and the occurrence of atrioventricular blockages was evaluated. The numerical data were submitted to Profile analysis and Kruskall-Wallis. The results allow to conclude that desflurane reduces in a more efficient way the arrhythmia produced by epinephrine and also the occurrence of atrioventricular blockages.

Os anestésicos inalatórios sensibilizam o miocárdio ou seu sistema de condução à ação das catecolaminas endógenas e/ou exógenas, predispondo o animal às arritmias cardíacas. Dentre os anestésicos voláteis, o sevoflurano e o desflurano são fármacos relativamente recentes e, embora sejam dotados de características relacionadas a não sensibilização do miocárdio às catecolaminas, desconhecem-se estudos que comparem suas eventuais propriedades antiarritmogênicas. Com o objetivo de estudar, comparativamente, o comportamento do ritmo cardíaco e observar eventuais bloqueios atrioventriculares em cães anestesiados pelo sevoflurano e desflurano e submetidos à infusão contínua de adrenalina, foram utilizados 20 animais adultos, os quais foram separados em dois grupos de igual número (G1 e G2). Aos cães do G1, foi administrado propofol, na dose média de 10mmg.kg-1; em seguida os animais receberam sevoflurano, a 1,5CAM. Decorridos 30 minutos do início da administração do anestésico volátil, iniciou-se a infusão de adrenalina na dose de 1mmg.kg-1.min-1. A cada 10 minutos, a dose da catecolamina foi acrescida em uma unidade, cessando-se a administração em 6mmg.kg-1.min-1. Para o G2, empregou-se a mesma metodologia, substituindo-se o sevoflurano pelo desflurano, administrado a 1,5CAM. A cada dose de adrenalina, foi feita contagem de batimentos ventriculares ectópicos, bem como a observação de bloqueios atrioventriculares. Os achados foram tratados pelos métodos estatísticos de Análise de Perfil e Kruskall-Wallis. Os resultados permitiram concluir que o desflurano minimiza de maneira mais eficiente a arritmia induzida pela adrenalina, além de reduzir a incidência de bloqueios atrioventriculares.

Sevoflurano e desflurano sobre o ritmo cardíaco de cães tratados com infusão contínua de doses crescentes de adrenalina

The volatile anesthetics increase the sensibility of the myocardium or its conduction system to the action of endogenous and/or exogenous epinephrine, predisposing the animal to cardiac arrhythmias. Among the volatile anesthetics, sevoflurane and desflurane are quite recent drugs and even though they have antiarrhythmogenic characteristics, there arent studies comparing these properties. The aim of this work was to study comparatively the cardiac rhythm and observe occasional atrioventricular blockages in dogs anesthetized with desflurane and sevoflurane, receiving increasing doses of epinephrine. 20 healthy adult male and female mongrel dogs were used. The animals were separated in two groups (G1 and G2). In G1, anesthesia was induced with propofol (10mmg-1.kg-1IV) and maintained with sevoflurane (1.5 MAC). Thirty minutes after the begin of volatile anesthetic administration, the epinephrine infusion was initiated at a dose of 1mmg.kg-1.min-1. At each 10 minutes the dose was increased in 1mmg.kg-1.min-1 until 6mmg.kg-1.min-1. For G2, the same methodology was used, except that sevoflurane was replaced by desflurane (1.5 MAC). At each epinephrine dose, the non-sinusal cardiac beats were counted and the occurrence of atrioventricular blockages was evaluated. The numerical data were submitted to Profile analysis and Kruskall-Wallis. The results allow to conclude that desflurane reduces in a more efficient way the arrhythmia produced by epinephrine and also the occurrence of atrioventricular blockages.

Os anestésicos inalatórios sensibilizam o miocárdio ou seu sistema de condução à ação das catecolaminas endógenas e/ou exógenas, predispondo o animal às arritmias cardíacas. Dentre os anestésicos voláteis, o sevoflurano e o desflurano são fármacos relativamente recentes e, embora sejam dotados de características relacionadas a não sensibilização do miocárdio às catecolaminas, desconhecem-se estudos que comparem suas eventuais propriedades antiarritmogênicas. Com o objetivo de estudar, comparativamente, o comportamento do ritmo cardíaco e observar eventuais bloqueios atrioventriculares em cães anestesiados pelo sevoflurano e desflurano e submetidos à infusão contínua de adrenalina, foram utilizados 20 animais adultos, os quais foram separados em dois grupos de igual número (G1 e G2). Aos cães do G1, foi administrado propofol, na dose média de 10mmg.kg-1; em seguida os animais receberam sevoflurano, a 1,5CAM. Decorridos 30 minutos do início da administração do anestésico volátil, iniciou-se a infusão de adrenalina na dose de 1mmg.kg-1.min-1. A cada 10 minutos, a dose da catecolamina foi acrescida em uma unidade, cessando-se a administração em 6mmg.kg-1.min-1. Para o G2, empregou-se a mesma metodologia, substituindo-se o sevoflurano pelo desflurano, administrado a 1,5CAM. A cada dose de adrenalina, foi feita contagem de batimentos ventriculares ectópicos, bem como a observação de bloqueios atrioventriculares. Os achados foram tratados pelos métodos estatísticos de Análise de Perfil e Kruskall-Wallis. Os resultados permitiram concluir que o desflurano minimiza de maneira mais eficiente a arritmia induzida pela adrenalina, além de reduzir a incidência de bloqueios atrioventriculares.

Alterações cardiovasculares e intracranianas promovidas pela buprenorfina em cães anestesiados com desflurano

The aim of this work was to study the possible alterations on cardiovascular and intracranial parameters caused by buprenorphine, in dogs anesthetized with desflurane. Eight adult healthy male and female mongrel dogs were used. The anesthetic induction was made using propofol (IV), and immediately after, the dogs were intubated and the tube was connected to a volatile anesthetic circuit, and desflurane was administrated at 1.5 MAC. The dogs were intrumented and 20 minutes after the introduction of the intracranial catheter, they received buprenorphine (0.02 mg/kg/IV). The animals were on mechanical ventilation during all the experimental period. Intracranial pressure (ICP), cerebral perfusion pressure (CPP), Heart Rate (HR); Systolic, Diastolic and Mean Arterial Blood Pressure (SAP, DAP and MAP, respectivelly); Cardiac Output (CO); Central Venous Pressure (CVP) and Pulmonar Arterial Pressure (PAP) were evaluated. The measurements were realized 20 minutes after the introduction of the intracranial catheter (M1); 15 minutes after buprenorphine administration (M2); and at each 15 minutes after M2 (M3, M4 and M5). The numerical data were analysed by use of ANOVA followed by a Tukeys test (p 0.05). Intracranial pressure was stable during all the experimental period, being observed only a decrease of the CPP after buprenorphine administration (M2). After buprenorphine administration (M2), there was a reduction in cardiovascular values: HR, PAP, SAP, DAP and MAP. During all the study, these values remained lower than the initial values, but were within normal values to the species. The CO and CVP were also decreased, but not statistically significant. The results allow us to conclude that buprenorphine didnt interfere with intracranial pressure. Although, the marked decrease of arterial pressure due to buprenorphine administration caused a reduction of the cerebral perfusion pressure in dogs anesthetized with desflurane.

Objetivou-se com a realização deste experimento, estudar possíveis alterações nas variáveis cardiovasculares e intracranianas promovidas pela buprenorfina, em cães anestesiados com desflurano. Para tanto, foram utilizados oito cães adultos, clinicamente saudáveis. A anestesia foi induzida com propofol (8 mg/kg IV) e em seguida os animais foram intubados com sonda orotraqueal de Magill, a qual foi conectada ao aparelho de anestesia volátil para administração de desflurano (1,5 CAM). Os animais foram mantidos sob ventilação controlada durante todo o período experimental. Após 20 minutos do posicionamento do cateter de pressão intracraniana (PIC), administrou-se buprenorfina (0,02 mg/kg IV). Foram avaliados: PIC; pressão de perfusão cerebral (PPC); FC; PAS, PAM e PAD; débito cardíaco (DC); pressão venosa central (PVC); e pressão da artéria pulmonar (PAP). As colheitas foram feitas nos seguintes momentos: M1 - 20 minutos após o posicionamento do cateter de PIC; M2 - 15 minutos após a administração do opióide; M3, M4 e M5 - de 15 em 15 minutos após M2. A avaliação estatística dos dados foi efetuada por meio de ANOVA seguida do Teste de Tukey (p 0,05). A PIC permaneceu estável durante todo o período experimental. Entretanto, registrou-se uma queda acentuada, estatisticamente significativa, da PPC após o M2. As variáveis cardiovasculares FC, PAS, PAM, PAD, DC e PAP, apresentaram redução significativa de seus valores após M2, mantendo-se estáveis no restante do período experimental. Quanto à PVC, o teste estatístico não registrou alterações significativas. Assim, pôde-se concluir que a buprenorfina não interferiu na PIC. Entretanto, a queda dos índices cardiovasculares, especialmente da PAM, determinada pela administração do opióide, causa redução da PPC em cães anestesiados com desflurano.

Efeitos da infusão contínua de cetamina sobre a pressão intra-ocular em cães hipovolêmicos anestesiados com desflurano / Effects of continuous infusion of ketamine on intraocular pressure in hypovolemic dogs during desflurane anesthesia

Compararam-se os efeitos de duas doses de cetamina, administradas em infusão contínua, sobre a pressão intra-ocular (PIO) de 18 cães submetidos à hipovolemia e à anestesia com desflurano. Promoveu-se a hipovolemia em todos os cães, retirando-se 40 ml de sangue/kg de peso. A anestesia foi induzida com desflurano, através de máscara facial, até que a intubação orotraqueal fosse permitida. Decorridos 30 minutos, para estabilização dos parâmetros, iniciou-se a infusão contínua de cetamina. Os cães foram distribuídos, aleatoriamente, em três grupos (n= 6). O grupo I (controle) recebeu solução salina estéril; o grupo II (GII) recebeu cetamina, na dose de 100mg/kg/min, e o grupo III (GIII), cetamina na dose de 200mg/kg/min. A PIO foi medida por tonometria de aplanação. Foram mensurados freqüência cardíaca (FC), ritmo cardíaco, pressão arterial média (PAM), débito cardíaco (DC), pressão venosa central (PVC) e pressão parcial de CO2 no final da expiração (ETCO2). O desflurano não influenciou os resultados da PIO, porém observou-se discreta ação da cetamina em todos os grupos. Foi possível estabelecer relação direta entre os valores de PIO e de ETCO2. A PIO apresentou relação direta somente com a ETCO2.(AU)

Effects of two dosages of continuous infusion of ketamine on the intraocular pressure (IOP) of 18 dogs, subjected to hypovolemia and anesthesia with desflurane were studied. Hypovolemia was induced in all dogs by withdrawal of 40ml of blood/kg of body weight. Initially, anesthesia was induced through face mask and then by tracheal intubation. After a delay of 30 minutes, for parameters stabilization, continuous infusion of ketamine was initiated. Dogs were randomly allotted in three groups (n =6): group I (control group) received continuous infusion of saline solution, group II received 100mg/kg/min of ketamine and group III received 200mg/kg/min of ketamine. IOP was measured by applanation tonometry. It was not possible to establish direct correlation between alterations of the mean arterial pressure and central venous pressure to those obtained to intraocular pressure. Desflurane did not affected values of intraocular pressure, however, direct action of ketamine was observed in all groups. It was possible to establish direct correlation between values of intraocular pressure and values of exhaled CO2.(AU)

Alterações cardiovasculares e intracranianas promovidas pela buprenorfina em cães anestesiados com desflurano

The aim of this work was to study the possible alterations on cardiovascular and intracranial parameters caused by buprenorphine, in dogs anesthetized with desflurane. Eight adult healthy male and female mongrel dogs were used. The anesthetic induction was made using propofol (IV), and immediately after, the dogs were intubated and the tube was connected to a volatile anesthetic circuit, and desflurane was administrated at 1.5 MAC. The dogs were intrumented and 20 minutes after the introduction of the intracranial catheter, they received buprenorphine (0.02 mg/kg/IV). The animals were on mechanical ventilation during all the experimental period. Intracranial pressure (ICP), cerebral perfusion pressure (CPP), Heart Rate (HR); Systolic, Diastolic and Mean Arterial Blood Pressure (SAP, DAP and MAP, respectivelly); Cardiac Output (CO); Central Venous Pressure (CVP) and Pulmonar Arterial Pressure (PAP) were evaluated. The measurements were realized 20 minutes after the introduction of the intracranial catheter (M1); 15 minutes after buprenorphine administration (M2); and at each 15 minutes after M2 (M3, M4 and M5). The numerical data were analysed by use of ANOVA followed by a Tukey’s test (p 0.05). Intracranial pressure was stable during all the experimental period, being observed only a decrease of the CPP after buprenorphine administration (M2). After buprenorphine administration (M2), there was a reduction in cardiovascular values: HR, PAP, SAP, DAP and MAP. During all the study, these values remained lower than the initial values, but were within normal values to the species. The CO and CVP were also decreased, but not statistically significant. The results allow us to conclude that buprenorphine didn’t interfere with intracranial pressure. Although, the marked decrease of arterial pressure due to buprenorphine administration caused a reduction of the cerebral perfusion pressure in dogs anesthetized with desflurane.

Objetivou-se com a realização deste experimento, estudar possíveis alterações nas variáveis cardiovasculares e intracranianas promovidas pela buprenorfina, em cães anestesiados com desflurano. Para tanto, foram utilizados oito cães adultos, clinicamente saudáveis. A anestesia foi induzida com propofol (8 mg/kg IV) e em seguida os animais foram intubados com sonda orotraqueal de Magill, a qual foi conectada ao aparelho de anestesia volátil para administração de desflurano (1,5 CAM). Os animais foram mantidos sob ventilação controlada durante todo o período experimental. Após 20 minutos do posicionamento do cateter de pressão intracraniana (PIC), administrou-se buprenorfina (0,02 mg/kg IV). Foram avaliados: PIC; pressão de perfusão cerebral (PPC); FC; PAS, PAM e PAD; débito cardíaco (DC); pressão venosa central (PVC); e pressão da artéria pulmonar (PAP). As colheitas foram feitas nos seguintes momentos: M1 - 20 minutos após o posicionamento do cateter de PIC; M2 - 15 minutos após a administração do opióide; M3, M4 e M5 - de 15 em 15 minutos após M2. A avaliação estatística dos dados foi efetuada por meio de ANOVA seguida do Teste de Tukey (p 0,05). A PIC permaneceu estável durante todo o período experimental. Entretanto, registrou-se uma queda acentuada, estatisticamente significativa, da PPC após o M2. As variáveis cardiovasculares FC, PAS, PAM, PAD, DC e PAP, apresentaram redução significativa de seus valores após M2, mantendo-se estáveis no restante do período experimental. Quanto à PVC, o teste estatístico não registrou alterações significativas. Assim, pôde-se concluir que a buprenorfina não interferiu na PIC. Entretanto, a queda dos índices cardiovasculares, especialmente da PAM, determinada pela administração do opióide, causa redução da PPC em cães anestesiados com desflurano.

Efeitos eletrocardiográficos do butorfanol em cães anestesiados pelo desfluorano

The aim of this work was to evaluate the alterations due to butorphanol administration in desflurane anesthetized dogs over heart rate (HR) and electrocardiography (ECG). Twenty adult dogs, males and females, clinically healthy were randomly distributed in two groups of ten animals each (GS and GB). General anesthesia was induced by intravenous administration of propofol (8.4± 0.8mg kg-1) and immediately, the dogs were intubated and submitted to inhalatory anesthesia with desflurane (10V%). After 40 minutes of induction, animals from GS received saline solution at 0.9% (0.05mL kg-1) and from GB received butorphanol (0.4mg kg-1), both applied intramuscularly. Observations of the variables heart rate (HR), duration and amplitude of P wave (Ps e PmV), P-R intervals (PR), QRS complex duration (QRSs), R wave amplitude (RmV), Q-T intervals (QT) and R-R intervals (RR) started immediately before the application of the agents (M0). Serial measurements were carried out in 15 minute intervals after the administration of butorphanol or saline up to 75 minutes, respectively M15, M30, M45, M60 and M75. Numeric data were submitted to Profile Analysis (p 0.05). Heart rate (HR) decreased significantly after butorphanol administration while RR and QT intervals increased. These results allowed to conclude that butorphanol administration in desflurane anesthetized dogs decreases heart rate and promotes a delay in ventricular repolarization.

Objetivou-se com este experimento avaliar as possíveis alterações eletrocardiográficas decorrentes do uso do butorfanol em cães, durante anestesia geral inalatória com desfluorano. Para tal, foram utilizados vinte cães adultos, clinicamente saudáveis, distribuídos em dois grupos (n=10) denominados de GS e GB. Os animais foram induzidos à anestesia com propofol (8,4 ± 0,8mg kg-1, IV) intubados com sonda orotraqueal de Magill e submetidos à anestesia inalatória pelo desfluorano (10V%). Decorridos 40 minutos da indução, foi administrado aos animais do GS, por via intramuscular, 0,05mL kg-1 de solução fisiológica a 0,9% (salina), enquanto que no GB, foi aplicado butorfanol na dose de 0,4mg kg-1 pela mesma via e em volume equivalente ao empregado no grupo anterior. As observações das variáveis freqüência cardíaca (FC), duração e amplitude da onda P (Ps e PmV), intervalo entre as ondas P e R (PR), duração do complexo QRS (QRSs), amplitude da onda R (RmV), duração do intervalo entre as ondas Q e T (QT) e intervalo entre duas ondas R (RR) tiveram início imediatamente antes da aplicação do opióide ou salina (M0). Novas mensurações foram realizadas 15 minutos após a administração do butorfanol ou salina (M15) e as demais colheitas foram realizadas à intervalos de 15 minutos, por um período de 60 minutos (M30, M45, M60 e M75). Os dados numéricos destas variáveis foram submetidos à Análise de Perfil (p 0,05). A freqüência cardíaca apresentou alteração no GB, com média de M0 maior que as demais enquanto que os intervalos RR e QT apresentaram valores de M0 menor que os demais no GB. Os resultados obtidos permitem concluir que a administração do butorfanol em cães submetidos à anestesia pelo desfluorano reduz a freqüência cardíaca e promove retardo na repolarização ventricular.