Hemodynamic effects of incremental doses of acepromazine in isoflurane-anesthetized dogs.

OBJECTIVE: To evaluate the effects of incremental doses of acepromazine on hemodynamics in isoflurane-anesthetized dogs. STUDY DESIGN: Prospective, experimental study. ANIMALS: Healthy, adult, mixed-breed dogs (two male and four female) weighing 16.8 ± 5.1 kg (mean ± standard deviation). METHODS: Dogs were anesthetized with propofol (7 mg kg-1) intravenously (IV) and isoflurane. Thermodilution and arterial catheters were placed for hemodynamic monitoring and arterial blood sampling for blood gas analysis. Baseline measurements were performed with stable expired concentration of isoflurane (Fe'Iso) at 1.8%. Each dog was then administered four incremental acepromazine injections (10, 15, 25 and 50 µg kg-1) IV, and measurements were repeated 20 minutes after each acepromazine injection with Fe'Iso decreased to 1.2%. The four acepromazine injections resulted in cumulative doses of 10, 25, 50 and 100 µg kg-1 (time points ACP10, ACP25, ACP50 and ACP100, respectively). RESULTS: Compared with baseline, cardiac index (CI) increased significantly by 34%, whereas systemic vascular resistance index (SVRI) decreased by 25% at ACP50 and ACP100. Arterial oxygen content (CaO2) was significantly lower than baseline after all acepromazine injections (maximum decreases of 11%) and was lower at ACP50 and ACP100 than at ACP10. No significant change was found in heart rate, stroke index, oxygen delivery index and systolic, mean and diastolic blood pressures. Hypotension (mean arterial pressure < 60 mmHg) was observed in one dog at baseline, ACP10, ACP25 and ACP100, and in two dogs at ACP50. CONCLUSIONS AND CLINICAL RELEVANCE: Compared with isoflurane alone, anesthesia with acepromazine-isoflurane resulted in increased CI and decreased SVRI and CaO2 values. These effects were dose-related, being more pronounced at ACP50 and ACP100. Under the conditions of this study, acepromazine administration did not change blood pressure.

Hemodynamic, respiratory and sedative effects of progressively increasing doses of acepromazine in conscious dogs.

OBJECTIVE: To evaluate the effects of progressively increasing doses of acepromazine on cardiopulmonary variables and sedation in conscious dogs. STUDY DESIGN: Prospective, experimental study. ANIMALS: A group of six healthy, adult, mixed-breed dogs weighing 16.5 ± 5.0 kg (mean ± standard deviation). METHODS: Dogs were instrumented with thermodilution and arterial catheters for evaluation of hemodynamics and arterial blood gases. On a single occasion, acepromazine was administered intravenously to each dog at 10, 15, 25 and 50 µg kg-1 at 20 minute intervals, resulting in cumulative acepromazine doses of 10 µg kg-1 (ACP10), 25 µg kg-1 (ACP25), 50 µg kg-1 (ACP50) and 100 µg kg-1 (ACP100). Hemodynamic data and sedation scores were recorded before (baseline) and 20 minutes after each acepromazine dose. RESULTS: Compared with baseline, all acepromazine doses significantly decreased stroke index (SI), mean arterial pressure (MAP) and arterial oxygen content (CaO2) with maximum decreases of 16%, 17% and 21%, respectively. Cardiac index (CI) decreased by up to 19% but not significantly. Decreases of 26-38% were recorded for oxygen delivery index (DO2I), with significant differences for ACP50 and ACP100. Systemic vascular resistance index (SVRI) and heart rate did not change significantly. No significant difference was found among acepromazine doses for hemodynamic data. After ACP10, mild sedation was observed in five/six dogs and moderate sedation in one/six dogs, whereas after ACP25, ACP50 and ACP100, moderate sedation was observed in five/six or six/six dogs. CONCLUSIONS AND CLINICAL RELEVANCE: In conscious dogs, acepromazine decreased MAP, SI, CaO2 and DO2I, but no significant dose effect was detected. SVRI was not significantly changed, suggesting that the reduction in MAP resulted from decreased CI. The ACP25, ACP50 and ACP100 doses resulted in moderate sedation in most dogs; ACP10 resulted in only mild sedation.

Correcting Campylorrhinus Lateralis in a Foal by Bone Distraction: A Case Report.

Campylorrhinus lateralis, also known as "wry nose," is a congenital malformation that mainly affects Thoroughbreds. These horses have a unilateral deviation of the maxillae that may be to one side or the other side, and it causes airway obstruction and dental malocclusion. The choice of treatment is not necessarily operation; however, the treatment of choice, which aims to repair the maxillae deviation, is surgical to improve the horse's respiratory condition and correct the dental occlusion. There are currently no reports describing the first surgical technique for such deformity described by Valdez et al. The present study describes the case of a 2-month-old foal of the Mangalarga Marchador breed that was diagnosed with wry nose. The foal presented with accentuated maxillae deviation to the right side, malocclusion of the incisor teeth, and respiratory noises. After diagnosis and physical examination, the foal was treated by surgical correction of the deviation. To correct the deviation, the bone distraction technique with unilateral osteotomy of the right maxillae and fixation of the external bone distractor was chosen. After 90 days, the bone distractor was removed; consequently, malocclusion of the incisors was greatly improved, and respiratory noises were eliminated.

Effects of 3 morphine doses, in combination with acepromazine, on sedation and some physiological parameters in dogs.

This study evaluated the effects of 3 morphine doses combined with acepromazine, on sedation and physiological parameters in 5 clinically healthy dogs. Four treatments were administered intramuscularly in a randomized, blinded, crossover design: acepromazine, 0.05 mg/kg, alone (ACP) and acepromazine plus morphine at doses of 0.25, 0.5, and 1.0 mg/kg body weight (BW) (AM0.25, AM0.5, and AM1.0, respectively). Sedation scores and cardiorespiratory variables were evaluated for 120 min after drug administration. The sedation scores were significantly higher with the AM0.25 and AM1.0 treatments than with the ACP treatment. At 30 min the scores were 36% to 66% higher with AM1.0 than with AM0.25 and AM0.5, respectively, but these differences were not significant. The physiological variables remained acceptable for dogs. The results of this study do not support the use of AM0.5 over AM0.25 to improve sedation in dogs, but they do indicate that sedation may be greater with AM1.0 than with AM0.25 and AM0.5. Studies with a greater number of samples are warranted to confirm this statement.

Cette étude visait à évaluer les effets de trois doses de morphine combinées à de l'acépromazine, sur la sédation et des paramètres physiologiques chez cinq chiens cliniquement en santé. Quatre traitements furent administrés par voie intramusculaire dans un design croisé randomisé à l'aveugle : acépromazine, 0,05 mg/kg seule (ACP) et acépromazine plus morphine à des doses de 0,25, 0,5, et 1,0 mg/kg de poids corporel (AM0,25, AM0,5, et AM1,0, respectivement). Les pointages de sédation et des variables cardiorespiratoires furent évalués pour 120 min après l'administration des drogues. Les pointages de sédation étaient significativement plus élevés avec les traitements AM0,25 et AM1,0 qu'avec le traitement ACP. À 30 min, les pointages étaient 36 % et 66 % plus élevés avec AM1,0 qu'avec AM0,25 et AM0,5, respectivement, mais ces différences n'étaient pas significatives. Les variables physiologiques sont demeurées acceptables pour les chiens. Les résultats de cette étude ne militent pas en faveur de l'utilisation d'AM0,5 par rapport à AM0,25 pour améliorer la sédation chez les chiens, mais ils indiquent que la sédation peut être plus grande avec AM1,0 qu'avec AM0,25 et AM0,5. Des études avec un plus grand nombre d'échantillons sont requises pour confirmer cet énoncé.(Traduit par Docteur Serge Messier).

Establishment of an experimental model of small intestinal ischemia and reperfusion injuries in New Zealand rabbits / Estabelecimento de modelo experimental de indução da lesão de isquemia e reperfusão de intestino delgado em coelhos Nova Zelândia

The present study aimed to establish a methodology capable to cause intestinal ischemia and reperfusion injuries, to perform clamping of the jejunal segment of the extramural peri-intestinal marginal artery branch. For this, 37, 10-week-old male New Zealand breed rabbits were used. One rabbit was used to establish the anatomic references for the procedure and was not part of the six experimental groups; the rest were allocated into six experimental groups: Sham group, negative control, subjected only to midline celiotomy; group I1H undergoing vascular occlusion for an hour; group I2H submitted to vascular occlusion for two hours; group I1H/R2H undergoing vascular occlusion for one hour followed by two hours of reperfusion; group I2H/R1H undergoing vascular occlusion for two hours, followed by reperfusion for one hour, and group I2H/R5H undergoing vascular occlusion for two hours followed by reperfusion for five hours. The rabbits were evaluated for the macroscopic aspects (color and peristalsis) of the jejunal segment, as well as the histological aspect, checking for presence or absence of mucosal destruction, edema, hemorrhaging, lymphatic vessel dilatation, and the presence of polymorphonuclear cells. It was observed that the macroscopic and histopathological lesions accentuated in larger employed ischemia and reperfusion times. Rabbits subjected to ischemia for two hours followed by reperfusion for five hours (I2H/R5H) made up the experimental group which was easily reproducible and showed moderate intestinal injury, different from the other groups.(AU)

O presente estudo objetivou estabelecer uma metodologia capaz de causar lesões de isquemia e reperfusão intestinal, realizando clipagem de um ramo de artéria marginal peri-intestinal extramural em segmento jejunal. Para tal foram utilizados 37 coelhos da raça Nova Zelândia, machos, de 10 semanas de idade, alocados em seis grupos experimentais: grupo Sham, controle negativo, submetido apenas a celiotomia mediana; grupo I1H submetido à oclusão vascular por uma hora; grupo I2H submetido a oclusão vascular por duas horas; grupo I1H/R2H submetido a oclusão vascular por uma hora, seguida de reperfusão por duas horas; grupo I2H/R1H submetido a oclusão vascular por duas horas, seguida de reperfusão por uma hora e grupo I2H/R5H submetido a oclusão vascular por duas horas seguida de reperfusão por cincos horas. Os animais foram avaliados quanto o aspecto macroscópico (coloração e peristaltismo) do segmento jejunal e quanto ao aspecto histopatológico, verificando presença ou ausência de destruição de mucosa, edema, hemorragia, dilatação de vasos linfáticos e presença de polimorfonucleares. Observou-se que as lesões macroscópicas e histopatológicas se acentuaram nos maiores tempos de isquemia e reperfusão empregados. Os animais submetidos à isquemia durante duas horas, seguida de reperfusão por cinco horas (I2H/R5H) compuseram o grupo experimental de fácil reprodução e foram os que apresentaram uma lesão intestinal moderada, diferentes dos demais grupos.(AU)

Allogenic mesenchymal stem cell intravenous infusion in reparation of mild intestinal ischemia/reperfusion injury in New Zealand rabbits / Infusão intravenosa de células tronco mesenquimais alógenas na reparação da lesão branda de isquemia/reperfusão intestinal em coelhos Nova Zelândia

The present study aimed to evaluate the efficacy of mesenchymal stem cell (MSC) infusion, derived from adipose tissue, on reduction of local and remote tissue damage caused by the event of experimental intestinal I/R in New Zealand breed rabbits. For obtaining, characterization, and cultivation of MSC derived from adipose tissue (MSC-Adp), 3 juvenile animals (four months old) were used. The cells were considered to be viable for therapy after the fourth passage (in vitro phase). For the in vivo stage, 24 young adult animals (six months old) were used, weighing approximately 3.5 kg, in which were randomly divided into two groups, called: IR treated with MSC (I2H/R5H MSC 3D; I2H/R5H MSC 7D); IR treated with PBS (I2H/R5H PBS 3D; I2H/R5H PBS 7D). The animals were anesthetized and submitted to pre-retro-umbilical midline celiotomy. The extramural peri-intestinal marginal artery was located and clamped (predetermined and standardized region) with the aid of a vascular clip, promoting a 2 hour blood flow interruption. After this period, blood flow was reestablished, inhalatory anesthesia was suspended, and the animals awaken. After 5 hours of reperfusion, the treatments were performed by intravenous infusion according to the experimental groups. The animals were evaluated 72 hours and seven days after the treatment as for the macroscopic appearance (color and peristaltism) of the jejunal segment, and by histological evaluation of the ischemic segment for the presence or absence of destruction of the intestinal mucosa, edema, bleeding, dilation of lymph vessels, and presence of polymorphonuclear inflammatory cells, both in the mucosa and submucosa. The observed results revealed that the groups treated with MSC-Adp obtained smaller mucosal and submucosal lesions when compared to the groups treated with PBS. Also, MSC-Adp treated groups obtained controlled inflammatory response and higher mitotic rate, outcomes related to the therapeutic potential of MSC. Infusion of stem cells attenuated the lesions caused by intestinal I/R in both MSC groups when compared to the group treated with PBS.(AU)

O presente estudo teve como principal objetivo avaliar a eficácia da infusão células tronco mesenquimais (CTM) derivada de tecido adiposo sobre diminuição das lesões teciduais locais e remotas, causadas pelo evento de I/R intestinal experimental, em coelhos da raça Nova Zelândia. Para obtenção, cultivo e caracterização das CTM provenientes de tecido adiposo (ADCTM) foram utilizados 3 animais jovens. As células foram consideradas viáveis para terapia a partir da quarta passagem (fase in vitro). Para etapa in vivo foram utilizados 24 animais, adulto-jovens, pesando aproximadamente 3,5kg, divididos aleatoriamente em dois grupos experimentais, denominados IR Tratado com CTM (I2H/R5H CTM 3D; I2H/R5H CTM 7D); IR Tratado PBS (I2H/R5H PBS 3D; I2H/R5H PBS 7D). Os animais foram anestesiados e submetidos à celiotomia mediana pré-retroumbilical. A artéria marginal peri-intestinal extramural foi localizada e clampeada (região predeterminada e padronizada) com auxílio de um clipe vascular, promovendo uma interrupção do fluxo sanguíneo durante 2 horas. Após esse período, o fluxo sanguíneo foi restabelecido, a anestesia inalatória suspendida e os animais despertados. Após 5 horas de reperfusão realizou-se os tratamentos por infusão endovenosa, conforme grupos experimentais. Os animais foram avaliados 72 horas e sete dias após o tratamento quanto ao aspecto macroscópico (coloração e peristaltismo) do segmento jejunal e por meio de avaliação histológica do segmento isquemiado quanto à presença ou ausência de destruição de mucosa intestinal, edema, hemorragia, dilatação de vasos linfáticos e presença de células inflamatórias polimorfornucleares, tanto em mucosa quanto submucosa. Os resultados observados revelaram que os grupos tratados com ADCTM obtiveram menores lesões em mucosa e submucosa quando comprados aos grupos tratados com PBS. Ainda os grupos tratados com ADCTM obtiveram resposta inflamatória controlada e maior taxa mitótica, resultados relacionados ao potencial terapêutico das CTM.(AU)

Tramadol does not enhance sedation induced by acepromazine in dogs.

The sedative effect of acepromazine combined with 2 doses of tramadol [3 and 5 mg/kg body weight (BW)] was compared with the sedative effect of acepromazine alone in dogs and the effects of each sedative protocol on cardiorespiratory variables were examined. This was a prospective, randomized, blinded, crossover study. Each of 6 dogs received 3 treatments at 1-week intervals. During all anesthetic episodes, dogs received 0.05 mg/kg BW acepromazine. Approximately 25 min later, dogs were given physiological saline (control) or tramadol [3 mg/kg BW (TR3) or 5 mg/kg BW (TR5)]. All drugs were administered intravenously. Variables evaluated included heart rate (HR), respiratory rate (RR), systolic, mean, and diastolic blood pressures (SAP, MAP, and DAP), and sedation [by use of a simple descriptive scale (SDS, range: 0 to 3) and a numeric rating scale (NRS, range: 0 to 10)]. Variables were recorded 25 min after acepromazine and for 80 min after saline or tramadol. Acepromazine administration resulted in mild sedation in most dogs and decreased RR, SAP, MAP, and DAP in all treatments. Tramadol administration did not significantly increase SDS or NRS scores compared to acepromazine alone. The only exception to this rule was observed at 20 min after TR3, when NRS was higher in this group than in the control treatment. Administration of tramadol (TR3 and TR5) decreased HR. Under the conditions of this study, sedation induced by acepromazine with tramadol was similar to that of acepromazine alone. The main adverse effects of the combination were a decrease in blood pressure and HR, without clinical significance.

L'effet sédatif de l'acépromazine combiné à deux doses de tramadol [3 et 5 mg/kg de poids corporel (PC)] a été comparé à l'effet sédatif de l'acépromazine seul chez des chiens et les effets de chaque protocole de sédation sur des variables cardio-respiratoires ont été examinés. Il s'agissait d'une étude prospective croisée, randomisée, réalisée à l'aveugle. Chacun des six chiens a reçu trois traitements à des intervalles de 1 semaine. Durant tous les épisodes anesthétiques, les chiens ont reçu 0,05 mg/kg PC d'acépromazine. Environ 25 min plus tard, les chiens ont reçu de la saline physiologique (témoin) ou du tramadol [3 mg/kg PC (TR3) ou 5 mg/kg PC (TR5)]. Toutes les drogues étaient administrées par voie intraveineuse. Les variables évaluées incluaient le rythme cardiaque (RC), le rythme respiratoire (RR), les pressions sanguines systolique, moyenne, et diastolique (PSS, PSM, et PSD), et la sédation [en utilisant une échelle descriptive simple (EDS, écart : 0 à 3) et une échelle de gradation numérique (EGN, écart : 0 à 10)]. Les variables ont été enregistrées 25 min après l'acépromazine et pendant 80 min après l'administration de saline ou de tramadol. L'administration d'acépromazine a résulté en une légère sédation chez la plupart des chiens et on nota une diminution de RR, PSS, PSM, et PSD avec tous les traitements. L'administration de tramadol ne fit pas augmenter de manière significative les pointages EDS et EGN lorsque comparée à l'acépromazine seul. La seule exception à cette règle a été observée à 20 min après TR3, alors que l'EGN était plus élevée dans ce groupe comparativement au témoin. L'administration de tramadol (TR3 et TR5) entraîna une diminution du RC. Dans les conditions de la présente étude, la sédation induite par l'acépromazine avec du tramadol était similaire à celle de l'acépromazine seul. Les principaux effets adverses de la combinaison étaient une diminution de la pression sanguine et du RC, mais sans signification clinique.(Traduit par Docteur Serge Messier).

Effects of a prolonged infusion of fentanyl, with or without atropine, on the minimum alveolar concentration of isoflurane in dogs.

OBJECTIVES: To evaluate the effect of a prolonged constant rate infusion (CRI) of fentanyl on the minimum alveolar concentration (MAC) of isoflurane (ISOMAC ) and to establish whether concurrent atropine administration influences ISOMAC in dogs. STUDY DESIGN: Prospective, crossover study. ANIMALS: Six healthy dogs weighing 13.0 ± 4.1 kg. METHODS: Dogs were anesthetized with isoflurane under conditions of normocapnia and normothermia. Arterial blood pressure was monitored invasively. Each dog was administered two treatments, on different occasions, in a crossover design. The dogs were administered intravenously (IV) an atropine bolus 0.02 mg kg(-1) and CRI at 0.04 mg kg(-1) hour(-1) (fentanyl-atropine treatment) or no atropine (fentanyl treatment). For each dog, baseline ISOMAC was measured in duplicate using a tail clamp technique. Subsequently, all dogs were administered a fentanyl bolus (5 µg kg(-1)) and CRI (9 µg kg(-1) hour(-1)) IV, and ISOMAC was re-determined at 120 and 300 minutes after initiation of the fentanyl CRI. RESULTS: Baseline ISOMAC values in the fentanyl and fentanyl-atropine treatments were 1.38 ± 0.16% and 1.39 ± 0.14%, respectively. Fentanyl significantly decreased the ISOMAC by 50 ± 9% and 47 ± 13% after 120 minutes and by 51 ± 14% and 50 ± 9% after 300 minutes (p < 0.001) in the fentanyl and fentanyl-atropine treatments, respectively. Compared with baseline, heart rate decreased significantly in the fentanyl treatment by 35% and 43% at 120 and 300 minutes, respectively. In the fentanyl-atropine treatment, heart rate did not change significantly over time. In both treatments, systolic arterial pressure increased from baseline after fentanyl. CONCLUSIONS AND CLINICAL RELEVANCE: In this study, fentanyl reduced the ISOMAC by approximately 50%. The ISOMAC remained stable throughout the 300 minute CRI of fentanyl, suggesting no cumulative effect of the opioid. Atropine did not influence ISOMAC in dogs.