Effects of pulse-delivered inhaled nitric oxide administration on pulmonary perfusion and arterial oxygenation in dorsally recumbent isoflurane-anesthetized horses.

OBJECTIVE: To image the spatial distribution of pulmonary blood flow by means of scintigraphy, evaluate ventilation-perfusion (VA/Q) matching and pulmonary blood shunting (Qs/Qt) by means of the multiple inert gas elimination technique (MIGET), and measure arterial oxygenation and plasma endothelin-1 concentrations before, during, and after pulse-delivered inhaled nitric oxide (PiNO) administration to isoflurane-anesthetized horses in dorsal recumbency. ANIMALS: 3 healthy adult Standardbreds. PROCEDURES: Nitric oxide was pulsed into the inspired gases in dorsally recumbent isoflurane-anesthetized horses. Assessment of VA/Q matching, Qs/Qt, and Pao2 content was performed by use of the MIGET, and spatial distribution of pulmonary blood flow was measured by perfusion scintigraphy following IV injection of technetium Tc 99m-labeled macroaggregated human albumin before, during, and 30 minutes after cessation of PiNO administration. RESULTS: During PiNO administration, significant redistribution of blood flow from the dependent regions to the nondependent regions of the lungs was found and was reflected by improvements in VA/Q matching, decreases in Qs/Qt, and increases in Pao2 content, all of which reverted to baseline values at 30 minutes after PiNO administration. CONCLUSIONS AND CLINICAL RELEVANCE: Administration of PiNO in anesthetized dorsally recumbent horses resulted in redistribution of pulmonary blood flow from dependent atelectatic lung regions to nondependent aerated lung regions. Because hypoxemia is commonly the result of atelectasis in anesthetized dorsally recumbent horses, the addition of nitric oxide to inhaled gases could be used clinically to alleviate hypoxemia in horses during anesthesia.

The effects of pulse-delivered inhaled nitric oxide on arterial oxygenation, ventilation-perfusion distribution and plasma endothelin-1 concentration in laterally recumbent isoflurane-anaesthetized horses.

OBJECTIVES: Anaesthetized horses commonly become hypoxaemic due to ventilation/perfusion (V·A/Q·) mismatch and increased pulmonary shunt fraction (Qs·/Qt·). Pulse-delivered inhaled nitric oxide may improve oxygenation but may increase plasma concentration of the potent vasoconstrictor, endothelin-1 (ET-1). Objectives: Study 1) compare arterial oxygen concentration (PaO2) and saturation (SaO2), calculated Qs·/Qt· and ET-1 concentration; and Study 2) assess V·A/Q· matching and measured Qs·/Qt· in isoflurane-anaesthetized horses in left lateral recumbency receiving pulse-delivered inhaled nitric oxide (PiNO group) or inhalant gas only (C group). STUDY DESIGN: Prospective research trial. ANIMALS: Ten Healthy adult Standardbred horses. Two horses were anaesthestized in both groups in a random cross-over design with >4 weeks between studies. METHODS: Study 1) Cardiopulmonary data including PaO2, SaO2, Qs·/Qt· and ET-1 concentration were measured or calculated prior to and at various points during PiNO administration in 6PiNO and 6C horses. Two-way repeated measures anova with Bonferroni significant difference test was used for data analysis with p < 0.05 considered significant. Study 2) V·A/Q· matching and Qs·/Qt· were determined using the multiple inert gas elimination technique in 3 horses. Data were collected after 60 minutes of anaesthesia without PiNO (baseline) and 15 minutes after PiNO was pulsed during the first 30%, and then the first 60%, of inspiration. Data were descriptive only. RESULTS: Study 1) PaO2 and SaO2 were higher and calculated Qs·/Qt· was lower in the PiNO group than the C group at most time points. ET-1 was not different over time or between groups. Study 2) V·A/Q· matching and measured Qs·/Qt· were improved from baseline in all horses but PiNO60% provided no improvement when compared to PiNO30%. CONCLUSIONS AND CLINICAL RELEVANCE: PiNO delivered in the initial portion of the inspiration effectively relieves hypoxaemia in anaesthetized horses by improving V·A/Q· matching and decreasing Qs·/Qt· without affecting ET-1.

Oxygenation and plasma endothelin-1 concentrations in healthy horses recovering from isoflurane anaesthesia administered with or without pulse-delivered inhaled nitric oxide.

OBJECTIVE: To assess oxygenation, ventilation-perfusion (V/Q) matching and plasma endothelin (ET-1) concentrations in healthy horses recovering from isoflurane anaesthesia administered with or without pulse-delivered inhaled nitric oxide (iNO). STUDY DESIGN: Prospective experimental trial. ANIMALS: Healthy adult Standardbred horses. METHODS: Horses were anaesthetized with isoflurane in oxygen and placed in lateral recumbency. Six control (C group) horses were anaesthetized without iNO delivery and six horses received pulse-delivered iNO (NO group). After 2.5 hours of anaesthesia isoflurane and iNO were abruptly discontinued, inhaled oxygen was reduced from 100% to approximately 30%, and the horses were moved to the recovery stall. At intervals during a 30-minute period following the discontinuation of anaesthesia, arterial and mixed venous blood gas values, shunt fraction (Qs/Qt), plasma ET-1 concentration, pulse rate and respiratory rate were measured or calculated. Repeated measures anova and a Bonferroni post hoc test was used to analyze data with significance set at p < 0.05. RESULTS: At all time points in the recovery period, NO horses maintained better arterial oxygenation (oxygen partial pressure: NO 13.2 ± 2.7-11.1 ± 2.7 versus C 6.7 ± 1.1-7.1 ± 1.1 kPa) and better V/Q matching (Qs/Qt NO 0.23 ± 0.05-0.14 ± 0.06 versus C 0.48 ± 0.03-0.32 ± 0.08%) than C horses. Mixed venous oxygenation was higher in NO for 25 minutes following the discontinuation of anaesthesia (NO 6.3 ± 0.2-4.5 ± 0.07 versus C 4.7 ± 0.6-3.7 ± 0.3 kPa). In both groups of horses arterial oxygenation remained fairly stable; venous oxygenation declined over this time period in the NO group but still remained higher than venous oxygen in the C group. ET-1 concentrations were higher at most time points in C than NO. Changes in other parameters were either minor or absent. CONCLUSIONS AND CLINICAL RELEVANCE: Delivery of iNO to healthy horses during anaesthesia results in better arterial and venous oxygenation and V/Q matching (as determined by lower Qs/Qt) and lower ET-1 concentrations throughout a 30-minute anaesthetic recovery period.

Effect of sedation with detomidine and butorphanol on pulmonary gas exchange in the horse.

BACKGROUND: Sedation with alpha2-agonists in the horse is reported to be accompanied by impairment of arterial oxygenation. The present study was undertaken to investigate pulmonary gas exchange using the Multiple Inert Gas Elimination Technique (MIGET), during sedation with the alpha2-agonist detomidine alone and in combination with the opioid butorphanol. METHODS: Seven Standardbred trotter horses aged 3-7 years and weighing 380-520 kg, were studied. The protocol consisted of three consecutive measurements; in the unsedated horse, after intravenous administration of detomidine (0.02 mg/kg) and after subsequent butorphanol administration (0.025 mg/kg). Pulmonary function and haemodynamic effects were investigated. The distribution of ventilation-perfusion ratios (VA/Q) was estimated with MIGET. RESULTS: During detomidine sedation, arterial oxygen tension (PaO2) decreased (12.8 +/- 0.7 to 10.8 +/- 1.2 kPa) and arterial carbon dioxide tension (PaCO2) increased (5.9 +/- 0.3 to 6.1 +/- 0.2 kPa) compared to measurements in the unsedated horse. Mismatch between ventilation and perfusion in the lungs was evident, but no increase in intrapulmonary shunt could be detected. Respiratory rate and minute ventilation did not change. Heart rate and cardiac output decreased, while pulmonary and systemic blood pressure and vascular resistance increased. Addition of butorphanol resulted in a significant decrease in ventilation and increase in PaCO2. Alveolar-arterial oxygen content difference P(A-a)O2 remained impaired after butorphanol administration, the VA/Q distribution improved as the decreased ventilation and persistent low blood flow was well matched. Also after subsequent butorphanol no increase in intrapulmonary shunt was evident. CONCLUSION: The results of the present study suggest that both pulmonary and cardiovascular factors contribute to the impaired pulmonary gas exchange during detomidine and butorphanol sedation in the horse.

Effects of acepromazine on pulmonary gas exchange and circulation during sedation and dissociative anaesthesia in horses.

OBJECTIVE: To study pulmonary gas exchange and cardiovascular responses to sedation achieved with romifidine and butorphanol (RB) alone, or combined with acepromazine, and during subsequent tiletamine-zolazepam anaesthesia in horses. ANIMALS: Six (four males and two females) healthy Standardbred trotters aged 3-12 years; mass 423-520 kg. STUDY DESIGN: Randomized, cross-over, experimental study. MATERIALS AND METHODS: Horses were anaesthetized on two occasions (with a minimum interval of 1 week) with intravenous (IV) tiletamine-zolazepam (Z; 1.4 mg kg(-1)) after pre-anaesthetic medication with IV romifidine (R; 0.1 mg kg(-1)) and butorphanol (B; 25 microg kg(-1) IV). At the first trial, horses were randomly allocated to receive (protocol ARBZ) or not to receive (protocol RBZ) acepromazine (A; 35 microg kg(-1)) intramuscularly (IM) 35 minutes before induction of anaesthesia. Each horse was placed in left lateral recumbency and, after tracheal intubation, allowed to breathe room air spontaneously. Respiratory and haemodynamic variables and ventilation-perfusion (; multiple inert gas elimination technique) ratios were determined in the conscious horse, after sedation and during anaesthesia. One- and two-way repeated-measures anova were used to identify within- and between-technique differences, respectively. RESULTS: During sedation with RB, arterial oxygen tension (PaO(2)) decreased compared to baseline and increased mismatch was evident; there was no O(2) diffusion limitation or increase in intrapulmonary shunt fraction identified. With ARB, PaO(2) and remained unaffected. During anaesthesia, intrapulmonary shunt occurred to the same extent in both protocols, and mismatching increased. This was less in the ARBZ group. Arterial O(2) tension decreased in both protocols, but was lower at 25 and 35 minutes of anaesthesia in RBZ than in ARBZ. During sedation, heart rate (HR) and cardiac output (Qt) were lower while arterial-mixed venous oxygen content differences and haemoglobin concentrations were higher in RBZ compared with ARBZ. Total systemic vascular resistance, mean systemic, and mean pulmonary arterial pressures were higher during anaesthesia with RBZ compared to ARBZ. CONCLUSIONS AND CLINICAL RELEVANCE: Acepromazine added to RB generally improved haemodynamic variables and arterial oxygenation during sedation and anaesthesia. Arterial oxygenation was impaired as a result of increased shunt and mismatch during anaesthesia, although acepromazine treatment reduced disturbances and falls in PaO(2) to some extent. Haemodynamic variables were closer to baseline during sedation and anaesthesia when horses received acepromazine. Acepromazine may confer advantages in healthy normovolaemic horses.