Few safe and effective anesthesia regimens have been described for use in rabbits, partially because of the susceptibility of this species to sometimes fatal respiratory depression. Although inhalant anesthetics are generally safer than injectable anesthetics, their use may be limited by lack of equipment or facilities. This study was conducted to compare effects of several injectable anesthetics in rabbits on response to noxious stimuli, heart rate, respiratory rate, and rectal temperature. Six injectable anesthetic combinations were administered to rabbits: xylazine-ethyl-(l-methyl-propyl) malonyl-thio-urea salt (EMTU), ketamine-EMTU, xylazine-pentobarbital, xylazine-acepromazine-ketamine (XAK), ketamine-chloral hydrate, and ketamine-xylazine. All combinations induced a depression of respiratory rate. Although rectal temperature values were reduced to some degree in each group, the most profound hypothermia was induced by XAK. The combination that induced the longest duration of anesthesia was XAK. It was concluded that XAK was preferable for longer periods of anesthesia (60 to 120 minutes), although it induces severe hypothermia. For short periods of anesthesia, xylazine-pentobarbital, xylazine-EMTU, or ketamine-xylazine were deemed adequate; however, xylazine-EMTU induced the best survivability and consistency.

The cardiopulmonary effects of thiopental sodium were studied in hypovolemic dogs from completion of until 1 hour after administration of the drug. Hypovolemia was induced by withdrawal of blood from dogs until mean arterial pressure of 60 mm of Hg was achieved. After stabilization at this pressure for 1 hour, 8 mg of thiopental/kg of body weight was administered IV to 7 dogs, and cardiopulmonary effects were measured. After blood withdrawal and prior to thiopental administration, heart rate and oxygen utilization ratio increased, whereas mean arterial pressure, mean pulmonary arterial pressure, central venous pressure, pulmonary wedge pressure, cardiac index, oxygen delivery, mixed venous oxygen tension, and mixed venous oxygen content decreased from baseline. Three minutes after thiopental administration, heart rate, mean arterial pressure, mean pulmonary arterial pressure, pulmonary vascular resistance, and mixed venous oxygen tension increased, whereas oxygen utilization ratio and arterial and mixed venous pH decreased from values measured prior to thiopental administration. Fifteen minutes after thiopental administration, heart rate was still increased; however by 60 minutes after thiopental administration, all measurements had returned to values similar to those obtained prior to thiopental administration.

The central arterial pharmacokinetics of alfentanil, a short-acting opioid agonist, were studied in rabbits, sheep, and dogs after short-duration infusion of the drug. Alfentanil was infused until a set end point (high-amplitude, slow-wave activity on the EEG) was reached. This required a larger alfentanil dose and a higher alfentanil arterial concentration in sheep, compared with rabbits and dogs. The plasma concentration-time data for each animal were fitted, using nonlinear regression, and in all animals, were best described by use of a triexponential function. In this study, differences in the disposition kinetics of alfentanil among the 3 species were found for only distribution clearance and initial distribution half-life. In dogs, compared with rabbits and sheep, the first distribution half-life was longer, probably because of pronounced drug-induced bradycardia (mean +/- SD, 48 +/- 21 beats/min). Distribution clearance was faster in sheep, compared with dogs, also probably because of better blood flow in sheep. Elimination half-life was similar in all species (rabbits, 62.4 +/- 11.3 minutes; sheep, 65.1 +/- 27.1 minutes; dogs, 58.3 +/- 10.3 minutes). This rapid half-life resulted from a small steady-state volume of distribution (rabbits, 908.3 +/- 269.0 ml/kg; sheep, 720.0 +/- 306.7 ml/kg; dogs, 597.7 +/- 290.2 ml/kg) and rapid systemic clearance (rabbits, 19.4 +/- 5.3 ml/min/kg; sheep, 13.3 +/- 3.0 ml/min/kg; dogs, 18.7 +/- 7.5 ml/min/kg). On the basis of these pharmacokinetic variables, alfentanil should have short duration of action in rabbits, sheep, and dogs. This may be beneficial in veterinary practice where rapid recovery would be expected after bolus administration for short procedures or after infusion for longer procedures.

Central venous pressure (CVP), portal pressure (PP), and heart rate (HR) were monitored in 6 female, sexually intact, middle-age Beagles during temporary portal vein obstruction, anesthetic recovery, abdominal bandaging, and propranolol administration. Intraoperative baseline PP was 7.3 mm of Hg (+/- 1.7 SD). Portal pressure was significantly increased throughout portal vein occlusion, but returned to baseline values 2 minutes after release of the ligature. Central venous pressure was significantly decreased throughout portal vein occlusion, but did not differ significantly from baseline values 3 minutes after release of the portal vein ligature. Portal pressure increased significantly (8 +/- 3.3 mm of Hg) over baseline values after application of an abdominal bandage; however, CVP did not change significantly. During postoperative monitoring, CVP and PP did not change significantly from respective 18-hour mean postoperative values in resting dogs. At 60 and 75 minutes after surgery, heart rate was significantly increased over the 18-hour mean. Portal pressure and CVP, respectively, were significantly increased over intraoperative baseline values in the first hour and the first 8 hours after surgery. Postoperative CVP and HR were significantly correlated. Individual measurements of PP in dogs that were abdominal pressing during barking or defecation were significantly increased (9 +/- 3 mm of Hg) above measurements taken after cessation of abdominal press. Portal pressure measurements in standing dogs decreased 7.5 +/- 2 mm of Hg, compared with measurements of the same dog in lateral recumbency. Central venous pressure was inaccurate in dogs performing abdominal press. Portal pressure did not decrease significantly from baseline after injection of propranolol (2 mg/kg, IV). Central venous pressure was significantly decreased at 2.5 and 3.0 hours after propranolol injection, and HR was significantly decreased from 1 to 3.5 hours after injection. Heart rate quickly returned to normal values if the dogs became excited. After propranolol administration, significant correlations were found between PP and HR, and between CVP and HR.

The effect of various confinement conditions on physical fitness in dogs was evaluated. Eighteen 9.5- to 10-month-old female purpose-bred Beagles were maintained individually for 3 months at a time in 1 of 6 confinement conditions: Condition A--an outdoor housing area with a conventional dog house and free access to a 6.1 X 9.1-m pen; condition B--outdoor kennel with a conventional dog house and free access to a 1.8 X 6.1-m run; condition C--indoor environmentally controlled 1.2 X 3.66-m run; condition D--0.9 X 1.2 X 0.84-m conventional laboratory cage in an indoor environmentally controlled room; condition E--0.9 X 1.2 X 0.84-m conventional laboratory cage in an indoor environmentally controlled room with treadmill exercise (7 km/h at a 10% grade) for 30 min/d, 5 d/wk; condition F--0.71 X 0.86 X 0.69-m conventional laboratory cage in an indoor environmentally controlled room. During the final week of each 3-month interval, muscle succinate dehydrogenase enzyme activities and submaximal exercise heart rates (during treadmill exercise) were determined to estimate physical fitness. Also, 5 days after being moved into a different housing condition, blood samples were collected for plasma cortisol determination. The type of confinement condition for dogs had little effect on muscle succinate dehydrogenase activity, but had a modest effect on submaximal exercise heart rates of dogs. At the fifth and tenth minutes of the treadmill exercise period, heart rates of dogs maintained in the smallest cages (condition F) were higher than those of dogs maintained in outside pens and runs (conditions A and B), indicating decreased fitness in the dogs maintained in the smallest cages. Differences in heart rates were not detected among dogs in other conditions. The confinement conditions used in this study had no detectable effect on plasma cortisol concentrations. We concluded that neither cage or pen size nor a regular mandatory exercise program substantially impacted on physical fitness of laboratory confined dogs, as long as the cages complied with federal standards and guidelines. Dogs maintained in substandard cages did have modest decreases in fitness.

The effects of IV administered amiodarone, a class-III antiarrhythmic agent, on myocardial contractility, early myocardial relaxation, and hemodynamic variables were evaluated in normal canine hearts and those with infarcts. In the normal canine heart, amiodarone had important, but relatively mild, depressant effects on left ventricular contractility (assessed by maximal positive first derivative of left ventricular pressure (+dP/dt(max)) and maximal elastance (Emax)) and heart rate when given IV at a dose of 10 mg/kg of body weight. An effect on contractility or active relaxation (assessed by maximal negative first derivative of left ventricular pressure(-dP/dt(max)) and the time constant of isovolumic pressure decrease) was not identified with smaller doses. Myocardial infarction itself caused a predictable and marked depressant effect on myocardial contractility, as indicated by decreases in +dP/dt(max) ejection fraction, Emax, and-dP/dt(max), and elevation in end diastolic pressure. Additional depressive effects on contractility and active relaxation resulted when 10 mg of amiodarone/kg was administered to dogs with myocardial infarction and these effects were sufficient to worsen acute myocardial infarction-induced heart failure. Significant changes attributable to heart rate alone could not be identified. On the basis of our findings, we suggest that amiodarone administered IV should be used with caution in dogs with compromised ventricular function.

Dynamic baroreflex sensitivity for increasing arterial pressure (DBSI) was used to quantitatively assess the effects of anesthesia on the heart rate/arterial pressure relationship during rapid (less than or equal to 2 minutes) pressure changes in the horse. Anesthesia was induced with IV administration of xylazine and ketamine and maintained with halothane at a constant end-tidal concentration of 1.1 to 1.2% (1.25 to 1.3 minimal alveolar concentration). Systolic arterial pressure (SAP) was increased a minimum of 30 mm of Hg in response to an IV bolus injection of phenylephrine HCl. Linear regression was used to determine the slope of the R-R interval/SAP relationship. During dynamic increases in SAP, a significant correlation between R-R interval and SAP was observed in 8 of 8 halothane-anesthetized horses. Correlation coefficients between R-R interval and sap were > 0.80 in 5 of 8 horses. Mean (+/- SD) DBSI was 4.8 +/- 3.4 ms/mm of Hg in anesthetized horses. A significant correlation between R-R interval and SAP was observed in only 3 of 6 awake horses during dynamic increases in SAP. Lack of correlation between R-R interval and SAP in 3 of 6 awake horses indicated that rapidly increasing SAP with an IV phenylephrine bolus is a poor method to evaluate baroreceptor-mediated heart rate changes in awake horses. Reflex slowing of heart rate in response to a rising arterial pressure appeared to have been overridden by the effects of excitement. Mean (+/- SD) DBSI (3 horses) was 7.3 +/- 3.3 ms/mm of Hg in awake horses.

The steady-state response characteristics of a pulse oximeter were evaluated on intestinal segments of seven clinically normal halothane-anesthetized horses. Arterial oxygen tension > 200 mm of Hg, end tidal carbon dioxide from 30 to 35 mm of Hg, and systemic mean arterial pressure > 70 mm of Hg were maintained throughout the recording periods. Values for percentage of pulse oximeter oxygen saturation, pulsatile blood flow, and percentage of signal strength were recorded from jejunum, ileum, cecum, left ventral colon, left dorsal colon, and descending colon. Probe placement on intestinal segments was recorded as over or not over visible subserosal or transmural vessels. There was no significant difference between median values on the basis of vessel codes for pulse oximeter oxygen saturations, pulsatile flow, and signal strength. Median values recorded for pulse oximeter oxygen saturation were 93% from jejunum and ileum and 95% from cecum, left ventral colon, left dorsal colon, and descending colon; median values for pulsatile flow were 576 from jejunum, 560 from ileum, 560 from cecum, 574 from left ventral colon, 578 from left dorsal colon, and 560 from descending colon; median values for signal strength were 50% from jejunum, 67.5% from ileum, 60% from cecum, 75% from left ventral colon, 50% from left dorsal colon, and 52.5% from descending colon. Median values obtained from each anatomic location were not significantly different for pulsatile flow or signal strength. Median pulse oximetry oxygen values recorded from jejunum and ileum were significantly lower than values obtained from other intestinal segments. When calculated arterial oxygen saturation was compared with oxygen saturation determined by the pulse oximeter, pulse oximeter oxygen saturation was consistently lower by 6.7% (jejunum and ileum) and 4.7% (cecum, left ventral colon, left dorsal colon, and descending colon). Equine and human absorption spectra were generated and compared for reduced hemoglobin and oxyhemoglobin at wavelengths of 600 nm (red) to 950 nm (infrared). Extinction coefficients calculated at wavelengths used by the pulse oximeter (660 nm and 940 nm) were nearly identical. The pulse oximeter is a self-calibrating instrument that displays oxygen saturation, heart rate, plethysmographic waveform, and signal strength indicator. Probe application was rapid and easy. Response time for the appearance of a plethysmographic waveform ranged from 5 to 25 seconds.

Three doses of an alpha2-adrenoreceptor antagonist, atipamezole, were administered to reverse xylazine-induced sedation, bradycardia, and ruminal atony in calves. Once a week for 4 weeks, each of 6 calves was administered IV 1 treatment of:0.3 mg of xylazine/kg of body weight, followed in 10 minutes by 1 ml of 0.9% NaCl; 0.3 mg of xylazine/kg, followed in 10 minutes by 3 microgram of atipamezole/kg; 0.3 mg of xylazine/kg, followed in 10 minutes by 10 microgram of atipamezole/kg; or 0.3 mg of xylazine/kg, followed in 10 minutes by 30 microgram of atipamezole/kg. The order of the 4 treatments in each calf was selected at random. Xylazine alone caused lateral recumbency for 33.6 +/- 7.1 minutes (mean +/-SEM). Atipamezole administered at dosages of 3, 10, and 30 microgram/kg shortened xylazine-induced lateral recumbency to 20.5 +/- 3.0, 10.2 +/- 0.2, and 9.3 +/- 0.5 minutes, respectively. Calves given xylazine alone stood at > 60 minutes after the onset of recumbency. Atipamezole given at 3, 10, and 30 microgram/kg shortened the time from onset of lateral recumbency to standing to 40.2 +/- 6.9, 12.8 +/- 1.1, and 10.0 +/- 0.7 minutes, respectively. Drowsiness was found in calves given the lowest dosage of atipamezole (3 microgram/kg) after the calves stood. Atipamezole given at dosages of 10 and 30 microgram/kg reversed xylazine-induced ruminal atony in a dose-dependent manner. In addition, 30 microgram of atipamezole/kg reversed xylazine-induced bradycardia, but the lower dosages of this antagonist did not. Results indicated that 30 microgram of atipamezole/kg should be a useful antidote for xylazine overdose in cattle.

Fourteen adult beavers (Castor canadensis) weighing 16.5 +/- 4.14 kg (mean +/- SD) were anesthetized for surgical implantation of radio telemetry devices. Beavers were anesthetized with diazepam (0.1 mg/kg) and ketamine (25 mg/kg) administered IM, which provided smooth anesthetic induction and facilitated tracheal intubation. Anesthesia was maintained with halothane in oxygen via a semiclosed circle anesthetic circuit. Values for heart rate, respiratory rate, esophageal temperature, direct arterial blood pressure, end-tidal halothane concentration, and end-tidal CO2 tension were recorded every 15 minutes during the surgical procedure. Arterial blood samples were collected every 30 minutes to determine pH, PaO2, and PaCO2. Values for plasma bicarbonate, total CO2, and base excess were calculated. Ventilation was spontaneous in 7 beavers and controlled to maintain normocapnia (PaCO2 approx 40 mm of Hg) in 7 others. Vaporizer settings were adjusted to maintain a light surgical plane of anesthesia. Throughout the surgical procedure, all beavers had mean arterial pressure < 60 mm of Hg and esophageal temperature < 35 C. Mean values for arterial pH, end-tidal CO2, PaO2, and PaCO2 were significantly (P < 0.05) different in spontaneously ventilating beavers, compared with those in which ventilation was controlled. Respiratory acidosis during halothane anesthesia was observed in spontaneously ventilating beavers, but not in beavers maintained with controlled ventilation. All beavers recovered unremarkably from anesthesia.