The Cardiovascular Response of Sheep to Tiletamine–Zolazepam and Butorphanol Tartrate Anesthesia

Butorphanol tartrate (0.5 mg/kg intravenously [IV]) was administered to six ewes (group 1), 10 minutes before administration of tiletamine-zolazepam (12 mg/kg IV). In six ewes (group 2), butorphanol tartrate and tiletamine-zolazepam were administered simultaneously. Time of administration of butorphanol did not alter hemodynamics or duration of anesthesia significantly. Anesthesia was adequate for 25 to 45 minutes (mean, 31 min) in group 1. The sheep in group 2 were anesthetized effectively for 25 to 50 minutes (mean, 39 min). Neither dosing regimen caused significant changes in right atrial pressure, heart rate, pulmonary vascular resistance, or pulmonary capillary wedge pressure. Mean arterial blood pressure (MABP) decreased an average of 18% from baseline values of 113 mm Hg to a minimum of 84 mm Hg at minute 60 in group 1, and from 111 mm Hg to 92 mm Hg at minute 75 in group 2. The decrease was significant only for group 1. Cardiac output (CO) was significantly decreased 24% from 6.6 L/min at minute 45 in group 1, and 32% from 6.3 L/min at minute 15 in group 2. Systemic vascular resistance (SVR) was increased significantly at minute 15, 11% in group 1 and 37% in group 2. Mild respiratory acidosis was measured by significant decreases in arterial pO2 and pH and a significant increase in pCO2 without significant changes in HCO3-. Results of this study show that (1) tiletamine-zolazepam and butorphanol tartrate produce adequate anesthesia for 25 to 50 minutes; (2) the cardiovascular and anesthetic effects of the dosing schedules were similar; and (3) tiletamine-zolazepam and butorphanol result in decreased CO and MABP with a concomitant increase in SVR, and mild respiratory acidosis.     

Xylazine-Ketamine and Detomidine-Tiletamine-Zolazepam Anesthesia in Horses

Eight horses were anesthetized three times, by intravenous administration of xylazine (1.1 mg/kg) and ketamine (2.2 mg/kg), detomidine (0.02 mg/kg) and tiletamine-zolazepam (1.1 mg/kg), or detomidine (0.04 mg/kg) and tiletamine-zolazepam (1.4 mg/kg). The sequences were randomized. The duration of analgesia and the times to sternal and standing positions were recorded. Heart rate, arterial pressure, pHa, PaCO2, and PaO2 were measured before and during anesthesia. The duration of analgesia with the two doses of detomidine-tiletamine-zolazepam, 26 +/- 4 minutes and 39 +/- 11 minutes, respectively, was significantly longer than the 13 +/- 6 minutes obtained with xylazine-ketamine. Bradycardia occurred after administration of detomidine, but heart rates returned to baseline values 5 minutes after administration of tiletamine and zolazepam. Arterial pressure was significantly higher and PaO2 significantly lower during anesthesia with detomidine-tiletamine-zolazepam than with xylazine-ketamine. Some respiratory acidosis developed with all anesthetic combinations. The authors conclude that detomidine-tiletamine-zolazepam can provide comparable anesthesia of a longer duration than xylazine and ketamine, but hypoxemia will develop in some horses.     

The effects on cardio-respiratory and acid-base variables of the anaesthetic alfaxalone in a 2-hydroxypropyl-β-cyclodextrin (HPCD) formulation in sheep

The objective of this study was to determine the pharmacodynamic effects in sheep of the anaesthetic alfaxalone in a 2-hydroxypropyl-β-cyclodextrin formulation. Seven Ripollesa sheep, weighing 43.0±6.6 kg, were used in the study. Twenty-four hours after instrumentation, the sheep were anesthetised with alfaxalone (2 mg/kg bodyweight IV) in cyclodextrin. Heart rate, arterial blood pressure, respiratory rate and arterial blood gases were recorded. Alfaxalone administration resulted in minimal cardio-respiratory depression. Time to standing from anaesthesia was 22.0±10.6 min. Apnoea was not observed in any of the sheep. Significant differences from baseline were not observed in respiratory rate or arterial blood pressure. Heart rate increased significantly (P<0.05) immediately after administration, returning to control values at 20 min. The calculated haemoglobin saturation (SO2) decreased significantly during the first 15 min after alfaxalone administration. The arterial pH decreased significantly during the first 30 min of the study, although no significant differences from basal values were observed in the arterial partial pressure of carbon dioxide (PaCO2). The results showed that alfaxalone in 2-hydroxypropyl-β-cyclodextrin administered as an IV bolus at 2 mg/kg produced minimal adverse effects and an uneventful recovery from anaesthesia in sheep.     

Xylazine and tiletamine-zolazepam anesthesia in horses

The cardiopulmonary and anesthetic effects of xylazine in combination with a 1:1 mixture of tiletamine and zolazepam were determined in 6 horses. Each horse was given xylazine IV or IM, as well as tiletamine-zolazepam IV on 4 randomized occasions. Anesthetics were administered at the rate of 1.1 mg of xylazine/kg of body weight, IV, 1.1 mg of tiletamine-zolazepam/kg, IV (treatment 1); 1.1 mg of xylazine/kg, IV, 1.65 mg of tiletamine-zolazepam/kg, IV (treatment 2); 1.1 mg of xylazine/kg, IV, 2.2 mg of tiletamine-zolazepam/kg, IV (treatment 3); and 2.2 mg of xylazine/kg, IM, 1.65 mg of tiletamine-zolazepam/kg, IV (treatment 4). Tiletamine-zolazepam doses were the sum of tiletamine plus zolazepam. Xylazine, when given IV, was given 5 minutes before tiletamine-zolazepam. Xylazine, when given IM, was given 10 minutes before tiletamine-zolazepam. Tiletamine-zolazepam induced recumbency in all horses. Duration of recumbency in group 1 was 31.9 +/- 7.2 (mean +/- 1 SD) minutes. Increasing the dosage of tiletamine-zolazepam (treatments 2 and 3) significantly (P less than 0.05) increased the duration of recumbency. Xylazine caused significant (P less than 0.05) decreases in heart rate and cardiac output and significant (P less than 0.05) increases in central venous pressure and mean pulmonary artery pressure 5 minutes after administration. Respiratory rate was decreased. Arterial blood pressures increased significantly (P less than 0.05) after xylazine was administered IV in treatments 1 and 3, but the increases were not significant in treatment 2. Xylazine administered IM caused significant (P less than 0.05) increases in central venous pressure and significant (P less than 0.05) decreases in cardiac output.(ABSTRACT TRUNCATED AT 250 WORDS)     

Cardiorespiratory Effects of the Intravenous Administration of Tiletamine-Zolazepam to Dogs

The anesthetic, hemodynamic, and respiratory effects of an intravenously administered 1:1 combination of tiletamine and zolazepam were evaluated in dogs. Each dog received tiletamine-zolazepam (6.6, 13.2, 19.8 mg/kg) on two occasions, once when awake and a second time with residual isoflurane anesthesia while instrumented for the recording of hemodynamic data. Tiletamine-zolazepam administered to conscious dogs resulted in good, rapid induction of anesthesia. Time to sternal recumbency (recovery) was dose-dependent. Character of recovery tended to be better with the lower dose. Tiletamine-zolazepam caused significant increases in heart rate after all doses and significant increases in cardiac output after the two larger doses. All doses caused significant decreases in arterial blood pressure at 1 minute. Arterial blood pressures returned to baseline and then increased significantly above baseline values. The rate of development of left ventricular pressure was significantly decreased 1 minute after the two higher doses, returned to normal, and then was significantly increased above baseline for all doses. Peripheral vascular resistance increased transiently 1 minute after the 6.6 mg/kg dose. Peripheral vascular resistance decreased significantly after the 13.2 and 19.8 mg/kg doses. Minute ventilation was significantly decreased only after the 19.8 mg/kg dose.     

The Hemodynamic Response of Calves to Tiletamine-Zolazepam Anesthesia

Six isoflurane-anesthetized calves were instrumented for hemodynamic studies and allowed to recover from anesthesia. When the mean arterial blood pressure rose to 100 mmHg or when vigorous movement occurred, a 1:1 tiletamine-zolazepam mixture (4 mg/kg) was administered intravenously (IV). Values for cardiac output, cardiac index, stroke index, central venous pressure, and right ventricular stroke work index did not change significantly. Systolic, mean, and diastolic arterial blood pressures and systemic vascular resistance were significantly decreased below baseline at 5 minutes; they were significantly increased above baseline at 20 minutes and remained so throughout the 60 minute study. Changes in left ventricular stroke work index and rate pressure product were similar to those of arterial blood pressure and systemic vascular resistance, although they were not significant. Heart rate and pulmonary capillary wedge pressure decreased significantly but gradually returned to baseline at 40 minutes and then increased significantly above baseline by the end of the study. Minor venous-arterial shunting or perhaps mismatching of ventilation and perfusion appeared to have developed in the later stages of the study. This was reflected in a minor increase in the arterial partial pressure of carbon dioxide (PaCO2) and a decrease in the arterial partial pressure of oxygen (PaO2) and arterial pH. At the dose administered, the hemodynamic changes induced by tiletamine-zolazepam were minimal and were compatible with safe anesthesia in calves.     

Propofol infusion anaesthesia in dogs pre-medicated with medetomidine

Ten laboratory beagles pre-medicated with medetomidine (40 μg/kg bodyweight [bwt]) were anaesthetised using a rapid injection of propofol, followed by propofol infusion. A loading dose of 4 mg/kg bwt of propofol was administered intravenously (iv) as a bolus and, immediately after, a 60 min iv propofol infusion (150 μg/kg bwt/min) was initiated. After a transient increase, mean arterial blood pressure decreased significantly below the pre-propofol level. However, the lowest values recorded (115 ± 11 mmHg) remained within the physiological limits. Heart rate increased significantly (from 41 ± 7.3 to 58 ± 11 beats/min) after initiation of the propofol infusion. No significant changes were seen in respiratory frequency; pO₂ decreased transiently; minimum values (10 ± 2.3 kPa) recorded 5 mins after initiation of the propofol infusion differed significantly from the starting level. pCO₂ increased significantly and the highest values recorded were 6.1 ± 0.35 kPa. Accordingly, pH decreased reaching the lowest level (pH 7.29) 15 mins after initiation of the propofol infusion. The analgesic effect of the present combination was not studied, but the absence of the palpebral and pedal reflexes suggested a surgical stage of anaesthesia. Therefore, propofol infusion in beagles pre-medicated with medetomidine proved to be a promising anaesthetic regimen but, if used clinically, oxygen-enriched inspired air should be used.     

Administration of a low dose tiletamine-zolazepam combination to cats

A tiletamine-zolazepam mixture was administered subcutaneously at doses of 2.5 mg/kg, 5.0 mg/kg and 7.5 mg/kg to fifty-nine cats. The response to drug administration, effect on heart rate, pulse quality, respiratory rate and temperature, and intensity and duration of sedation were recorded. As the tiletamine-zolazepam dose was increased, intensity and duration of sedation increased. At the lowest dose, some cats became excited rather than sedated. Heart rate and respiratory rate changed minimally, but body temperature decreased.     

Doxapram: cardiopulmonary effects in the horse

The cardiopulmonary effects of 3 dosages of doxapram hydrochloride (0.275 mg/kg, 0.55 mg/kg, and 1.1 mg/kg, IV) were studied in 6 adult horses. Doxapram given IV significantly (P less than 0.05) decreased PaCO2 and increased respiratory rate, cardiac output arterial blood pressures (systolic, mean, and diastolic) arterial pH, and PaO2 at 1 minute after each dose was administered. Heart rate and mean and diastolic pulmonary arterial blood pressure were significantly (P less than 0.05) increased 1 minute after the 2 larger dosages of doxapram were given (0.55 mg/kg and 1.1 mg/kg, IV), but not after the smallest dosage was given. All measurements, except heart rate and cardiac output, had returned to base line by 5 minutes after each dosing. Heart rate remained significantly (P less than 0.05) increased 10 minutes after the 0.55 mg/kg dosage was given and 30 minutes after the 1.1 mg/kg dosage. Cardiac output remained significantly (P less than 0.05) increased at 10 minutes, 5 minutes, and 30 minutes after the 0.275, 0.55, and 1.1 mg/kg dosages, respectively, were given.     

A comparison of anesthetic and cardiorespiratory effects of tiletamine-zolazepam-butorphanol and tiletamine-zolazepam-butorphanol- medetomidine in cats

Using a randomized crossover design, this study compared the anesthetic and cardiorespiratory effects of three intramuscular anesthetic combinations in seven 2-year-old cats: tiletamine-zolazepam (8 mg/kg) and butorphanol (0.2 mg/kg) (TT); tiletamine-zolazepam (3 mg/kg), butorphanol (0.15 mg/kg), and medetomidine (15 microg/kg) (TTD); or the TTD protocol plus atipamezole (75 microg/kg IM) given 20 minutes later to reverse medetomidine. Analgesia was assessed using algometry and needle pricking. All three combinations effectively induced anesthesia suitable for orotracheal intubation within 5 minutes after injection. Hemoglobin oxygen saturation was lower than 90% at least once in all three groups between 5 and 15 minutes after drug administration. Blood pressure and heart and respiratory rates were within normal ranges. Both TT and TTD appeared to be effective injectable anesthetic combinations. TTD provided significantly better analgesia with a longer duration than did TT. Atipamezole administration shortened the duration of analgesia and decreased blood pressure but did not shorten total recovery time.     

Cardiovascular effects of xylazine recorded with telemetry in the dog

Cardiovascular effects of xylazine have not been studied with telemetry in dogs. In the present study, the effects on cardiovascular parameters after intramuscular (i.m.) administration of 2.0 mg/kg xylazine were studied via telemetry in unrestrained dogs. Telemetry transmitters were implanted subcutaneously (s.c.) with a pressure catheter in the femoral artery. Cardiovascular effects and body temperature effects were assessed after i.m. administration of xylazine. Heart rate decreased for about 10 min and was continuously depressed during 60 min. Thereafter, heart rate slowly increased but had not fully reached pre-dose values 4 h after treatment. Both systolic and diastolic blood pressure increased immediately after administration of xylazine. The systolic blood pressure showed a peak increase for about 5-10 min and then decreased below the baseline value not normalizing within 90 min. The diastolic blood pressure peaked 5-10 min after xylazine administration but did not return to baseline level until 50 min after administration. Body temperature decreased continuously for about 90 min and remained low for more than 4 h after treatment. An additional administration of xylazine to the same individuals after a recovery period of 4 weeks induced exactly the same response in systolic and diastolic blood pressure and in heart rate. By using the telemetric recording system it was possible to continuously evaluate xylazine-induced cardiovascular responses in a way that is not possible with conventional techniques.     

Comparison of two injectable anesthetic regimes in feral cats at a large-volume spay clinic

Same‐day mass sterilization of feral cats requires rapid onset, short‐duration anesthesia. The purpose of this study was to compare our current anesthetic protocol, Telazol–ketamine–xylazine (TKX) with medetomidine–ketamine–buprenorphine (MKB). Feral female cats received either IM TKX (n = 68; 0.25 mL cat^?1; tiletamine 12.5 mg, zolazepam 12.5 mg, K 20 mg, and X 5 mg per 0.25 mL) or MKB (n = 17; M 40 µg kg^?1, K 15 mg kg^?1, and B 10 µg kg^?1). Intervals measured included time from injection to recumbency, time to surgery, duration of surgery, and time from reversal of anesthesia (TKX: yohimbine 0.50 mg cat^?1 IV; MKB: atipamezole 0.50 mg cat^?1 IM) to sternal recumbency. Following instrumentation (Vet/Ox 4403 and Vet/BP Plus 6500), physiological measurements were recorded at 5‐minute intervals, and included rectal temperature, heart rate (HR), respiratory rate (RR), SpO₂ (lingual or rectal probes), and indirect mean arterial blood pressure (MAP) (oscillometric method). Nonparametric means were compared using Mann–Whitney U‐tests. Parametric means were compared using a two‐factorial anova with Bonferroni's t‐tests. The alpha‐priori significance level was p < 0.05. Values were mean ± SD. Body weight (TKX: 2.9 ± 0.5 kg, MKB: 2.7 ± 0.7 kg), time to recumbency (TKX: 4 ± 1 minutes, MKB: 3 ± 1 minutes), time to surgery (TKX: 28 ± 7 minutes, MKB: 28 ± 5 minutes), and duration of surgery (TKX: 11 ± 7 minutes, MKB: 8 ± 5 minutes) did not differ between groups. In contrast, MKB cats required less time from reversal to sternal recumbency (TKX: 68 ± 41 minutes, MKB: 7 ± 2 minutes) and were recumbent for shorter duration (TKX: 114 ± 39 minutes, MKB: 53 ± 6 minutes). Temperature decreased during the study in both groups, but overall temperature was higher in MKB cats (38.0 ± 0.95 °C) than in TKX cats (37.5 ± 0.95 °C). RR, HR, and SpO₂ did not change during the study in either group. However, overall HR and RR were higher in TKX cats (RR: 18 ± 8 breaths minute^?1, HR: 153 ± 30 beats minute^?1) compared to MKB cats (RR: 15 ± 7 breaths minute^?1, HR: 128 ± 19 beats minute^?1). In contrast, overall SpO₂ was lower in the TKX group (90 ± 6%) compared to the MKB group (94 ± 4%). MAP was also lower in the TKX group (112 ± 29 mm Hg) compared to that in the MKB group (122 ± 20 mm Hg). However, MAP increased in the TKX group during surgery compared to pre‐surgical values, but did not change in the MKB group. The results of this study suggested that MKB might be more suitable as an anesthetic for the purpose of mass sterilization of feral female cats.     

Cardiorespiratory Effects of the Intravenous Administration of Tiletamine-zolazepam to Cats

The hemodynamic and respiratory effects of three doses (9.7, 15.8, and 23.7 mg/kg intravenous [IV]) of a 1:1 combination of tiletamine and zolazepam were studied after isoflurane anesthesia in cats instrumented for the recording of hemodynamic data. Systolic, mean, and diastolic arterial blood pressures were decreased 1 minute after drug administration but then increased above baseline with all three doses. Cardiac output was decreased briefly at 1 minute with the 15.8 and 23.7 mg/kg doses. The rate of development of left ventricular pressure and peripheral vascular resistance decreased at 1 minute but returned to baseline or above by 10 minutes. There were no significant changes in heart rate, central venous pressure, or left ventricular end diastolic pressure. The arterial pH and blood gas measurements reflected the development of respiratory acidosis after administration of 23.7 mg/kg. These results support the conclusions that tiletamine-zolazepam administered intravenously is a useful and comparatively safe anesthetic agent in the cat.     

Midazolam and ketamine induction before halothane anaesthesia in ponies: cardiorespiratory, endocrine and metabolic changes

Six Welsh gelding ponies were premedicated with 0.03 mg/kg of acepromazine intravenously (i.v.) prior to induction of anaesthesia with midazolam at 0.2 mg/kg and ketamine at 2 mg/kg i.v.. Anaesthesia was maintained for 2 h using 1.2 % halothane concentration in oxygen. Heart rate, electrocardiograph (ECG), arterial blood pressure, respiratory rate, blood gases, temperature, haematocrit, plasma arginine vasopressin (AVP), dynorphin, ß-endorphin, adrenocorticotropic hormone (ACTH), cortisol, dopamine, noradrenaline, adrenaline, glucose and lactate concentrations were measured before and after premedication, immediately after induction, every 20 min during anaesthesia, and at 20 and 120 min after disconnection. Induction was rapid, excitement-free and good muscle relaxation was observed. There were no changes in heart and respiratory rates. Decrease in temperature, hyperoxia and respiratory acidosis developed during anaes-thesia and slight hypotension was observed (minimum value 76 ± 10 mm Hg at 40 mins). No changes were observed in dynorphin, ß-endorphin, ACTH, catecholamines and glucose. Plasma cortisol concentration increased from 220 ± 17 basal to 354 ± 22 nmol/L at 120 min during anaesthesia; plasma AVP concentration increased from 3 ± 1 basal to 346 ± 64 pmol/L at 100 min during anaesthesia and plasma lactate concentration increased from 1.22 ± 0.08 basal to 1.76 ± 0.13 mmol/L at 80 min during anaesthesia. Recovery was rapid and uneventful with ponies taking 46 ± 6 min to stand. When midazolam/ketamine was compared with thiopentone or detomidine/ketamine for induction before halothane anaesthesia using an otherwise similar protocol in the same ponies, it caused slightly more respiratory depression, but less hypotension. Additionally, midazolam reduced the hormonal stress response commonly observed during halothane anaesthesia and appears to have a good potential for use in horses.     

Acute haemolysis associated with etomidate-propylene glycol infusion in dogs

Acute haemolysis occurred in medetomidine-atropine premedicated dogs (n=6) after infusion of etomidate in 35% propylene glycol (etomidate-PG). Free plasma haemoglobin concentration was 12.0 +3.5 μg/dl at baseline. After premedication (medetomidine 15 μg/kg, IM; atropine 0.044 mg/kg, IM) values were 14 ± 5.2 and 20 ± 4.8 mg/dl, at 5 and 10 minutes, respectively. Plasma haemoglobin values increased significantly (p±0.05; 121 +24.2 mg/dl) 5 minutes after etomidate-PG loading dose (0.5 mg/kg) and infusion (50μg/kg/min) and remained significantly elevated (127 ± 12.7 to 310.6 ± 69.3 mg/dl) throughout the 60-minute infusion period. Acute haemolysis was also observed in dogs (n=3) that received etomidate-PG infusion alone (2 mg/kg loading dose followed by 110 μg/ kg/ min constant infusion). In addition, fresh dog blood (n=3) was incubated alone or with either 0.9% saline or etomidate-PG in test tubes for 5 minutes and free plasma haemoglobin concentration measured. Free plasma haemoglobin concentrations were 18.3 ± 6.8, 11.7 +4.5 and 1712.0 ± 309.6 mg/dl for blood alone, saline-blood and etomidate-PG-blood, respectively. It was concluded that etomidate-PG caused acute haemolysis in dogs both in vivo and in vitro. The clinical significance of this amount of haemolysis is not clear at this time and thus, requires further study.     

Effects of acepromazine and butorphanol on tiletamine-zolazepam anesthesia in llamas

OBJECTIVE: To evaluate sedative, antinociceptive, and physiologic effects of acepromazine and butorphanol during tiletamine-zolazepam (TZ) anesthesia in llamas. ANIMALS: 5 young adult llamas. PROCEDURES: Llamas received each of 5 treatments IM (1-week intervals): A (acepromazine, 0.05 mg/kg), B1 (butorphanol, 0.1 mg/kg), AB (acepromazine, 0.05 mg/kg, and butorphanol, 0.1 mg/kg), B2 (butorphanol, 0.2 mg/kg), or C (saline [0.9% NaCl] solution). Sedation was evaluated during a 30-minute period prior to anesthesia with TZ (2 mg/kg, IM). Anesthesia and recovery characteristics and selected cardiorespiratory variables were recorded at intervals. Antinociception was assessed via a toe-clamp technique. RESULTS: Sedation was not evident following any treatment. Times to sternal and lateral recumbency did not differ among treatments. Duration of lateral recumbency was significantly longer for treatment AB than for treatment C. Duration of antinociception was significantly longer for treatments A and AB, compared with treatment C, and longer for treatment AB, compared with treatment B2. Treatment B1 resulted in a significant decrease in respiratory rate, compared with treatment C. Compared with treatment C, diastolic and mean blood pressures were lower after treatment A. Heart rate was increased with treatment A, compared with treatment B1 or treatment C. Although severe hypoxemia developed in llamas anesthetized with TZ alone and with each treatment-TZ combination, hemoglobin saturation remained high and the hypoxemia was not considered clinically important. CONCLUSIONS AND CLINICAL RELEVANCE: Sedation or changes in heart and respiratory rates were not detected with any treatment before administration of TZ. Acepromazine alone and acepromazine with butorphanol (0.1 mg/kg) prolonged the duration of antinociception in TZ-treated llamas.     

The effects of L‐659,066, a peripheral α2‐adrenoceptor antagonist,and verapamil on the cardiovascular influences of dexmedetomidine in conscious sheep

Raekallio M. R., Honkavaara J. M., Vainio O. M. The effects of L‐659,066, a peripheral α₂‐adrenoceptor antagonist, and verapamil on the cardiovascular influences of dexmedetomidine in conscious sheep. J. vet. Pharmacol. Therap. 33 , 434–438. We investigated whether administration of L‐659,066, a peripheral α₂‐adrenoceptor antagonist, or verapamil, a calcium‐channel antagonist, would prevent the cardiovascular effects of dexmedetomidine. Eleven sheep received three intravenous treatments with a randomized, cross‐over design: dexmedetomidine (5 μg/kg, DEX); DEX with L‐659,066 (250 μg/kg, DEX + L); and verapamil (0.05 mg/kg) 10 min prior to DEX (Ver + DEX). Haemodynamics were recorded at intervals upto 40 min. Acute increases in mean arterial pressure (MAP) (106 ± 10.7 to 120.8 ± 11.7 mmHg), central venous pressure (CVP) (3.3 ± 3.2 to 14.7 ± 5.0 mmHg) and systemic vascular resistance (SVR) (1579 ± 338 to 2301 ± 523 dyne s/cm⁵), and decreases in cardiac output (CO) (5.36 ± 0.87 to 3.93 ± 1.30 L/min) and heart rate (HR) (88.6 ± 15.3 to 49.7 ± 5.5/min) were detected with DEX. The peak SVR remained lower after Ver + DEX (1835 ± 226 dyne s/cm⁵) than DEX alone, but the other parameters did not significantly differ between these treatments. 2 min after drug delivery, differences between DEX and DEX + L were statistically significant for all measured haemodynamic parameters. With DEX + L, an early decrease in MAP (99.9 ± 6.8 to 89.3 ± 6.6 mmHg) was detected, and DEX + L induced a slight but significant increase in CVP and a decrease in HR at the end of the observation period, while SVR and CO did not significantly change. All animals were assessed as deeply sedated from 2–20 min with no differences between treatments. L‐659,066 has great potential for clinical use to prevent the cardiovascular effects of dexmedetomidine mediated by peripheral α₂‐adrenoceptors, whereas the effects of verapamil were marginal.     

Antagonism of pancuronium neuromuscular blockade in halothane-anesthetized ponies using neostigmine and edrophonium

Efficacy of neostigmine (0.04 mg/kg of body weight) and edrophonium (1 mg/kg), as antagonists for pancuronium neuromuscular blockade in halothane-anesthetized ponies, was evaluated. Neostigmine and edrophonium were satisfactory antagonists, with edrophonium having a significantly (P less than 0.01) more rapid onset of action than did neostigmine. Muscarinic activity of neostigmine and edrophonium was also evaluated. Neither antagonist was administered with atropine. Gastrointestinal effects, increased salivation, and increased airway secretions were minimal with edrophonium, but were marked after neostigmine. Blood pressure increased within 1 to 2 minutes of antagonist administration. Heart rate decreased after edrophonium injection, but this occurred after blood pressure increase. Heart rate increased or did not change after neostigmine administration.     

Alteration in the arrhythmogenic dose of epinephrine (ADE) following xylazine administration to halothane-anesthetized dogs

The arrhythmogenic dose of epinephrine (ADE) was determined in six dogs during halothane (1.35%) anesthesia before and after xylazine administration (1.1 mg/kg, i.v. bolus; 1.1 mg/kg/hr, i.v. infusion). The arrhythmogenic dose was determined by constant infusion of freshly mixed epinephrine (100 microgram/ml). The ADE was defined as the total dose of epinephrine which produced four or more intermittent or continuous premature ventricular contractions within a 15-sec period. Total dose was calculated as a function of infusion rate and time to arrhythmia. Following xylazine administration, ADE significantly decreased from 6.28 +/- 0.522 to 4.17 +/- 0.679 micrograms/kg. At the end of i.v. xylazine bolus administration, heart rate significantly decreased (115 +/- 4 to 99 +/- 4.9 b.p.m.), and mean arterial pressure significantly increased (83 +/- 4.0 to 122 +/- 3.4 mm Hg). Heart rate measured immediately prior to epinephrine-induced arrhythmia formation was significantly increased following xylazine administration (177 +/- 8 vs 78 +/- 3 b.p.m.). Mean arterial blood pressure was unchanged. Apparently, xylazine, a mixed alpha agonist, potentiated halothane-induced myocardial sensitization to ventricular arrhythmogenesis and was associated with a significant increase in heart rate, but not blood pressure, during subsequent epinephrine infusions.     

Hypotension in the horse induced by acepromazine maleate

The hypotensive effect of acepromazine maleate was related to both the dose and route of administration. The degree and duration of hypotension varied between individual horses. In general, intravenous administration produced a more rapid maximum effect than intramuscular injection and the larger the dose the longer blood pressure remained at low levels. Average systolic pressure (of 6 horses) remained significantly below control values for more than 6 h after an intramuscular injection of 0.05 mg acepromazine maleate/kg body weight. Respiratory rate was markedly decreased, with the duration, but not the degree of bradypnoea related to the dose administered. A slight, transient decrease in body temperature was observed. Heart rate was not significantly influenced by administration of acepromazine maleate.