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Abstract

Objectives

To determine the concentrations of sevoflurane and compound A (a degradation product of sevoflurane) in the anesthetic circuit when sevoflurane was delivered with an in-circuit vaporizer, and to determine the cardiorespiratory effects of sevoflurane in dogs.

Animals

6 mixed-breed dogs.

Procedure

In-circuit vaporizers were connected to the inspiratory limb of a circle rebreathing system connected to a ventilator. A reservoir bag was attached to the Y-piece connector to act as an artificial lung, and sevoflurane concentrations in the anesthetic circuit were measured at vaporizer settings of 1, 3, 5, 7, and 10 and oxygen flow rates of 250 and 500 ml/min. Cardiorespiratory effects of sevoflurane were determined in dogs while they were breathing spontaneously, during controlled ventilation, and during closed circuit anesthesia. Concentrations of compound A were determined by means of gas chromatography with flame ionization.

Results

The concentration of sevoflurane in the anesthetic circuit increased with vaporizer setting and time. For oxygen flow rates of 250 and 500 ml/min, vaporizer settings between 5 and 7 and between 7 and 10, respectively, produced sevoflurane concentrations closest to values reported to produce surgical anesthesia in dogs. Significant differences were not observed in cardiorespiratory variables with time or among anesthetic conditions. Concentrations of compound A in the anesthetic circuit were less than values reported to produce renal toxicoses and death in rats.

Conclusion

Results suggested that sevoflurane can be administered to nonsurgically stimulated dogs, using an in-circuit vaporizer and low (< 15 ml/kg/min) oxygen flow rates, without causing significant cardiorespiratory depression or clinically important concentrations of compound A. (Am J Vet Res 1998;59:603–608)

Free access
in American Journal of Veterinary Research

Summary

Mechanisms responsible for the positive inotropic effects of dopexamine were investigated in 8 halothane-anesthetized horses. The hemodynamic effects of increasing infusions of dopexamine (5, 10, 15 μg/kg of body weight/min) were determined before and after sequential administration of specific antagonists. Using glycopyrrolate and chlorisondamine, and atenolol and ICI 118,551, muscarinic and nicotinic ganglionic, and β1, and β2-adrenergic receptor blockade, respectively, was induced. Dopexamine infusions induced increase in heart rate, cardiac output, systolic and mean arterial blood pressure, and maximal rate of left ventricular pressure development (+ dP/dtmax). Right atrial pressure and systemic vascular resistance decreased. Parasympathetic and ganglionic blockade attenuated cardiac output, systolic and mean aortic blood pressures, and + dP/dtmax responses to dopexamine infusion. Dopexamine-induced increase in heart rate was potentiated by parasympathetic and ganglionic blockade. β1-Adrenergic receptor blockade decreased heart rate, cardiac output, arterial blood pressure, and + dP/dtmax from baseline values and markedly reduced the response to dopexamine infusion. β2-Adrenergic receptor blockade induced further decrease in hemodynamic variables from baseline values and completely abolished the cardiostimulatory effects of dopexamine on + dP/dtmax. These data indicate that baroreflex activity, β1- and β2-adrenergic receptor stimulation may be an important cause of dopexamine's positive inotropic effects in horses.

Free access
in American Journal of Veterinary Research

SUMMARY

Complete atrioventricular block was induced in 26 pentobarbital-anesthetized dogs to determine the effects of the α2-adrenergic receptor agonists, xylazine and medetomidine, on supraventricular and ventricular automaticity. Prazosin and atipamezole, α- adrenoceptor antagonists, were administered to isolate α1- or α2-adrenoceptor effects. Six dogs served as controls and were given glycopyrrolate (0.1 mg/ kg of body weight, iv) and esmolol (50 to 75 μg/kg/ min, iv) to induce parasympathetic and β1-adrenergic blockade, respectively. Eight dogs were given sequentially increasing doses of xylazine (n = 5), 0.000257 mg (10−9 M) to 25.7 mg (10−4 M) and medetomidine (n = 3), 0.000237 mg (10−9 M) to 2.37 mg (10−5 M) after parasympathetic and β1-adrenergic blockade. Twelve dogs were given xylazine (n = 6, 1.1 mg/kg, iv) or medetomidine (n = 6, 0.05 mg/kg, iv) after parasympathetic and β1-adrenergic blockade. Three dogs given xylazine and 3 dogs given medetomidine were administered prazosin (0.1 mg/kg, iv) followed by atipamezole (0.3 mg/kg, iv). The order of prazosin and atipamezole was reversed in the remaining 3 dogs given either xylazine or medetomidine.

Complete atrioventricular block and administration of glycopyrrolate and esmolol resulted in stable supraventricular and ventricular rates over a 4-hour period. Increasing concentration of xylazine or medetomidine did not cause signficant changes in supraventricular or ventricular rate. Xylazine and medetomidine, in the presence of the α-adrenoceptor antagonists, prazosin (α1) and atipamezole (α2), did not cause significant changes in supraventricular or ventricular rate. α2-Adrenoceptor agonists do not induce direct α1- or α2-adrenoceptor-mediated depression of supraventricular or ventricular rate in dogs with complete atrioventricular block.

Free access
in American Journal of Veterinary Research

SUMMARY

Eight adult horses were used in a study to determine ketamine's ability to reduce halothane requirement. To obtain steady-state plasma concentrations of 0.5, 1.0, 2.0, 4.0, and 8.0 μg/ml, loading doses and constant infusions for ketamine were calculated for each horse on the basis of data from other studies in which the pharmacokinetic properties of ketamine were investigated. Blood samples for determination of plasma ketamine concentrations were collected periodically during each experiment. Plasma ketamine concentrations were determined by capillary gas chromatography/mass spectrometry under electron-impact ionization conditions, using lidocaine as the internal standard. Halothane minimal alveolar concentration (mac; concentration at which half the horses moved in response to an electrical stimulus) and plasma ketamine concentration were determined after steady-state concentrations of each ketamine infusion had been reached. Plasma ketamine concentrations > 1.0 μg/ml decreased halothane mac. The degree of mac reduction was correlated directly with the square root of the plasma ketamine concentration, reaching a maximum of 37% reduction at a plasma ketamine concentration of 10.8 ± 2.7 μg/ml. Heart rate, mean arterial blood pressure, and the rate of increase of right ventricular pressure did not change with increasing plasma ketamine concentration and halothane mac reduction. Cardiac output increased significantly during ketamine infusions and halothane mac reduction. Our findings suggest that plasma ketamine concentrations > 1.0 μm/ml reduce halothane mac and produce beneficial hemodynamic effects.

Free access
in American Journal of Veterinary Research

Abstract

Objective

To examine effects of atipamezole on detomidine midsacral subarachnoidally-induced analgesia, cardiovascular and respiratory activity, head ptosis, and position of pelvic limbs in healthy mares.

Animals

10 healthy mares.

Procedure

Using a randomized, blinded, crossover study design, mares received detomidine (0.03 mg/kg of body weight, diluted in 3 ml of CSF) midsacral subarachnoidally, followed by atipamezole (0.1 mg/kg [test]) or sterile saline (0.9% NaCl) solution (control), IV 61 minutes later and saline solution (3 ml, midsacral subarachnoidally) on a separate occasion, at least 2 weeks later. Analgesia was determined by lack of sensory perception to electrical stimulation at the perineal dermatome and no response to needle-prick stimulation extending from the coccygeal to T15 dermatomes. Arterial acid-base (pH, standard bicarbonate, and base excess values), gas tensions (PO2 , PCO2 ), PCV, total solids concentration, heart and respiratory rates, rectal temperature, and arterial blood pressure were determined, and mares were observed for sweating and urination. Mean scores of perineal analgesia, head ptosis, position of pelvic limbs, and cardiovascular and respiratory data were compared for the 3-hour test period.

Results

Subarachnoidally administered detomidine induced perineal analgesia (mean ± SD onset, 9.0 ± 4.6 minutes; duration, 130 ± 26 minutes), marked head ptosis, moderate changes in pelvic limb position, cardiovascular and respiratory depression, sweating in analgesic zones, and diuresis. Intravenously administered atipamezole significantly reduced mean scores of detomidine-induced perineal analgesia, head ptosis, pelvic limb position, sweating and diuresis; partially antagonized detomidine-induced bradycardia; and did not effect detomidine-induced bradypnea.

Conclusions and Clinical Relevance

Most effects of midsacral subarachnoidally administered detomidine, except bradycardia and bradypnea, were reversed by atipamezole (0.1 mg/kg, IV), indicating that most of the actions of detomidine were mediated via activation of α2-adrenergic receptors. (Am J Vet Res 1998;59:468–477)

Free access
in American Journal of Veterinary Research

Abstract

Objective

To examine and compare effects of 2α2 - adrenergic receptor agonists, xylazine and detomidine, administered into the sacrococcygeal epidural space to induce safe and effective perineal analgesia on cardio-vascular and respiratory functions, head ptosis, and po-sition of pelvic limbs in healthy mares.

Animals

8 healthy mares.

Procedure

Blood samples were drawn and systemic hemodynamics were determined, including cardiac output and pulmonary arterial, systemic arterial, and right atrial pressures. Two-way ANOVA with repeated measures was used to detect significant (P < 0.05) differences between mean scores of perineal analgesia, cardiorespiratory variables, head ptosis, and position of pelvic limbs in mares before and during a 3-hour testing period. Analgesia was determined by lack of sensory perception to electrical stimulation at the perineal dermatome and no response to needle prick stimulation in dermatomes extending from the coccyx to T15. Avoidance responses to electrical current and needle prick stimulation and behavioral changes (head ptosis, position of pelvic limbs) were quantitatively assessed by use of a scoring system.

Results

Epidurally administered xylazine induced perineal analgesia and variable bilateral caudal analgesia extending from the coccyx to S3 dermatome, with minimal cardiovascular and respiratory depression, head ptosis, changes in position of pelvic limbs, and no urination in standing mares. Epidurally administered detomidine in-duced perineal analgesia, variable bilateral analgesia with dermatomal spread ranging from coccyx to S3 and coccyx to T15, with cardiovascular depression, marked head ptosis, changes in position of pelvic limbs, and diuresis in standing mares. Onset of perineal analgesia after xylazine and detomidine administrations was 13.1 ± 3.7 and 12.5 ± 2.7 minutes (mean ± SD), respectively. The period of perineal analgesia was significantly (P < 0.05) longer in mares after epidural xylazine administration than after epidural detomidine administration (165 to > 180 minutes vs 160 ± 8 minutes).

Conclusions

Caudal epidurally administered xylazine (0.25 mg/kg of body weight in 8 ml of 0.9% NaCI) offers the most desirable conditions in mares: long-term perineal analgesia (> 2.5 hours), with minimal cardiopulmonary depression, head ptosis, changes in pelvic limb position, and no urination in standing mares during a 3- hour test period. (Am J Vet Res 1996;57:1338-1345)

Free access
in American Journal of Veterinary Research

Abstract

Objective

To examine effects of 0.25 mg of xylazine/kg of body weight diluted to a total volume of 6 ml/450 kg with sterile 0.9% NaCl, administered into the epidural space of the sacrococcygeal joint on perineal analgesia, sedation, ataxia, and respiratory and cardiovascular function in standing mares:

Design

Randomized, blinded study, using xylazine (treatment) and 0.9% NaCl (controls). At least 2 weeks elapsed between the treatments.

Animals

Eight healthy mares.

Procedure

Blood samples were drawn. Systemic hemodynamics were determined, including cardiac output and pulmonary arterial, systemic arterial, and right atrial pressures. Two-way ANOVA with repeated measures was used to detect significant (P < 0.05) differences between mean scores of analgesia, sedation, ataxia, and cardiorespiratory variables before and during a 3-hour testing period. Analgesia was determined by lack of sensory perception to electrical stimulation at the perineal dermatome and no response to needle prick stimulation extending from coccyx to S3 dermatomes. Sedation was determined by head ptosis.

Results

Epidurally administered xylazine induced variable bilateral caudal analgesia extending from coccyx to S3, with minimal sedation, ataxia, and cardiovascular and respiratory depression in standing mares. Analgesia was attained at 15 ± 6 minutes and lasted for 165 to over 180 minutes. Heart and respiratory rates, systolic, diastolic, and mean arterial blood pressure, PCV, hemoglobin concentration, arterial oxygen content, and oxygen transport were decreased after xylazine, but not 0.9% NaCl, treatment. Cardiac output, stroke volume, mean right atrial pressure, mean pulmonary artery pressure, systemic vascular resistance, pulmonary vascular resistance, arterial and mixed venous pH and gas tensions (Po2 and Pco2 ), oxygen consumption, blood temperature, and rectal temperature did not change significantly (P < 0.05) after epidural administration of xylazine or 0.9% NaCl.

Conclusions

Caudal epidurally administered xylazine (0.25 mg/kg in 6 ml of 0.9% NaCl) can be given safely to induce prolonged (> 2 hours) caudal analgesia with minimal sedation, ataxia, and circulatory and respiratory disturbances in conscious, standing mares.

Free access
in American Journal of Veterinary Research

Summary

Seven adult mares were used to determine the analgesic, cns, and cardiopulmonary effects of detomidine hydrochloride solution after epidural or subarachnoid administration, using both regimens in random sequence. At least 1 week elapsed between experiments.

A 17-gauge Huber point (Tuohy) directional needle was used to place a catheter with stylet into either the epidural space at the first coccygeal interspace or the subarachnoid space at the lumbosacral intervertebral junction. Catheters were advanced so that the tips lay at the caudal sacral (S5 to S4) epidural space or at the midsacral (S3 to S2) subarachnoid space. Position of the catheter was confirmed radiographically. A 1% solution of detomidine HCl was injected into the epidural catheter at a dosage of 60 µg/kg of body weight, and was expanded to a 10-ml volume with sterile water to induce selective caudal epidural analgesia (cea). A dose of 30 µg of detomidine HCl/kg expanded to a 3-ml volume with spinal fluid was injected into the subarachnoid catheter to induce caudal subarachnoid analgesia (csa). Analgesia was determined by lack of sensory perception to electrical stimulation (avoidance threshold > 40 V, 0.5-ms duration) at the perineal dermatomes and no response to superficial and deep muscular pinprick stimulation at the pelvic limb and lumbar and thoracic dermatomes. Maximal cea and csa extended from the coccyx to spinal cord segments T15 and T14 at 10 to 25 minutes after epidural and subarachnoid drug administrations in 2 mares. Analgesia at the perineal area lasted longer after epidural than after subarachnoid administration (142.8 ± 28.8 minutes vs 127.1 ± 27.7 minutes). All mares remained standing. Both cea and csa induced marked sedation, moderate ataxia, minimal cardiopulmonary depression, increased frequency of second-degree atrioventricular heart block, and renal diuresis. All treatments resulted in significantly (P < 0.05) decreased heart rate, respiratory rate, systemic arterial blood pressure, pcv, and plasma total solids concentration. To the contrary, arterial carbon dioxide tension, plasma bicarbonate, and standard base excess concentrations were significantly (P < 0.05) increased. Arterial oxygen tension, pH, and rectal temperature did not change significantly from baseline values.

Results indicate that use of detomidine for cea and csa in mares probably induces local spinal and cns effects, marked sedation, moderate ataxia, mild cardiopulmonary depression, and renal diuresis.

Free access
in American Journal of Veterinary Research

SUMMARY

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/dtmax) 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/dtmax) 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/dtmax, ejection fraction, Emax, and — dP/dtmax, 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.

Free access
in American Journal of Veterinary Research

SUMMARY

The ventricular arrhythmogenic dose of epinephrine (ade) was determined in 6 dogs anesthetized with halothane alone or with halothane after injection of tiletamine/zolazepam (tz). Respiratory rate and tidal volume were controlled and sodium bicarbonate was administered to maintain arterial pH and blood gas values within reference range. Heart rate and arterial blood pressure were recorded during determination of the ade. The ade (mean ± sd) was no different during anesthesia with use of halothane alone (8.9 ± 4.3) than it was when injections of tz preceded administration of halothane (6.7 ± 2.8). Tiletamine/zolazepam was also administered iv immediately after determination of the ade during halothane-induced anesthesia. The tz administered in this manner did not alter the ade. Blood pressure and heart rate were significantly greater during infusion of epinephrine than immediately prior to infusion. The administration of tz did not alter blood pressure response.

The ade was also determined in 6 cats anesthetized with halothane preceded by administration of tz. The ade (mean ± sd) was 0.7 ± 0.23 μg/kg, a value similar to that reported for cats during anesthesia with halothane alone.

Free access
in American Journal of Veterinary Research