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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

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

Abstract

Objective—To determine the effects of xylazine on canine coronary artery smooth muscle tone.

Sample Population—Hearts of 26 healthy dogs.

Procedure—Dogs were anesthetized with pentobarbital, and vascular rings of various diameters were prepared from the epicardial coronary arteries. Vascular rings were placed in tissue baths to which xylazine was added (cumulative concentrations ranging from 10–10 to 10–4M), and changes in vascular ring tension were continuously recorded. Effects of the nitric oxide inhibitor NG-nitro-L-arginine methyl ester (L-NAME; 5mM), the α1-adrenoceptor antagonist prazosin (10mM), and the α2-adrenoceptor antagonist atipamezole (10mM) on xylazine-induced changes in vascular ring tension were determined. Results were expressed as percentage of maximal contraction for each vascular ring preparation.

Results—Xylazine induced vasoconstriction of small (< 500-µm-diameter) and medium (500- to 1,000-µmdiameter) vascular rings but not of large (> 1,000-µmdiameter) rings. For large vascular rings, L-NAME, atipamezole, and prazosin did not significantly affect the contractile response to xylazine. For small vascular rings, the contractile response following addition of xylazine to rings treated with L-NAME was not significantly different from the contractile response following addition of xylazine to control rings, except at a xylazine concentration of 10–6M. Xylazine-induced vasoconstriction of small vascular rings was blocked by atipamezole, but the addition of prazosin had no effect on xylazine-induced vasoconstriction.

Conclusions and Clinical Relevance—Results suggest that xylazine increases smooth muscle tone of small canine coronary arteriesand that this effect is predominantly mediated by stimulation of α2adrenoceptors.( Am J Vet Res 2004;65:431–435)

Full access
in American Journal of Veterinary Research

Abstract

Objective— To determine the hemodynamic effects of IM administration of romifidine hydrochloride in propofol-anesthetized cats.

Animals—15 adult domestic shorthair cats.

Procedure—Cats were randomly assigned to receive romifidine (0, 400, or 2,000 µg/kg, IM). Cats were anesthetized with propofol and mechanically ventilated with oxygen. The right jugular vein, left carotid artery, and right femoral artery and vein were surgically isolated and catheterized. Heart rate; duration of the PR, QRS, and QT intervals; mean pulmonary artery pressure; mean right atrial pressure; systolic, diastolic, and mean arterial pressures; left ventricular systolic pressure; left ventricular end-diastolic pressure; and cardiac output were monitored. Systemic vascular resistance, rate of change of left ventricular pressure, and rate pressure product were calculated. Arterial and venous blood samples were collected anaerobically for determination of pH and blood gas tensions (PO2 and PCO2).

Results—Administration of romifidine at 400 and 2,000 µg/kg, IM, decreased heart rate, cardiac output, rate of change of left ventricular pressure, rate pressure product, and pH. Arterial and pulmonary artery pressures, left ventricular pressure, left ventricular end-diastolic pressure, and right atrial pressure increased and then gradually returned to baseline values. Arterial blood gas values did not change, whereas venous PCO2 increased and venous PO2 decreased. Significant differences between low and high dosages were rare, suggesting that the dosages investigated produced maximal hemodynamic effects.

Conclusion and Clinical Relevance—Romifidine produces cardiovascular effects that are similar to those of other α2-agonists. High dosages of romifidine should be used with caution in cats with cardiovascular compromise. (Am J Vet Res 2002;63:1241–1246)

Full access
in American Journal of Veterinary Research

Abstract

Objective—To evaluate the effects of the α2-adrenoceptor agonist medetomidine on respiratory rate (RR), tidal volume (VT), minute volume (VM), and central respiratory neuromuscular drive as determined by inspiratory occlusion pressure (IOP) during increasing fractional inspired concentrations of carbon dioxide (FiCO2) in conscious dogs.

Animals—6 healthy dogs (3 males and 3 females).

Procedure—Dogs were administered 0, 5, or 10 µg of medetomidine/kg IV. We measured RR, VT, VM, and IOP for the first 0.1 second of airway occlusion (IOP0.1) during FiCO2 values of 0%, 2.5%, 5.0%, and 7.5% at 15 minutes before and 5, 30, and 60 minutes after administration of medetomidine.

Results—Increases in FiCO2 significantly increased RR, VT, and VM. The IV administration of 5 and 10 µg of medetomidine/kg significantly decreased RR and VM at 5, 30, and 60 minutes for FiCO2 values of 2.5% and 5.0% and at 30 and 60 minutes for an FiCO2 value of 7.5%. The IOP0.1 was decreased after 30 minutes only for an FiCO2 value of 7.5% in dogs administered 5 and 10 µg of medetomidine/kg. The IOP0.1 was decreased at 60 minutes after administration of 10 µg of medetomidine/kg for an FiCO2 value of 7.5%.

Conclusions and Clinical Relevance—The IV administration of medetomidine decreases RR, VM, and central respiratory drive in conscious dogs. Medetomidine should be used cautiously and with careful monitoring in dogs with CNS depression or respiratory compromise. (Am J Vet Res 2004;65: 720–724)

Full access
in American Journal of Veterinary Research

Abstract

Objective—To compare the effects of lactated Ringer's solution (LRS) with those of a physiologically balanced 6% hetastarch plasma expander administered to isoflurane-anesthetized dogs with hypotension induced by blood withdrawal.

Animals—12 healthy Beagles.

Procedure—Blood was withdrawn from isofluraneanesthetized dogs (volume withdrawn measured) to a systolic arterial blood pressure (SAP) of 80 mm Hg. Six dogs each received either LRS or hetastarch solution (90 mL/kg/h, IV). Hemodynamic variables, pH, blood gas concentrations, PCV, serum electrolyte and total protein concentrations, and colloid osmotic pressure (COP) were determined at baseline, while SAP was 80 mm Hg, and after fluid treatment. The volume of fluid administered and rate of return of SAP to within 10% of baseline values were recorded.

Results—Mean ± SD volume of blood withdrawn to decrease SAP to 80 mm Hg was 173 ± 38 mL. Hemodynamic variables decreased after blood withdrawal but returned to baseline values more rapidly after infusion of a smaller volume of hetastarch solution, compared with the response to LRS infusion. Whereas PCV and serum total protein concentration decreased after administration of either solution, COP decreased only after administration of LRS. The total volume of hetastarch solution and LRS required to restore and maintain SAP to within 10% of baseline values was 1.1 ± 0.9 and 4.4 ± 1.7 times greater than the volume of blood removed, respectively.

Conclusions and Clinical Relevance—Compared with LRS infusion, smaller volumes of hetastarch solution normalized and maintained SAP without lowering COP in isoflurane-anesthetized dogs after blood withdrawal. (Am J Vet Res 2004;65:1189–1194)

Full access
in American Journal of Veterinary Research

Abstract

Objective—To evaluate the effect of medetomidine on minimum alveolar concentration (MAC), respiratory rate, tidal volume, minute volume (VM), and maximum inspiratory occlusion pressure (IOCPmax) in halothane- and isoflurane-anesthetized dogs.

Animals—6 healthy adult dogs (3 males and 3 females).

Procedure—The MAC of both inhalants was determined before and 5, 30, and 60 minutes after administration of medetomidine (5 μg/kg, IV). Dogs were subsequently anesthetized by administration of halothane or isoflurane and administered saline (0.9% NaCl) solution IV or medetomidine (5 μg/kg, IV). Respiratory variables and IOCPmax were measured at specific MAC values 15 minutes before and 5, 30, and 60 minutes after IV administration of medetomidine while dogs breathed 0% and 10% fractional inspired carbon dioxide (FICO2). Slopes of the lines for VM/FICO2 and IOCPmax/FICO2 were then calculated.

Results—Administration of medetomidine decreased MAC of both inhalants. Slope of VM/FICO2 increased in dogs anesthetized with halothane after administration of medetomidine, compared with corresponding values in dogs anesthetized with isoflurane. Administration of medetomidine with a simultaneous decrease in inhalant concentration significantly increased the slope for VM/FICO2, compared with values after administration of saline solution in dogs anesthetized with halothane but not isoflurane. Values for IOCPmax did not differ significantly between groups.

Conclusions and Clinical Relevance—Equipotent doses of halothane and isoflurane have differing effects on respiration that are most likely attributable to differences in drug effects on central respiratory centers. Relatively low doses of medetomidine decrease the MAC of halothane and isoflurane in dogs.

Full 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