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  • Author or Editor: Clifford Swanson x
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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

We investigated the influence of parasympathetic tone on the arrhythmogenicity of graded dobutamine infusions in horses anesthetized under clinical conditions. Six horses were used in 9 trials. Two consecutive series of graded dobutamine infusions were given iv; each continuous graded dobutamine infusion was administered for 20 minutes. The dobutamine infusion dosage (5, 10, 15, and 20 μg/kg of body weight/min) was increased at 5-minute intervals. Isovolumetric saline solution vehicle (v) or atropine (a; 0.04 mg/kg) was administered iv, or bilateral vagotomy (vg) was performed as a treatment before the second series of dobutamine infusions. Treatment was not administered prior to the first dobutamine infusion. Significant interaction between treatment and dosage of dobutamine infusion existed for differences from baseline for mean arterial pressure, systolic arterial pressure, diastolic arterial pressure, heart rate, and cardiac index at dosages of 5 and 10 μg of dobutamine/kg/min, given iv and for heart rate at dosage of 15 μg of dobutamine/kg/ min, given iv. Results for group-v horses were different from those for group-A and group-VG horses, but were not different between group-A and group-VG horses in all aforementioned cases, except for heart rate and cardiac index at dosage of 5 p.g of dobutamine/kg/min, given iv. Normal sinus rhythm, second-degree atrioventricular block, and bradyarrhythmias predominated during low dobutamine infusion rates during the first infusion series (nontreated horses) and in group-v horses during the second infusion series. Only tachyarrhythmias were observed during the second infusion series in the horses of the A and VG groups. The modulating influence of parasympathetic nervous system activity on hemodynamics and development of arrhythmia was conspicuous during low dobutamine infusion rates. Significant differences were not observed in hemodynamic responses to dobutamine, with respect to parasympathetic influence at high dobutamine infusion rates.

Free access
in American Journal of Veterinary Research

Summary

Plasma cortisol concentrations were compared in canine surgical patients given etomidate (2 mg/kg of body weight, iv) or thiopental sodium (12 mg/kg, iv) for anesthetic induction. Blood samples to determine plasma concentrations of etomidate were obtained at 0, 5, 10, 15, and 30 minutes and 1, 2, 3, 4, 5, 6, 8, 12, and 24 hours after induction. Adrenocortical function was evaluated before surgery by use of adrenocorticotropic hormone stimulation tests. Dogs in both induction groups had high plasma cortisol concentrations after induction. Dogs given thiopental had a significant increase (P < 0.05) in plasma cortisol concentration from baseline at 2, 3, 4, 5, 6, 8, and 12 hours after induction. Dogs given etomidate had a significant increase (P < 0.05) in plasma cortisol concentration from baseline at 5, 6, and 8 hours after induction. A comparison of plasma cortisol concentrations determined at 2, 3, 4, 5, and 6 hours after induction with thiopental or etomidate revealed a higher (P < 0.05) concentration in dogs given thiopental.

The disposition of etomidate was best described by a 2-compartment model, with a redistribution half-life of 0.12 ± 0.04 minute and a terminal half-life of 1.70 ± 0.27 minute. Plasma cortisol concentrations did not correlate with plasma etomidate concentrations.

We conclude that, compared with thiopental, a single bolus injection of etomidate reduces the adrenocortical response to anesthesia and surgery from 2 to 6 hours after induction. Because cortisol concentrations were significantly higher than baseline, and because cardiopulmonary function is maintained after a single bolus injection of etomidate, it can be considered a safe induction agent in dogs.

Free access
in American Journal of Veterinary Research

Abstract

Objective—To compare the anesthetic efficacy and physiologic changes associated with exposure to tricaine methanesulfonate and clove oil (100% eugenol).

Animals—15 adult cultured red pacu (Piaractus brachypomus).

Procedure—Fish were exposed to each of 6 anesthetic concentrations in a within-subjects complete crossover design. Stages of anesthesia and recovery were measured, and physiologic data were collected before and during anesthesia.

Results—Interval to induction was more rapid and recovery more prolonged in fish exposed to eugenol, compared with those exposed to tricaine methanesulfonate. The margin of safety for eugenol was narrow, because at the highest concentration, most fish required resuscitation. Mixed venous-arterial PO2 consistently decreased with anesthesia, while PCO2 consistently increased with anesthesia in all fish regardless of anesthetic agent. The increase in PCO2 was accompanied by a decrease in pH, presumably secondary to respiratory acidosis. Anesthesia was associated with increased blood glucose, potassium, and sodium concentrations as well as Hct and hemoglobin. Fish anesthetized with eugenol were more likely to react to a hypodermic needle puncture than fish anesthetized with tricaine methanesulfonate.

Conclusions and Clinical Relevance—Anesthesia induced with tricaine methanesulfonate or eugenol contributes to hypoxemia, hypercapnia, respiratory acidosis, and hyperglycemia in red pacu. Similar to tricaine methanesulfonate, eugenol appears to be an effective immobilization compound, but eugenol is characterized by more rapid induction, prolonged recovery, and a narrow margin of safety. Care must be taken when using high concentrations of eugenol for induction, because ventilatory failure may occur rapidly. In addition, analgesic properties of eugenol are unknown. (Am J Vet Res 2001;62:337–342)

Full access
in American Journal of Veterinary Research

Abstract

Objective—To evaluate the effect of acepromazine maleate administered IV on platelet function assessed in healthy dogs by use of a modified thromboelastography assay.

Animals—6 healthy adult mixed-breed dogs.

Procedures—Dogs received each of 3 treatments (saline [0.9% NaCl] solution [1 to 2 mL, IV] and acepromazine maleate [0.05 and 0.1 mg/kg, IV]) in a randomized crossover study with a minimum 3-day washout period between treatments. From each dog, blood samples were collected via jugular venipuncture immediately before and 30 and 240 minutes after administration of each treatment. A modified thromboelastography assay, consisting of citrated kaolin–activated (baseline assessment), reptilase-ADP–activated (ADP-activated), and reptilase-arachidonic acid (AA)–activated (AA-activated) thromboelastography, was performed for each sample. Platelet inhibition was evaluated by assessing the percentage change in maximum amplitude for ADP-activated or AA-activated samples, compared with baseline values. Percentage change in maximum amplitude was analyzed by use of Skillings-Mack tests with significance accepted at a family-wise error rate of P < 0.05 by use of Bonferroni corrections for multiple comparisons.

Results—No significant differences were found in the percentage change of maximum amplitude from baseline for ADP-activated or AA-activated samples among treatments at any time.

Conclusions and Clinical Relevance—Platelet function in dogs, as assessed by use of a modified thromboelastography assay, was not inhibited by acepromazine at doses of 0.05 or 0.1 mg/kg, IV. This was in contrast to previous reports in which it was suggested that acepromazine may alter platelet function via inhibition of ADP and AA.

Full access
in American Journal of Veterinary Research

Summary

We evaluated the effects of clenbuterol HCl (0.8 μg/kg, of body weight, iv), a β2, agonist, on ventilation-perfusion matching and hemodynamic variables in anesthetized (by iv route), laterally recumbent horses. The multiple inert gas elimination technique was used to assess pulmonary gas exchange. Clenbuterol HCl induced a decrease in arterial oxygen tension (from 57.0 ± 1.8 to 49.3 ± 1.2 mm of Hg; mean ± sem) as a result of increased shunt fraction (from 6.6 ± 2.1 to 14.4 ± 3.1%) and ventilation to regions with high ventilation-perfusion ratios. In contrast, no changes in these variables were found in horses given sterile water. In horses given clenbuterol HCl, O2 consumption increased from 2.23 ± 0.18 to 2.70 ± 0.14 ml · min-1 · kg-1, and respiratory exchange ratio decreased from 0.80 ± 0.02 to 0.72 ± 0.01. Respiratory exchange ratio and O, consumption were not significantly modified in sterile water-treated (control) horses. Clenbuterol HCl administration was associated with increased cardiac index (from 57.4 ± 4.0 to 84.2 ± 6.3 ml. min-1 · kg-1), decreased total peripheral vascular resistance (from 108.3 ± 9.3 to 47.6 ± 2.8 mm of Hg · s · kg · ml-1), and decreased pulmonary vascular resistance (from 31.3 ± 3.8 to 13.6 ± 0.7 mm of Hg · s · kg · ml-1). Our findings indicated that clenbuterol HCl may potentiate hypoxemia as a result of increased shunt fraction in horses anesthetized by the iv route, and caused changes in hemodynamic variables that were consistent with its ability to stimulate β2-adrenergic receptors.

Free access
in American Journal of Veterinary Research