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  • Author or Editor: Colin I. Dunlop x
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Summary

The hemodynamic effects of 2 dosages of ephedrine were studied in 6 dogs anesthetized with isoflurane only (end-tidal concentration equivalent to 1.5 times minimum alveolar concentration). Following instrumentation, baseline (time 0) measurements included heart rate (hr), respiratory rate, mean arterial blood pressure (map), cardiac output, and blood gas tensions. Cardiac index (ci), stroke volume (sv), systemic vascular resistance (svr), arterial oxygen content (Cao2 ), and oxygen delivery and consumption (Do2 and Vo2 , respectively) were calculated. Three dogs were given ephedrine iv at a dosage of 0.1 mg/kg of body weight, and 3 dogs were given ephedrine iv at a dosage of 0.25 mg/kg. Measurements were recorded at 5, 10, 15, 30, and 60 minutes. Each dog then received the alternate dosage of ephedrine, and measurements were again recorded at the same intervals. Effects of ephedrine varied with dosage. Neither dosage was associated with significant changes in pH, Pao2 , Paco2 , Vo2 , or respiratory rate. Ephedrine at a dosage of 0.1 mg/kg caused transient significant increases in map, ci, sv, Cao2 , and Do2 , significant decreases in hr and svr, and a late, slight decrease in Cao2 . Ephedrine at a dosage of 0.25 mg/kg caused a greater and more prolonged increase in map, as well as increases in ci, sv, and svr, and a decrease in hr. The higher dosage of ephedrine also caused a pronounced increase in hemoglobin concentration and CaO2 , resulting in a 20 to 35% increase in Do2 throughout the 60-minute experiment.

Free access
in American Journal of Veterinary Research

Summary

Cardiopulmonary and behavioral responses to detomidine, a potent α2-adrenergic agonist, were determined at 4 plasma concentrations in standing horses. After instrumentation and baseline measurements in 7 horses (X̄ ± sd for age and body weight, 6 ± 2 years, and 531 ± 48.5 kg, respectively), detomidine was infused to maintain 4 plasma concentrations: 2.1 ± 0.5 (infusion 1), 7.2 ± 3.5 (infusion 2), 19.1 ± 5.1. (infusion 3), and 42.9 ± 10 (infusion 4) ng/ml, by use of a computer-controlled infusion system.

Detomidine caused concentration-dependent sedation and somnolence. These effects were profound during infusions 3 and 4, in which marked head ptosis developed and all horses leaned heavily on the bars of the restraining stocks. Heart rate and cardiac index decreased from baseline measurements (42 ± 7 beats/min, 65 ± 11 ml·kg of body weight−1·min−1) in linear relationship with the logarithm of plasma detomidine concentration (ie, heart rate = −4.7 [loge detomidine concentration] + 44.3, P < 0.01; cardiac index = −10.5 [loge detomidine concentration] + 73.6, P < 0.01). Second-degree atrioventricular block developed in 5 of 7 horses during infusion 3, and in 6 of 7 horses during infusion 4. Mean arterial blood pressure increased significantly from 118 ± 11 mm of Hg at baseline to 146 ± 27 mm of Hg at infusion 4. Similar responses were observed for mean pulmonary artery and right atrial pressures. Systemic vascular resistance (baseline, 182 ± 28 mm of Hg·ml−1·min−1·kg−1) increased significantly during infusions 3 and 4 (to 294 ± 79 and 380 + 58, respectively). Plasma atrial natriuretic peptide concentration was significantly increased with increasing detomidine concentration (20.4 ± 3.8 pg/ml at baseline to 33.5 ± 9.1 at infusion 4). There were few significant changes in respiration rate and arterial blood gas and pH values. We conclude that maintenance of steady-state detomidine plasma concentrations resulted in cardiopulmonary changes that were quantitatively similar to those induced by detomidine bolus administration in horses.

Free access
in American Journal of Veterinary Research