Cardiopulmonary and behavioral responses to computer-driven infusion of detomidine in standing horses

David A. Daunt From the Departments of Molecular and Cellular Physiology (Daunt) and Anesthesiology (Shafer, Maze), Stanford University, Stanford, CA 94305; the Departments of Clinical Sciences (Dunlop, Hodgson, Tyler) and Statistics (Chapman), College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80523; and the Departments of Pharmacology and Toxicology (Ruskoaho) and Physiology (Vakkuri), University of Oulu, Oulu, Finland.

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Colin I. Dunlop From the Departments of Molecular and Cellular Physiology (Daunt) and Anesthesiology (Shafer, Maze), Stanford University, Stanford, CA 94305; the Departments of Clinical Sciences (Dunlop, Hodgson, Tyler) and Statistics (Chapman), College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80523; and the Departments of Pharmacology and Toxicology (Ruskoaho) and Physiology (Vakkuri), University of Oulu, Oulu, Finland.

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Phillip L. Chapman From the Departments of Molecular and Cellular Physiology (Daunt) and Anesthesiology (Shafer, Maze), Stanford University, Stanford, CA 94305; the Departments of Clinical Sciences (Dunlop, Hodgson, Tyler) and Statistics (Chapman), College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80523; and the Departments of Pharmacology and Toxicology (Ruskoaho) and Physiology (Vakkuri), University of Oulu, Oulu, Finland.

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Steven L. Shafer From the Departments of Molecular and Cellular Physiology (Daunt) and Anesthesiology (Shafer, Maze), Stanford University, Stanford, CA 94305; the Departments of Clinical Sciences (Dunlop, Hodgson, Tyler) and Statistics (Chapman), College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80523; and the Departments of Pharmacology and Toxicology (Ruskoaho) and Physiology (Vakkuri), University of Oulu, Oulu, Finland.

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Heikki Ruskoaho From the Departments of Molecular and Cellular Physiology (Daunt) and Anesthesiology (Shafer, Maze), Stanford University, Stanford, CA 94305; the Departments of Clinical Sciences (Dunlop, Hodgson, Tyler) and Statistics (Chapman), College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80523; and the Departments of Pharmacology and Toxicology (Ruskoaho) and Physiology (Vakkuri), University of Oulu, Oulu, Finland.

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Olli Vakkuri From the Departments of Molecular and Cellular Physiology (Daunt) and Anesthesiology (Shafer, Maze), Stanford University, Stanford, CA 94305; the Departments of Clinical Sciences (Dunlop, Hodgson, Tyler) and Statistics (Chapman), College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80523; and the Departments of Pharmacology and Toxicology (Ruskoaho) and Physiology (Vakkuri), University of Oulu, Oulu, Finland.

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David S. Hodgson From the Departments of Molecular and Cellular Physiology (Daunt) and Anesthesiology (Shafer, Maze), Stanford University, Stanford, CA 94305; the Departments of Clinical Sciences (Dunlop, Hodgson, Tyler) and Statistics (Chapman), College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80523; and the Departments of Pharmacology and Toxicology (Ruskoaho) and Physiology (Vakkuri), University of Oulu, Oulu, Finland.

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Liz M. Tyler From the Departments of Molecular and Cellular Physiology (Daunt) and Anesthesiology (Shafer, Maze), Stanford University, Stanford, CA 94305; the Departments of Clinical Sciences (Dunlop, Hodgson, Tyler) and Statistics (Chapman), College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80523; and the Departments of Pharmacology and Toxicology (Ruskoaho) and Physiology (Vakkuri), University of Oulu, Oulu, Finland.

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Mervyn Maze From the Departments of Molecular and Cellular Physiology (Daunt) and Anesthesiology (Shafer, Maze), Stanford University, Stanford, CA 94305; the Departments of Clinical Sciences (Dunlop, Hodgson, Tyler) and Statistics (Chapman), College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80523; and the Departments of Pharmacology and Toxicology (Ruskoaho) and Physiology (Vakkuri), University of Oulu, Oulu, Finland.

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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.

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.

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