Search Results

You are looking at 1 - 2 of 2 items for

  • Author or Editor: Liz M. Tyler x
  • Refine by Access: All Content x
Clear All Modify Search

Summary

The uterine hemodynamic response to maternal positioning in dorsal recumbency was evaluated in 7 conscious pregnant cows during the third trimester. Anesthetic or sedative drugs were not administered. Uterine artery flow was measured, using a previously implanted ultrasonic flow probe. Catheters implanted in the uterine artery and vein were used for measurement of blood pressure and for blood sample collections. Heart rate, systemic arterial pressure, uterine arterial blood flow, arterial and venous oxygen and carbon dioxide tensions, and pH were measured in cows in standing position. Cows were cast with ropes and positioned in dorsal recumbency, then measurements were repeated at 15 and 30 minutes. Compared with standing measurements, dorsal recumbency caused 50% increase in heart rate and 44% increase in arterial blood pressure. Uterine artery flow did not change significantly. Despite increased ventilation, arterial oxygenation was reduced during dorsal recumbency. There were minimal differences between measurements at 15 and 30 minutes of dorsal recumbency.

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