1University of Cambridge, United Kingdom; and 2Faculty of Veterinary Medicine and Animal Science, UNESP, Botucatu, SP, Brazil.
Equine anesthesia and surgery carry a higher mortality risk than other domestic species and man. Many of these deaths are related to cardiovascular system (CVS) dysfunction. Halothane depresses CVS function and activates the pituitary-adrenal axis (PAA), thus also increasing circulating beta endorphin. This endogenous opioid (EO) may itself contribute to CVS depression. The objective of this study was to investigate EO effects on the CVS and PAA during halothane anesthesia in ponies by studying the effects of opioid antagonism by naloxone. Six ponies (312 ± 50 kg) were anesthetized three times at two week intervals in a randomised cross-over study. On each occasion anesthesia was induced with thiopental and maintained with 1.2% end-tidal halothane for 2 hours. In treatment 1 (IV) naloxone was administered intravenously (0.5 mg/kg as a bolus followed by an infusion at 0.25 mg/kg/hr for 2 hours). In treatment 2 (IT), naloxone (0.5 mg) was injected intrathecally at the cisterna magna immediately after induction. In treatment 3 (control) saline replaced intravenous and intrathecal naloxone. Saline was given intrathecally in the IV group and intravenously in the IT group. Pulse and respiratory rates, arterial blood gases, cardiac output (CO), ECG, and plasma cortisol and ACTH concentrations were measured. Statistical analysis was performed using analysis of variance. Results are expressed as mean ± SEM. Differences were considered significant when P < 0.05. In all groups CVS was depressed (CO decreased by 40%) and plasma ACTH and cortisol increased (three-fold and two-fold respectively). There were no significant differences between groups. This suggests that endogenous opioids do not play a major role in halothane-induced CVS depression in ponies.
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