The effect of halothane on reflexes elicited by acute coronary artery occlusion in the dog

Abstract

Acute myocardial infarction in the intra- or perioperative period may be accompanied by either bradycardia and hypotension or tachycardia and hypertension. Different degrees of activation of cardiac and arterial receptors stimulated by the infarction may produce the seemingly dichotomous results. When infarction occurs intraoperatively, the effects of anesthesia may also play a role on the reflex responses observed. This study was performed for two reasons; 1) to study the effects of acute coronary artery occlusion (ACO) on vascular resistance; and 2) to study the effects of halothane (H) anesthesia on this ACO reflex. Snare occlusions of the left coronary arteries were performed in pentothal-anesthetized mongrel dogs, and changes in arterial presure, left ventricular length, hindlimb vascular resistance, and lumbar sympathetic efferent nerve activity were measured during 30- to 60-s occlusions at 0, 0.5, 1.0, and 1.5 per cent end tidal halothane concentrations. ACO produced a consistent depressor response, produced by withdrawal of sympathetic efferent activity, that was significantly attenuated by vagotomy. Increasing levels of H blunted the reflex depression in vascular resistance, and also produced decreases in baseline resistance and increases in left ventricular end diastolic length (LVEDL). Vagotomy blunted the dose-dependent decrease in baseline resistance with H. Therefore, the study has shown that: 1) ACO activates vagal afferents to initiate a reflex decrease in vascular resistance; 2) this reflex dilatation is attenuated with increasing levels of H; and 3) by producing increases in LVEDL, H stimulates cardiac receptors and reflexly reduces vascular resistance.