Acute blood pressure elevation and ventricular fibrillation threshold during coronary occlusion and reperfusion in the dog.
The effect of acute elevation of arterial blood pressure on the ventricular fibrillation threshold was examined in 19 closed chest dogs anesthetized with chloralose during 10 minutes of occlusion followed by abrupt reperfusion of the left anterior descending coronary artery. Ventricular fibrillation threshold was determined using two methods of electrical testing: sequential R/T pulsing and the train of stimuli method. Blood pressure was increased with an intravenous injection of the alpha adrenergic stimulator phenylephrine. Acute hypertension significantly diminished the enhanced vulnerability associated with coronary occlusion. After denervation of the carotid sinus and aortic arch baroreceptors, elevation of blood pressure failed to affect vulnerability during occlusion. In both intact and denervated animals, the predisposition to ventricular fibrillation after reperfusion was unchanged by the increase in blood pressure. It is suggested that withdrawal of sympathetic tone mediated by the baroreceptor reflex is the basis for the protection against ventricular fibrillation resulting from elevation of blood pressure. The failure of acute hypertension to alter vulnerability during reperfusion suggests that the predisposition to ventricular fibrillation during reperfusion is due to mechanisms other than those operating during coronary occlusion.
D000818:Animals; D001011:Aorta / Q000294:innervation; D001794:Blood Pressure / Q000187:drug effects; D002346:Carotid Sinus / Q000294:innervation; D003326:Coronary Circulation; D003327:Coronary Disease / Q000150:complications*; D003331:Coronary Vessels / Q000601:surgery; D003714:Denervation; D004195:Disease Models, Animal; D004285:Dogs; D008026:Ligation; D010656:Phenylephrine / Q000494:pharmacology; D014693:Ventricular Fibrillation / Q000209:etiology*
D010656:Phenylephrine