Abstract
The effect of vagal stimulation on the myocardial ischaemia produced by acute coronary occlusion during beta-receptor blockade has been examined. Epicardial ST-segment elevation, myocardial surface temperature and regional blood flow were determined 10 min after coronary occlusion in the dog. Coronary occlusion after beta-receptor blockade alone raised the average ST-segment from 0.5 ± 0.3 to 3.1 ± 0.5 mV (SEM) (P <0.001). Subsequent vagal stimulation with beta-receptor blockade, which reduced heart rate from 129 to 50 beats/min, mean arterial pressure from 123 to 78 mmHg, but increased cardiac output from 1164 to 1855 ml/min, resulted in marked reduction in ST-segment elevation to 0.3 ± 0.2 mV which was not different from the control before occlusion. Epicardial temperature was markedly decreased in the ischaemic area following coronary occlusion. The temperature difference between central ischaemic and surrounding areas became smaller after beta-receptor blockade, and vanished during vagal stimulation. Vagal stimulation caused a 55% decrease of blood flow in all non-ischaemic regions. A smaller reduction took place in the border zone where flow values close to those of the non-ischaemic myocardium were obtained. In the central ischaemic area blood flow remained unchanged despite the reduction in arterial pressure. Thus, vagal stimulation resulted in decreased collateral resistance in the ischaemic area and a marked reduction of myocardial oxygen requirement of both non-ischaemic and border zone myocardium, additional to that obtained with beta-receptor blockade. The provision of energy to the ischaemic myocardium is therefore very favourably balanced with its actual demand during vagal stimulation.