Reflex hypotension due to regional activation of left ventricular mechanoreceptors to explain the hypotension noted in clinical myocardial ischaemia or reperfusion.

To determine if regional increases in myocardial contractility, as may occur clinically in angina pectoris, myocardial infarction, or coronary thrombolysis, can initiate the reflex hypotension that sometimes accompanies these conditions, regional injections of positive inotropic agents were made into 32(3)% of the left ventricular myocardium in seven pneumonectomised dogs on total cardiac bypass. The coronary and systemic circulations were isolated and perfused separately. The systemic circulation was perfused at a constant rate so that changes in systemic pressure reflected changes in resistance. Regional injections of doses from 0.001 to 1.0 micrograms noradrenaline in a 0.1 ml volume appreciably increased regional contractility, detected visually and by strain gauge arches, whereas global contractility (left ventricular peak dP/dt) was increased much less. This caused a fall in the systemic pressure (resistance) of 14(2)% below the control value of 78(5)mm Hg, at the largest dose. The decreases in resistance were abolished by bilateral vagotomy, proving their reflex nature. The smaller (0.0001-0.01 micrograms) doses of noradrenaline and the smallest (0.25 micrograms) dose of veratridine increased regional contractility almost without increasing global contractility, indicating that the increase in regional contractility was the major cause of the reflex decrease in systemic resistance. In one animal a decrease in contractility in a control myocardial region occurred simultaneously with the experimentally produced increase in regional left ventricular contractility. This decrease may be analogous to the increase in contractility in the non-ischaemic left ventricular myocardium that occurs simultaneously with the decrease in contractility in the ischaemic region in clinical or experimental myocardial infarction. Left ventricular mechanoreceptors in the region with increased contractility probably initiate the reflex hypotension that sometimes occurs in both circumstances. Thus in angina pectoris or acute myocardial infarction the reflex hypotension probably originates in the hyperactive non-ischaemic myocardial region, whereas in coronary arterial thrombolysis it probably originates in the newly reperfused, formerly ischaemic, region.