Mutual interaction of vasoconstriction and endothelial damage in stenotic arteries.

Abstract

Coronary artery vasomotion may be important in the pathogenesis of angina pectoris. Numerous experimental studies demonstrated accentuated arterial vasomotion in endothelium-damaged vessels. We examined interactions of stenosis, arterial vasoconstriction, and endothelium denudation in a stenosed artery preparation in vitro. Canine carotid arteries and porcine coronary arteries were perfused with a physiological salt solution under constant pressure and a fixed distal resistance. Pressures at the proximal and distal ends of the artery, as well as the flow, were continuously recorded. Hemodynamic responses to serotonin, norepinephrine, and angiotensin II were separately studied. In intact arteries without stenosis, the agonists produced a 30-40% reduction in lumen diameter without altering flow or distal pressure. After a luminal stenosis was created, vasoconstriction produced by the agonists decreased flow and increased the pressure gradient across the stenosis. Flow decreased to (or near) zero, indicating occlusion at the stenotic site. After endothelial loss, this effect was amplified, demonstrating occlusion of the artery and suppression of the flow at significantly (P less than 0.05) lower concentrations of agonist (0.1-0.3) compared with endothelial intact arteries. These studies illustrate 1) the necessity for the presence of stenosis in large arteries for vasoconstriction to impair flow and 2) the protecting effect of intact endothelium in blunting the effects of arterial vasoconstriction in stenosed vessels. Through the reciprocal interaction of arterial stenosis, vasoconstriction, and endothelial damage, ischemic events associated with certain types of vasomotion can be explained.