Regional blood flow during reactive hyperemia in canine myocardium as determined by local washout of xenon-133.

The mechanisms regulating vascular tone in the myocardium were studied in open-chest anesthetized dogs by occlusions of the left anterior descending coronary artery (LAD) for 3 to 600 s. Cumulative excess blood flow (flow in excess of control flow), and repayment of flow debt (cumulative excess blood flow divided by blood flow deficity) were calculated using local injections of Xenon-133 for blood flow measurements. Release of vascular occlusion following 3 s of ischemia was not associated with any measurable hyperemia. Cumulative excess blood flow increased with increasing duration of ischemia from 5 to 600 s, but the increment in excess flow per unit extention of the occlusion time showed a considerable decline. Blood flow in excess exceeded blood flow diet incurred during the occlusion of 10 s duration of 161%; with prolongation of ischemia to 600 s repayment of flow debt declined markedly to about 10%. Oxygen lack in the tissue elicited by perfusion of LAD-for 10 s with constant perfusion rate-with deoxygenated blood produced a fall in peripheral coronary resistance of about 40% which closely corresponds to the fall in resistance observed after a period of LAD occlusion of similar duration. The results lead to the conclusion that 'vasodilator' metabolites formed in the tissue during periods of arterial occlusion are of prime importance for the fall in the tone on the vascular smooth muscle cell occurring in the post-occlusion period. The findings argue against a myogenic component in this response.