The results of reperfusion coronary circulatory alterations manifested by a rapid cessation of reactive hyperemia and a secondary increase in coronary vascular resistance were studied in acute canine experiments on a model of partial blood flow restriction by 30,, 50, 70, and 90% with subsequent reperfusion. It was shown that most frequently delayed disturbances of myocardial blood supply adequacy, which is qualified as a reperfusion coronarogenic mechanism of secondary coronary failure progression, which differs from the well-known phenomenon of unrestored coronary blood flow, which occurs after blood flow restriction to a greater extent.