Reactive hyperaemia in the dog heart: evidence for a myogenic contribution.

Temporary restriction of arterial inflow after release of eight second coronary artery occlusions greatly reduced reactive hyperaemia but prolonged its duration. Early repayment of the flow debt before restriction did not alter these changes. Despite reduced hyperaemia, there was evidence of subendocardial ischaemia during restriction. Yet occlusions of only one and two cardiac cycles produced marked hyperaemia without evidence of post-release subendocardial ischaemia. All these changes were associated with alterations in peripheral coronary artery pressure consistent with myogenic responses contributing to reactive hyperaemia.