Reactive hyperemia in the dog heart. Effects of temporarily restricting arterial inflow and of coronary occlusions lasting one and two cardiac cycles.

With electromagnetic flow transducers and pneumatic cuff occluders on the circumflex branch of the left coronary artery in conscious and in anesthetized dogs, we examined the effects of both a temporary reduction in postocclusion hyperemia and oneand twocardiac cycle occlusions of the artery on the size and the duration of the hyperemic response. After release of 8-second occlusions, flow was prevented from rising to more than 10-20% above the preocclusion value for the expected duration of the hyperemia. Peripheral coronary arterial pressure measurements established that this maneuver produced a pressure gradient. Temporary restriction of arterial inflow markedly reduced the percent repayment of the flow deficit from 618 ± 34% to 213 ± 17% (mean ± SE) and moderately prolonged the duration of the response from 95 ± 4 seconds to 129 ± 5 seconds (P < 0.0005 for both). In conscious dogs, the mean percent repayment after a one-cycle (0.7-second) occlusion was 227%. Much larger and longer-lasting responses were obtained with one-cycle (0.4-second) occlusions in anesthetized dogs in which heart rate and blood pressure were considerably higher. Since restricting arterial inflow resulted in a large reduction in reactive hyperemia with only a small increase in its duration, local mechanisms acting in the interstitial space and possibly in the vascular smooth muscle may be relatively more important for the hyperemia that occurs after short occlusions than is the myocardial release of freely diffusible metabolites that are removed by the blood stream. The results with oneand two-cycle occlusions suggest that myogenic responses contribute to the hyperemia, since it is unlikely that such brief occlusions produce myocardial hypoxia under resting conditions.