Coronary vascular reactivity is temporarily reduced in the immediate postreactive hyperemic period following brief coronary occlusions, independent of beta-adrenergic mechanisms or vasodilator metabolite depletion.
Using electromagnetic flow transducers on the circumflex branch of the left coronary artery in anesthetized dogs and in conscious dogs, we examined the effects of repeated brief coronary artery occlusions on reactive hyperemic responses and those of injected vasodilators given before the occlusions and in the immediate postreactive hyperemic period on coronary blood flow responses. Three successive occlusions (4 or 8 seconds) at 1-minute intervals were accompanied by decreasing reactive hyperemia; the full response was restored after 5 minutes. Beta-receptor blockade reduced resting coronary blood flow, blood pressure, and heart rate, but it did not change this response pattern. When injections of adenosine, glyceryl trinitrate, or papaverine were given before and after a sequence of a 4-second and an 8-second occlusion performed 1 minute apart, the postocclusion vasodilator responses were reduced for up to 3 minutes. We concluded that the coronary vascular reactivity in the immediate postreactive hyperemic period was temporarily reduced. The mechanisms are not understood, but the results suggest that the reduced reactivity was not due to the depletion of a vasodilator metabolite produced during ischemia or to the development of tachyphylaxis to the coronary vasodilating action of adenosine. Also, the reduction in reactivity was not mediated through beta action of catecholamines.
Eikens et al. (Sat,) studied this question.