Large coronary arteries exhibit reactive dilation following brief periods of occlusion, a response dependent on the marked increase in coronary blood flow (reactive hyperemia) rather than autonomic or prostaglandin-mediated mechanisms.
To study the response of large coronary arteries to short periods of myocardial ischemia a pair of ultrasonic dimension transducers, a flow probe and a hydraulic occluder were implanted around the left circumflex coronary artery for the instantaneous and continuous measurement of external coronary artery dimensions and coronary blood flow, respectively. At 6.1 +/- 0.4 seconds after release of a 15-second occlusion, mean coronary blood flow increased by 255 +/- 30% from a preocclusion flow of 32 +/- 4.1 ml/min. At this time, large coronary arterial cross-sectional area was unchanged but increased slowly, reaching a peak 28 +/- 4.4% above preocclusion levels 61 +/- 3.2 seconds after occlusion, i.e., reactive dilation. During maximal reactive dilation, coronary blood flow had already returned to control levels, and heart rate, mean arterial pressure, left ventricular systolic pressure, and left ventricular dP/dt were not different from control. The reactive dilation was not affected if the occlusion occurred proximal or distal to where diameter was measured, or by combined alpha- and beta-adrenergic receptor blockade, ganglionic blockade, inhibition of prostaglandin synthesis, or by aminophylline. When the reactive hyperemia was prevented by constricting the coronary artery upon release of the coronary occlusion, the reactive dilation was not observed. Thus, large coronary arteries respond to brief periods of occlusion with reactive dilation. The time course of this response is distinctly different from the accompanying reactive hyperemia, and could be eliminated by preventing the marked increase in coronary blood flow following release from the brief period of coronary artery occlusion.
Hintze et al. (1984) studied this question.