Coronary microvascular responses to reductions in perfusion pressure. Evidence for persistent arteriolar vasomotor tone during coronary hypoperfusion.

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Abstract
The goals of this study were to test the following hypotheses: 1) Coronary autoregulatory adjustments to decreases in perfusion pressure occur primarily in coronary arterioles (less than 150 microns in diameter). 2) Small coronary arteries (greater than 150 microns in diameter) can be recruited to participate in the autoregulatory adjustments as perfusion pressure is progressively lowered. 3) Small arterioles are the location of vasodilator reserve in the coronary microcirculation during hypoperfusion. Studies were performed in anesthetized open-chest dogs in which coronary perfusion pressures were reduced to 80, 60, 40, and 30 mm Hg. During reductions in coronary perfusion pressure, measurements were made of systemic hemodynamics, myocardial blood flow (radioactive microspheres), and coronary microvascular diameters. Arterial pressure and heart rate were largely unchanged during the experimental maneuvers. Measurements of microvascular diameters in the beating heart were performed during epi-illumination via a stroboscopic light source synchronized to the cardiac cycle using fluorescence intravital microscopy. Coronary autoregulatory adjustments were evident during reductions in perfusion pressure from control (96 mm Hg) to 80 and 60 mm Hg. Blood flow was unchanged from control, and active vasodilation of coronary arterioles was observed. At 80 mm Hg, only coronary arterioles dilated (4.4 +/- 1.2%), whereas at 60 mm Hg both small arteries (4.9 +/- 2.2%) and arterioles (6.9 +/- 1.2%) demonstrated significant vasodilation (p less than 0.05). The magnitude of dilation (i.e., percent increase in diameter) was inversely related to the initial diameter; that is, the arterioles dilated to a greater extent, percentage wise, than the small arteries. At 40 mm Hg, myocardial blood flow decreased slightly from that under control conditions, but coronary arterioles dilated to a greater extent than at 60 mm Hg (8.1 +/- 1.6%); yet, microvessels were incompletely vasodilated, because adenosine produced a further increase in microvessel diameter (12.5 +/- 2.1%) (p less than 0.05). At a perfusion pressure of 30 mm Hg, arterioles demonstrated a decrease in vascular diameter (-0.2 +/- 2.1%), which was reversed by adenosine (11.1 +/- 3.1%). From these results we concluded the following: 1) Coronary autoregulatory adjustments involve primarily coronary arteriolar vessels, but small coronary arteries can be recruited to participate in the autoregulatory response. 2) The magnitude of vessel dilation appears to be inversely related to vascular diameter. 3) Coronary arterioles are not maximally vasodilated during coronary hypoperfusion, and these vessels may be the source of persistent vasomotor tone during coronary insufficiency.