The objective of this study was to determine whether coronary vascular resistance remains constant during long diastoles and whether critical closure of arterial microvessels occurs at zero-flow pressure. For this purpose, we directly measured internal diameters and red blood cell velocities in arterial and venous coronary microvessels during long diastoles under maximal vasodilation. The epicardial coronary microcirculation was viewed in anesthetized, open-chest mongrel dogs through an intravital microscope equipped with a newly developed floating objective. Coronary microvascular diameters and red blood cell velocities were measured with high-speed cinematography. During maximal vasodilation (150 μg/kg body wt i.v. dilazep), long diastoles were induced by vagal nerve stimulation. Internal diameters of all small arteries and arterioles (N = 12) gradulally declined with decreasing aortic pressure during long diastoles, and the reduction of the diameter was greatest when aortic pressure was less than 35 mm Hg. The mean internal diameter (88.8 ± 52.2 μm) at minimal aortic pressure (19.2 ± 6.4 mm Hg) was significantly less than that at an aortic pressure of 100 mm Hg (116.2 ± 68.5 μm, p < 0.01). The internal diameters of small veins and venules remained nearly constant during long diastoles. When red blood cell progression in coronary microvessels stopped at the nadir of aortic pressure, all arterial coronary microvessels remained open; that is, there was no evidenc of 'critical closure'. Zero-flow pressure (13.6 ± 1.7 mm Hg), at which red blood cell progression in coronary microvessels stopped, was higher than right atrial pressure (3.2 ± 4.4 mm Hg, p < 0.01) and left ventricular end-diastolic pressure (8.6 ± 2.7 mm Hg, p < 0.05). The relations between pressure and red blood cell velocity in arterioles, capillaries, and venules were curvilinear at lower aortic pressures. These results indicate that coronary vascular resistance does not remain constant during long diastoles but gradually increases with the decline in prefusion pressure even in the maximally vasodilated condition and that, in the epimyocardium, zero-flow pressure is not caused by critical closure of arterial microvessels.
ASJC Scopus subject areas