Venules During Prolonged Diastole in Canine Left Ventricles

Using a needle-probe videomicroscope with a charge-coupled device (CCD) camera, we measured the diameter of subendocardial arterioles and venules during prolonged diastole beyond the time point at which coronary blood flow reached zero. In seven open-chest heart-blocked dogs, a sheathed needle probe with a doughnut-shaped balloon was introduced from the left atrial appendage and advanced into the left ventricle through the mitral valve. The tip of the probe was placed gently on the endocardial surface. Diameters of arterioles (n= 16) and venules (n= 16) at the beginning of long diastole ranged from 40 to 126 ,um and from 32 to 192 ,um, respectively. After cardiac arrest, the arteriolar diameter gradually declined with aortic pressure. Arteriolar diameters at zero flow decreased by 28±9% (mean±SD) compared with A rterial blood inflow into the myocardium is almost exclusively limited to diastole, since cardiac contraction impedes the coronary arterial flow in systole.1-3 To understand the mechanisms by which the myocardium is perfused during diastole, the coronary pressure-flow (P-F) relation during diastole has been investigated.4 In 1978, Bellamy5 observed that coronary arterial inflow during long diastole could become zero while aortic pressure was still substantially higher than right atrial pressure. He suggested that the collapse of arterioles may occur, causing a vascular waterfall phenomenon attributable to a high zero-flow pressure. If this happens, the high zero-flow pressure depends on the intramyocardial pressure around the vessels. The slope of the P-F relation and its intercept with the pressure axis were of major interest, since they were considered to indicate coronary vascular resistance and effective back pressure to flow. An alternative hypothesis for high zero-flow pressures, based on intramyocardial capacitance, was put forward by Spaan.6 He pointed out that intramyocardial vessels have a relatively large capacitance and that the resulting long time constant leads to an apparently high zero-flow pressure. Received November 9, 1993; accepted April 28, 1994. From the Department of Medical Engineering and Systems Cardiology, Kawasaki Medical School, Kurashiki, Okayama, Japan. Presented in part at the 65th Scientific Sessions of the American Heart Association, November 1992, New Orleans, La (Circulation. 1992;86[suppl I]:I-508). Correspondence to Osamu Hiramatsu and reprint requests to Fumihiko Kajiya, Professor, MD, PhD, Department of Medical Engineering and Systems Cardiology, Kawasaki Medical School, 577 Matsushima, Kurashiki, Okayama, 701-01, Japan. ©