Sabbah H N, Marzilli M, Liu Z Q, Stein P D
Clin Exp Pharmacol Physiol. 1986 Jun;13(6):477-86. doi: 10.1111/j.1440-1681.1986.tb00928.x.
The purpose of this study was to determine the extent to which coronary pressure at zero coronary flow (Pf=0) may relate to extravascular compressive forces determined by direct measurements of left ventricular intramyocardial pressure. Studies were performed in nine open-chest anaesthetized dogs in which the anterior descending coronary artery was cannulated and perfused from the carotid artery. Coronary pressure was measured at the tip of the cannula. Intramyocardial pressure was measured with a 1 mm diameter micromanometer inserted directly into the subepicardium. The atrioventricular node was obliterated by cautery and the heart was electrically paced. Long diastolic pauses, sufficient to allow coronary flow to reach zero, were produced by the cessation of electrical pacing. In the autoregulated coronary bed, Pf=0, 47 mmHg (s.e.m. = 9), exceeded subepicardial pressure at zero flow, 23 mmHg (s.e.m. = 2; P less than 0.001). During maximal vasodilatation with adenosine, Pf=0, 16 mmHg (s.e.m. = 11), was not significantly different from subepicardial pressure at zero flow, 21 mmHg (s.e.m. = 4). These observations indicate that, in addition to coronary vasomotor tone, diastolic myocardial tissue pressure is important in the genesis of Pf=0.