Cessation of arterial and venous flow at a finite driving pressure in porcine coronary circulation

We investigated the hypothesis that coronary capacitance is responsible for epicardial coronary artery flow stopping at arterial pressures greater than the coronary venous pressure. Using an in situ blood-perfused swine heart preparation, we compared the arterial pressures at which coronary artery inflow and coronary sinus outflow ceased. A pressure change was used that had the time course of aortic pressure during diastole. Data were obtained in hypocalcemic-arrested, adenosine-vasodilated preparations before and after pharmacologic interventions simulating the coronary circulation of the intact beating heart. The effect of extravascular compression was studied with barium contracture, while acetylcholine was infused to increase coronary vasomotor tone. The arterial pressure when arterial flow ceased was 13 +/- 5 mmHg in the arrested-vasodilated preparations, 37 +/- 10 mmHg after acetylcholine, and from 18 to 150 mmHg during barium contracture. Coronary sinus outflow ceased when arterial pressure was slightly less than the arterial pressure at which arterial flow had stopped. The differences between the arterial and venous zero flow arterial pressures were as follows: arrested-vasodilated 4 +/- 3 mmHg, acetylcholine 9 +/- 4, and barium contracture 0 +/- 3. The arteriovenous pressure gradients across the coronary bed at the instant venous flow ceased were as follows: arrested-vasodilated 5 +/- 6 mmHg, acetylcholine 23 +/- 6, and from 12 to 128 during barium contracture. These data do not support the suggestion that cessation of epicardial artery flow is solely a capacitance phenomenon.