AJP - Heart and Circulatory Physiology, Vol 245, Issue 3 453-H460, Copyright © 1983 by American Physiological Society
Determinants of systemic zero-flow arterial pressure
M. J. Brunner, A. S. Greene, K. Sagawa and A. A. Shoukas
Thirteen pentobarbital-anesthetized dogs whose carotid sinuses were
isolated and perfused at a constant pressure were placed on total cardiac
bypass. With systemic venous pressure held at 0 mmHg (condition 1),
arterial inflow was stopped for 20 s at intrasinus pressures of 50, 125,
and 200 mmHg. Zero-flow arterial pressures under condition 1 were 16.2 +/-
1.3 (SE), 13.8 +/- 1.1, and 12.5 +/- 0.8 mmHg, respectively. In condition
2, the venous outflow tube was clamped at the instant of stopping the
inflow, causing venous pressure to rise. The zero-flow arterial pressures
were 19.7 +/- 1.3, 18.5 +/- 1.4, and 16.4 +/- 1.2 mmHg for intrasinus
pressures of 50, 125, and 200 mmHg, respectively. At all levels of
intrasinus pressure, the zero-flow arterial pressure in condition 2 was
higher (P less than 0.005) than in condition 1. In seven dogs, at an
intrasinus pressure of 125 mmHg, epinephrine increased the zero-flow
arterial pressure by 3.0 mmHg, whereas hexamethonium and papaverine
decreased the zero-flow arterial pressure by 2 mmHg. Reductions in the
hematocrit from 52 to 11% resulted in statistically significant changes (P
less than 0.01) in zero-flow arterial pressures. Thus zero-flow arterial
pressure was found to be affected by changes in venous pressure,
hematocrit, and vasomotor tone. The evidence does not support the literally
interpreted concept of the vascular waterfall as the model for the finite
arteriovenous pressure difference at zero flow.
