Determinants of systemic zero-flow arterial pressure

M. J. Brunner, A. S. Greene, K. Sagawa, A. A. Shoukas

Research output: Contribution to journalArticle

Abstract

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 < 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 < 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.

Original languageEnglish (US)
Pages (from-to)H453-H460
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume14
Issue number3
StatePublished - Jan 1 1983

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

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