AJP - Heart and Circulatory Physiology, Vol 259, Issue 1 68-H73, Copyright © 1990 by American Physiological Society
Angiotensin and alpha-adrenoceptor activation play a role in hemodynamic response to aortic cross-clamping
S. Gelman, D. L. Bredle, W. E. Bradley and S. M. Cain
Department of Anesthesiology, University of Alabama, Birmingham 35233.
This study was designed to identify the possible role of vasoconstricting
compounds released from ischemic tissues in the hemodynamic response to
cross-clamping of the thoracic aorta. Twenty-one dogs were anesthetized
with pentobarbital sodium. The left hindlimb was denervated, vascularly
isolated, and pump perfused at a constant rate with blood drained from the
inferior vena cava after passing through a gas-exchanging membrane where
oxygen and carbon dioxide tensions were maintained within normal limits.
Left and right thoracotomies were performed, and the aorta and inferior
vena cava were cross-clamped. The cross-clamping was associated with 33-45%
increase in limb vascular resistance in denervated control animals (n = 6).
In animals pretreated with Enalaprilat (2 mg/kg, n = 6), an
angiotensin-converting enzyme inhibitor, limb vascular resistance did not
change significantly. In animals pretreated with phenoxybenzamine (3 mg/kg,
n = 6), an alpha-adrenoceptor antagonist, limb vascular resistance
significantly decreased to 43% of preclamped level. The study demonstrated
that vasoconstrictive compounds, such as angiotensin and catecholamines,
play a role in systemic hemodynamic changes, including arterial
hypertension, observed during cross-clamping of the thoracic aorta.
