Key result
Increasing mean aortic pressure by 50% with angiotensin or vasopressin significantly decreased cardiac output in dogs, whereas mechanical balloon occlusion maintained cardiac output.
Why the study?
How do angiotensin and vasopressin affect cardiac and peripheral circulatory responses compared to mechanical afterload increases in dogs?
How do angiotensin and vasopressin affect cardiac and peripheral circulatory responses compared to mechanical afterload increases in dogs?
Absolute Event Rate: 146% vs 161%
p-value: p=<0.01
Angiotensin and vasopressin exert distinct effects on the venous circulation that are independent of their mechanical effects on arterial pressure.
Suggests vasopressors may impair output via venous effects beyond afterload; leaves open translation to human hemodynamics.
To determine the cardiac and peripheral circulatory responses to changes in afterload with angiotension and vasopressin, we increased mean aortic pressure 25% and 50% above control in splenectomized and ganglion-blocked dogs. We compared these responses to similar mechanical increases in aortic pressure produced by partial balloon occlusion of the descending aorta. With 25% or 50% increases in aortic pressure, angiotensin, vasopressin, and balloon inflation produced no changes in heart rate, right atrial, and mean pulmonary artery pressures. At 25% increase in aortic pressure, cardiac output was maintained with angiotensin and balloon occlusion but decreased with vasopressin. At 50% increase in aortic pressure, cardiac output was maintained with only balloon occlusion and decreased with both angiotensin and vasopressin. Whenever cardiac output fell, central blood volume did not increase as after-load increased. These changes in preload can be explained by alterations in the venous circulation. Vasopressin did not alter venous compliance or unstressed vascular volume but increased resistance to venous return. Angiotensin also increased resistance to venous return but decreased venous compliance and did not change unstressed vascular volume. Balloon occlusion had no effects on these parameters. We conclude that: (a) angiotensin caused significant venoconstriction resulting in maintenance of cardiac output at 25% but not 50% increase in aortic pressure; (b) vasopressin increased the resistance to venous return without venoconstriction; this resulted in a fall in cardiac output even with a 25% increase in aortic pressure; and (c) the effects of the agents on the venous circulation were independent of the mechanical effects of a pressure increase in the arterial circulation.
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Lee et al. (1988) studied Normal hemodynamics (animal model) (n=11). Angiotensin and Vasopressin vs. Baseline / Mechanical balloon occlusion was evaluated on Cardiac index (ml/kg/min) at 50% increase in mean aortic pressure with angiotensin (p=<0.01). Increasing mean aortic pressure by 50% with angiotensin or vasopressin significantly decreased cardiac output in dogs, whereas mechanical balloon occlusion maintained cardiac output.
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