AJP - Heart and Circulatory Physiology, Vol 242, Issue 6 973-H979, Copyright © 1982 by American Physiological Society
Nonsympathetic increased inotropic state early after aortic insufficiency
B. Crozatier, D. Caillet, J. L. Chevrier and P. Y. Hatt
The very early left ventricular response to chronic volume overload induced
by aortic insufficiency (AI) was examined in conscious dogs previously
instrumented with a left ventricular micromanometer and ultrasonic crystals
measuring internal diameter, segmental length, and parietal wall thickness.
Acute volume loading with dextran (AVL) was compared with that 24 and 48 h
after AI induced by a perforation of the aortic valve. beta-Blockade was
also produced before and after AI. For a similar increase in preload in AVL
and after AI, the percent change in systolic shortening of diameters and
segments (% delta L) increased from 30.4 to 34.1% after AI (P less than
0.01). For matched calculated wall stress during AVL and AI, % delta L and
peak velocity of shortening were significantly increased after AI, and the
same results were reproduced after beta-blockade. We conclude that, at the
early phase of chronic volume overload before hypertrophy appears, left
ventricular hyperfunction is mainly due to a nonsympathetic increased
contractility and that, in the conscious dog, the inotropic state appears
to be modified by a sustained increased preload.
