AJP - Heart and Circulatory Physiology, Vol 259, Issue 3 796-H803, Copyright © 1990 by American Physiological Society
Captopril reduces left ventricular enlargement induced by chronic volume overload
R. G. Gay
Department of Internal Medicine, Veterans Administration Medical Center, Portland, Oregon.
The effect of captopril treatment on left ventricular (LV) function, mass,
and volume during chronic volume overload induced by production of aortic
insufficiency (AI) was studied. AI was caused by mechanical disruption of
the aortic valve in 175- to 225-g male Sprague-Dawley rats. At 24 h after
surgery, AI and sham-operated rats were divided into control and captopril
treatment (2 g/l drinking water) groups. After 2 mo of treatment,
hemodynamics were measured in open-chest rats, and the LV pressure-volume
relation was determined ex vivo. Compared with sham-operated rats, in the
untreated AI rats, aortic pulse pressure was increased nearly 100%, LV
end-diastolic pressure was 10 +/- 1 vs 3 +/- 1 mmHg, and LV end-diastolic
volume was 1.25 +/- 0.07 vs 0.36 +/- 0.03 ml. LV weight was increased 43%
and the LV pressure-volume relation was shifted rightward by AI. LV
systolic and diastolic wall stress were increased in rats with AI. Peak LV
pressure during aortic occlusion was decreased in AI rats, however, peak
wall stress during aortic occlusion was not different compared with
sham-operated rats. Captopril treatment decreased aortic pulse pressure and
LV systolic pressure. Both LV weight and LV end-diastolic volume measured
from the ex vivo pressure-volume relation at LV end-diastolic pressure were
increased by 33% in untreated AI rats compared with captopril-treated AI
rats. Captopril treatment of AI rats shifted the LV pressure-volume to the
left compared with untreated rats. LV pressure and wall stress during
aortic occlusion were not changed in captopril-treated AI rats.(ABSTRACT
TRUNCATED AT 250 WORDS)
