PROPORTIONAL ARTERIOLAR GROWTH ACCOMPANIES CARDIAC-HYPERTROPHY INDUCED BY VOLUME OVERLOAD

Citation
Yw. Chen et al., PROPORTIONAL ARTERIOLAR GROWTH ACCOMPANIES CARDIAC-HYPERTROPHY INDUCED BY VOLUME OVERLOAD, American journal of physiology. Heart and circulatory physiology, 36(6), 1994, pp. 80002132-80002137
Citations number
32
Categorie Soggetti
Physiology
ISSN journal
03636135
Volume
36
Issue
6
Year of publication
1994
Pages
80002132 - 80002137
Database
ISI
SICI code
0363-6135(1994)36:6<80002132:PAGACI>2.0.ZU;2-H
Abstract
Volume overload-induced cardiac hypertrophy is char acterized by norma l coronary reserve and maximal flow. Accordingly, we tested the hypoth esis that both arteriolar and capillary growth are proportional to the magnitude of hypertrophy in this model. Five months after performing an aortocaval fistula [arteriovenous (A-V) shunt] in young rats, right and left ventricles were 61 and 55%, respectively, heavier than their sham controls. Using morphometric methods and image analysis, we foun d that increases in cardiac myocyte cross-sectional area accounted for similar to 50% of the hypertrophy and that arteriolar length density (L(v)) (7.5 +/- 0.9 and 7.0 +/- 0.4 mm/mm(3)) and the frequency distri bution of arteriolar diameters were similar in the hearts from A-V shu nt and control rats. Capillary L(v) in the right ventricle was similar in the two groups; in the left ventricle a significantly lower L(v) f or the A-V shunt rats was noted only in the endomyocardium. Capillary volume density was not attenuated in the A-V shunt rats, since slightl y larger luminal diameters compensated for any decrements in L(v) in t he left ventricle. These findings provide an anatomic basis for the ob servation that maximal myocardial perfusion is not necessarily comprom ised in ventricular enlargement due to aortocaval fistula. Because dia stolic volume is increased in this model and thereby provides a stretc h on the microvasculature, our findings are consistent with those from other models of cardiac hypertrophy in which enhancement of mechanica l factors is associated with angiogenesis.