AJP - Heart and Circulatory Physiology, Vol 249, Issue 3 534-H539, Copyright © 1985 by American Physiological Society
Myocardial perfusion in compensated and failing hypertrophied left ventricle
D. G. Parrish, W. S. Ring and R. J. Bache
This study examined blood flow in the hypertrophied left ventricle with and
without failure. Left ventricular hypertrophy was produced in 20 dogs by
banding the ascending aorta at 6-7 wk of age; studies were performed after
animals reached adulthood. Sixteen dogs had compensated hypertrophy, while
four dogs had cardiac failure manifested by left ventricular dilatation and
end-diastolic pressures greater than 18 mmHg. The degree of hypertrophy,
assessed by left ventricular-to-body weight ratio, was similar in animals
with compensated hypertrophy (7.29 +/- 0.26 g/kg) and failure (8.45 +/-
0.15); both were greater than control (4.50 +/- 0.15, P less than 0.01).
Left ventricular systolic pressure was similar in compensated hypertrophy
(184 +/- 9 mmHg) and failure (226 +/- 29), as compared with control (130
+/- 4; P less than 0.01). Left ventricular blood flow measured with
microspheres was 0.89 +/- 0.07 ml X min-1 X g-1 in control animals, was
increased to 1.34 +/- 0.05 with compensated hypertrophy (P less than
0.001), and was further increased with failure to 1.86 +/- 0.40 (P less
than 0.05). The left ventricular wall thickness-to-cavity diameter ratio
was increased to 0.63 +/- 0.04 with compensated hypertrophy but was only
0.40 +/- 0.05 in dogs with failure (P less than 0.01), suggesting that wall
stress was greater in hearts with failure. These data suggest that
increased blood flow rates in dogs with failure resulted from increased
myocardial O2 requirements due to increased systolic wall stress. Need for
increased blood flow during resting conditions in dogs with failure would
impair the ability for further coronary vasodilation during periods of
cardiac stress.
