TY - JOUR
T1 - Myocardial perfusion in compensated and failing hypertrophied left ventricle
AU - Parrish, D. G.
AU - Ring, W. S.
AU - Bache, R. J.
PY - 1985
Y1 - 1985
N2 - 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 >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 < 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 < 0.01). Left ventricular blood flow measured with microspheres was 0.89 ± 0.07 ml·min-1·g-1 in control animals, was increased to 1.34 ± 0.05 with compensated hypertrophy (P < 0.001), and was further increased with failure to 1.86 ± 0.40 (P < 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 < 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.
AB - 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 >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 < 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 < 0.01). Left ventricular blood flow measured with microspheres was 0.89 ± 0.07 ml·min-1·g-1 in control animals, was increased to 1.34 ± 0.05 with compensated hypertrophy (P < 0.001), and was further increased with failure to 1.86 ± 0.40 (P < 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 < 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.
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U2 - 10.1152/ajpheart.1985.249.3.h534
DO - 10.1152/ajpheart.1985.249.3.h534
M3 - Article
C2 - 4037102
AN - SCOPUS:0022119869
SN - 0363-6135
VL - 18
SP - H534-H539
JO - American Journal of Physiology - Heart and Circulatory Physiology
JF - American Journal of Physiology - Heart and Circulatory Physiology
IS - 3
ER -