Effect of renal hypertension and left ventricular hypertrophy on the coronary circulation in dogs.
- 1 April 1978
- journal article
- research article
- Published by Wolters Kluwer Health in Circulation Research
- Vol. 42 (4), 543-549
- https://doi.org/10.1161/01.res.42.4.543
Abstract
The effects of pressure-induced left ventricular hypertrophy on the coronary circulation was investigated. Hypertrophy was induced by single-kidney renal vascular hypertension in 12 dogs. Ventricular mass in the dogs with hypertrophy was about 50% greater than in 11 controls. A 3rd group of 6 dogs, with a similar amount of left ventricular hypertrophy but normal blood pressure after repair of the renal artery stenosis, also was studied. Total and regional myocardial blood flow was measured with radioactive microspheres at rest, during pacing at a rate of 200 (in the control and hypertensive dogs), and during maximal vasodilation induced with adenosine (4.7 .mu.m/kg .times. min). Regional distribution of coronary flow was normal at rest in dogs with hypertension and left ventricular hypertrophy and in dogs with hypertrophy alone. Pacing caused a 16% decrease in the endocardial-epicardial perfusion ratio only in the hypertrophied ventricles of the hypertensive dogs. During maximal coronary vasodilation, the coronary vascular resistance of the entire left ventricle was no different among the 3 groups: the controls, the hypertensive dogs with left ventricular hypertrophy, and the normotensive dogs with left ventricular hypertrophy (0.14 .+-. 0.02 SEM, 0.16 .+-. 0.02, and 0.14 .+-. 0.02 mm Hg/ml .times. min, respectively). The use of the minimal coronary vascular resistance measured during maximal vasodilation as an index of the functional cross-sectional area of the coronary bed suggests that the cross-sectional area does not increase with hypertrophy. This failure of the cross-sectional area of the coronary bed to increase commensurate with the degree of hypertrophy is due to an anatomical or architectural alteration of the relationship between the coronary bed and the cardiac muscle and is not due to a functional alteration caused by hypertension alone. The hypertrophied ventricle may be at greater risk of ischemic injury.This publication has 16 references indexed in Scilit:
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