CARDIAC HYPERTROPHY IN THE ABSENCE OF PRESSURE OVERLOAD: AN EXPERIMENTAL AND CLINICAL REPORT

1. A simulated altitude of 7000 m was applied in rats chronically exposed to hypoxia in a hypobaric chamber. In these experimental conditions the contralateral ventricle not exposed to pressure overload (that is, the left) showed a significant degree of hypertrophy. The hypoxic stimulus did not affect systemic artery pressure or the heart rate.

[1]  J. Goodwin.  The frontiers of cardiomyopathy. , 1982, British heart journal.

[2]  M. Condorelli,et al.  Regression of myocardial hypertrophy in the rat following removal of acute or chronic hypobaric hypoxia. , 1982, European Heart Journal.

[3]  E. Frohlich,et al.  Is arterial pressure the sole factor responsible for hypertensive cardiac hypertrophy? , 1979, The American journal of cardiology.

[4]  A. Nadas,et al.  Rat pulmonary circulation after chronic hypoxia: hemodynamic and structural features. , 1979, The American journal of physiology.

[5]  T. Fujinami,et al.  Impedance cardiography for estimating cardiac output during submaximal and maximal work. , 1978, Journal of applied physiology: respiratory, environmental and exercise physiology.

[6]  R. Arcilla,et al.  Regression of myocardial hypertrophy. I. Experimental model, changes in heart weight, nucleic acids and collagen. , 1975, Journal of molecular and cellular cardiology.

[7]  Meerson Fz.  Development of modern components of the mechanism of cardiac hypertrophy. , 1974 .

[8]  D. H. Will,et al.  Cardiopulmonary responses of male and female swine to simulated high altitude. , 1973, Journal of applied physiology.

[9]  B. Highman,et al.  Effects of polycythemia and altitude hypoxia on rat heart and exercise tolerance. , 1971, The American journal of physiology.

[10]  E. Sonnenblick,et al.  Response of myocardial connective tissue to development of experimental hypertrophy. , 1969, The American journal of physiology.

[11]  J. Williams,et al.  Left ventricular function in patients with chronic obstructive pulmonary disease. , 1968, The Journal of clinical investigation.

[12]  D. Northup,et al.  Differences in Cardiac Hypertrophy in Exercise and in Hypoxia , 1965, Circulation research.

[13]  N. Weiner,et al.  The ability of tyramine to liberate catecholamines in vivo. , 1962, The Journal of pharmacology and experimental therapeutics.

[14]  N. Michelson,et al.  Bilateral ventricular hypertrophy due to chronic pulmonary disease. , 1960, Diseases of the chest.