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Effects of antagonism of platelet thromboxane receptors and α2-adrenoceptors on arrhythmogenesis and electrophysiology during myocardial ischaemia
J Mol Cell Cardiol 24 (Supplement I) (1992) p-07-46
REGRESSION OF CARDIAC HYPERTROPHY IN HYPERTENSIVE RATS Takaaki Iwai, Masahito Tsuchiya, Tohru Arino, Akira Tanamura, Izuru Nakamura, Tadanari Ohkubo, Nobuakira Takeda, Makoto Nagano. Department of Internal Medicine, Aoto Hospital, Jikei University School of Medicine, Tokyo, Japan. Regression of cardiac hypertrophy was investigated physiologically and biochemically in hypertensive rats (Goldblatt rats and SHR). Regression of cardiac hypertrophy was induced by lowering of blood pressure by nephrectmy on the affected side in Goldblatt rats or by long-term administration of ACE inhibitor in SHR. Blood pressure of nephrectomized Goldblatt rats was reduced almost to normal, and that of ACE inhibitor-treated SHR was slightly decreased, although to a significant extent. Active or rcsing tension of isometric contraction of isolated left ventricular papillary muscles remained unchanged. Speed parameters tended to be decreased in the hypertrophic myocardium, and returned to normal lcvcls upon regression of hypertrophy. The myocardial collagen content, assessed in terms of hydroxyproline concentration, was slightly increased in the hypertensive myocardium, but not significantly. The content did not change significantly upon regression of cardiac hypertrophy. The regression of cardiac hypertiophy observed in ACE inhibitor-treated SHR was less marked than that in nephrcctomizcd Goldblatt rats. It is concluded that the degree of reduction of cardiac mechanical overload must singnificantly influence the regression of cardiac hypertrophy.
p-07-47ABNORMAL CALCIUM HANDLING IN THE CHRONICALLY INFARCTED RAT HEART. Louise K Rix. Campbell H Thompson, George K Radda, and Anne-Marie L Seymour’. Dept. Biochemistry, Oxford University, Oxford, OX1 3QU, U.K. Dept. Cartfiithoracic Surgery, N.H.L.I., London SW3 6LY, U.K. Myocardial infarction (PMI) is known to cause both ventricular hypertrophy and failure. The aim of this study was to investigate the cardiac contractility of female Wistar rats (f60-18Og) following ligation of the left coronary artery. After 5 weeks the heart weight&@ weight ratio of the PMI hearts had increased by 29.6% (n=6, p
P-()7-46POSTZCHEMIC CONTRIBUTIONS
DIASTOLIC DYSFUNCTION OF DEPRESSED REFLOW
IN THE HYPERTROPHIED AND CORONARY VASCULAR
RAT HEART: TURGOR
THE RELATIVE
0 hyperemic re(low I depressedreflmv * pO.oS v C depressed refbw during early repetfusion, and (ii) may b;e due to a greater contribution to wall stiffness from coronary turgor. S.247
REGRESSION OF CARDIAC HYPERTROPHY IN HYPERTENSIVE RATS Takaaki Iwai, Masahito Tsuchiya, Tohru Arino, Akira Tanamura, Izuru Nakamura, Tadanari Ohkubo, Nobuakira Takeda, Makoto Nagano. Department of Internal Medicine, Aoto Hospital, Jikei University School of Medicine, Tokyo, Japan. Regression of cardiac hypertrophy was investigated physiologically and biochemically in hypertensive rats (Goldblatt rats and SHR). Regression of cardiac hypertrophy was induced by lowering of blood pressure by nephrectmy on the affected side in Goldblatt rats or by long-term administration of ACE inhibitor in SHR. Blood pressure of nephrectomized Goldblatt rats was reduced almost to normal, and that of ACE inhibitor-treated SHR was slightly decreased, although to a significant extent. Active or rcsing tension of isometric contraction of isolated left ventricular papillary muscles remained unchanged. Speed parameters tended to be decreased in the hypertrophic myocardium, and returned to normal lcvcls upon regression of hypertrophy. The myocardial collagen content, assessed in terms of hydroxyproline concentration, was slightly increased in the hypertensive myocardium, but not significantly. The content did not change significantly upon regression of cardiac hypertrophy. The regression of cardiac hypertiophy observed in ACE inhibitor-treated SHR was less marked than that in nephrcctomizcd Goldblatt rats. It is concluded that the degree of reduction of cardiac mechanical overload must singnificantly influence the regression of cardiac hypertrophy.
p-07-47ABNORMAL CALCIUM HANDLING IN THE CHRONICALLY INFARCTED RAT HEART. Louise K Rix. Campbell H Thompson, George K Radda, and Anne-Marie L Seymour’. Dept. Biochemistry, Oxford University, Oxford, OX1 3QU, U.K. Dept. Cartfiithoracic Surgery, N.H.L.I., London SW3 6LY, U.K. Myocardial infarction (PMI) is known to cause both ventricular hypertrophy and failure. The aim of this study was to investigate the cardiac contractility of female Wistar rats (f60-18Og) following ligation of the left coronary artery. After 5 weeks the heart weight&@ weight ratio of the PMI hearts had increased by 29.6% (n=6, p
P-()7-46POSTZCHEMIC CONTRIBUTIONS
DIASTOLIC DYSFUNCTION OF DEPRESSED REFLOW
IN THE HYPERTROPHIED AND CORONARY VASCULAR
RAT HEART: TURGOR
THE RELATIVE
0 hyperemic re(low I depressedreflmv * pO.oS v C depressed refbw during early repetfusion, and (ii) may b;e due to a greater contribution to wall stiffness from coronary turgor. S.247