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European Heart Journal 1993 14(10):1404-1409;
Copyright © 1993 by the European Society of Cardiology.
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© 1993 The Europen Society of Cardiology

Sequential changes in sympatho-neuronal regulation and contractile function following aortic regurgitation in rabbit heart

T. YOSHIKAWA, T. HANDA, T. YAMADA, Y. WAINAI, M. SUZUKI, K. NAGAMI, M. TANI and Y. NAKAMURA

Cardiopulmonary Division, Department of Internal Medicine, Keio University School of Medicine Tokyo, Japan, 160

accepted 18 May 1993.

Correspondence: Tsutomu Yoshikavva, M.D., Cardiopulmonary Division, Department of Internal Medicine. Keio University School of Medicine. 15 Shinanomachi, Shinjuku-ku, Tokyo, Japan, 160.

Abstract

This study was designed to determine the sequential changes in sympatho-neuronal regulation and contractile function of hearts exposed to volume overloading. Aortic regurgitation was produced by perforation of the aortic valve in 20 rabbits. Another 20 rabbits underwent sham operation. They were randomly assigned to a 1-day group, a 1-week group, and a 4-week group. Haemodynamics, myocardial beta-adrenoceptor binding number and catecholamines were measured in each period after production of aortic regurgitation. Left ventricular end-diastolic pressure increased and cardiac output decreased progressively over the week following production of aortic regurgitation, but they returned towards normal during the subsequent 3 weeks. Left ventricular free wall thickness increased 4 weeks after production of aortic regurgitation, and plasma norepinephrine increased 1 day after the procedure. Maximal binding sites of myocardial beta-adrenoceptors (125I-iodocyanopindolol) were decreased 1 day and 1 week after production of aortic regurgitation. Myocardial norepinephrine was also reduced. After 4 weeks, both beta-adrenoceptor binding sites and myocardial norepinephrine content were restored. Alterations in sympatho-neuronal regulation are related to the compensatory processes in volume overloaded hearts.

Key Words: Beta-adrenoceptor binding sites • catecholamines • heart failure • aortic regurgitation • hypertrophy


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