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DOI 10.1016/0735-1097(89)90181-2

Медицинская библиотека · Journal of the American College of Cardiology · 1989

Myocardial beta-adrenoceptor changes in heart failure: concomitant reduction in beta 1- and beta 2-adrenoceptor function related to the degree of heart failure in patients with mitral valve disease.

Brodde O E, Zerkowski H R, Doetsch N, Motomura S, Khamssi M, Michel M C

СтатьяПоддержка исследования: вне правительства СШАПеревод пока не подготовлен

Аннотация

In patients suffering from end-stage congestive cardiomyopathy, cardiac beta 1-adrenoceptor function is markedly reduced, whereas cardiac beta 2-adrenoceptor function is nearly normal. To determine whether beta 1-adrenoceptor function is impaired in heart failure selectively, beta 1- and beta 2-adrenoceptor density and functional responsiveness in the right and left atria and the left papillary muscles from patients with mitral valve disease (functional class III to IV) were studied. In all three tissues concomitantly beta 1- and beta 2-adrenoceptor density gradually declined when the degree of heart failure increased from functional class III to IV. This decrease in beta 1- and beta 2-adrenoceptor density was accompanied by similar decreases in the contractile response of isolated electrically driven right atrial and left ventricular papillary muscles to beta-adrenergic agonists. It is concluded that a decrease in cardiac beta-adrenoceptor function is a general phenomenon in heart failure, and its extent is related to the degree of heart failure. However, in contrast to congestive cardiomyopathy, in mitral valve disease the decrease in cardiac beta-adrenoceptor function is due to a concomitant decrease in beta 1- and beta 2-adrenoceptors.

Для цитирования: Brodde O E, Zerkowski H R, Doetsch N, Motomura S, Khamssi M, Michel M C. Myocardial beta-adrenoceptor changes in heart failure: concomitant reduction in beta 1- and beta 2-adrenoceptor function related to the degree of heart failure in patients with mitral valve disease.. Journal of the American College of Cardiology. 1989. DOI: 10.1016/0735-1097(89)90181-2.

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