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European Heart Journal 1994 15(Supplement D):35-36; doi:10.1093/eurheartj/15.suppl_D.35
Copyright © 1994 by the European Society of Cardiology.
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© 1994 The European Society of Cardiology

Contractile Function and Response to Agonists in Myocytes from Failing Human Heart

S. E. Harding, C. H. Davies, D. G. Wynne and P. A. Poole-Wilson

Department of Cardiac Medicine, National Heart and Lung Institute Dovehouse St., London SW3 6LY, U.K.

Correspondence: Dr Sian E. Harding, Department of Cardiac Medicine, National Heart and Lung Institute, Dovehouse St., London SW3 6LY, U.K.

Ventricular myocytes from failing human hearts have a similar maximum contraction amplitude in high Ca2+to those from non-failing heart at low stimulation rates (0.2 Hz, 32°C), but do not exhibit the same positive frequency-interval relationship. At higher stimulation rates (1 Hz) therefore, the amplitude is depressed in cells from failing hearts compared to controls. Slow relaxation is seen in myocytes from failing ventricle at all stimulation rates, and contraction velocity is also slightly reduced, β-adrenoceptor desensitization is evident, and increases with severity of disease. There is also a post-receptor defect in myocytes from failing heart since responses to forskolin and cyclic A MP analogues are reduced, and this is accompanied by decreased cyclic AMP levels in myocardium from patients in end-stage disease. Pertussis toxin treatment, which inactivates Gi, reverses most of the alterations in the β-adrenoceptor pathway. The role of the sympathetic system is indicated by the parallels between myocytes from failing human heart and those from the noradrenaline-treated guinea-pig, which show β-adrenoceptor desensitization, a post-receptor defect and reduced basal cyclic AMP levels. However, relaxation velocities are not slowed in these guinea-pig myocytes, indicating that basal cyclic AMP does not have a tonic role in speeding relaxation.

Key Words: β-adrenoceptor • desensitization • myocyte • human • heart failure


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