Abstract
The use of isolated human ventricular muscle preparations has provided evidence that the failing human heart exhibits strongly reduced responsiveness to cAMP-increasing positive inotropic agents such as β-adrenergic agents and phosphodiesterase inhibitors, write Wilhelm Schmitz, Hasso Scholz and Erland Erdmann. This probably explains the therapeutic failure of these agents in end-stage dilative cardiomyopathy and casts doubts on the value of extrapolations from data obtained on healthy laboratory animals. Since α 1-adrenoceptors and adenosine receptors mediating positive and negative inotropic effects, respectively, exist in the human myocardium, it is conceivable that a defect of these receptor systems may also play a role in human heart diseases as has been hypothesized from animal experiments.
Published Version
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