Impaired beta-adrenergic stimulation in the uninvolved ventricle post-acute myocardial infarction: reversible defect due to excessive circulating catecholamine-induced decline in number and affinity of beta-receptors.

@article{Baumann1981ImpairedBS,
  title={Impaired beta-adrenergic stimulation in the uninvolved ventricle post-acute myocardial infarction: reversible defect due to excessive circulating catecholamine-induced decline in number and affinity of beta-receptors.},
  author={Gert Baumann and G{\"u}nther Rie\ss and Wolfgang Erhardt and Stephan Burkhart Felix and L. F. Ludwig and G{\"u}nther Bl{\"u}mel and Hans Bl{\"o}mer},
  journal={American heart journal},
  year={1981},
  volume={101 5},
  pages={569-81}
}
Left ventricular infarction (AMI) was produced in experimental animals and the contractile response to isoproterenol was tested in the isolated perfused heart preparation. Adenylate cyclase activity, phosphodiesterase activity, and beta-receptor binding characteristics were determined in a sarcolemmal preparation of the right ventricle of the same hearts. Three days post-AMI the dose-response curve for isoproterenol of right ventricular dP/dtmax was significantly depressed, while the inotropic… CONTINUE READING

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