[Dopamine-induced secondary cardiomyopathy (author's transl)].
When myocardial fibre necrosis was produced experimentally in rats by high doses of dopamine, the main lesions were found in the left ventricular and septal myocardium. They could also be demonstrated in the left atrium. This report, which concerns clinical observations, is suggestive of a secondary cardiomyopathy in humans due to dopamine. The following pathogenetic mechanism is envisaged. The effects of dopamine are due to myocardial depletion of high energy phosphates following maximal stimulation and the increased, though inadequate adaptation of coronary resistance. The release of norepinephrine is also important. Aggravating factors may include the disturbed relationships of pulmonary ventilaltion to perfusion and the opening and dilatation of arterio-venous shunts in the lung, with subsequent hypoxaemia.
D000818:Animals; D009202:Cardiomyopathies / Q000139:chemically induced* / Q000473:pathology; D004298:Dopamine / Q000009:adverse effects*; D005260:Female; D006346:Heart Septum; D006352:Heart Ventricles; D000860:Hypoxia; D009206:Myocardium / Q000473:pathology; D009336:Necrosis; D009638:Norepinephrine; D051381:Rats; D014692:Ventilation-Perfusion Ratio
D004298:Dopamine; D009638:Norepinephrine
Dopamin-induzierte sekundäre Cardiomyopathie.