[Experimental myocardial infarct and supraventricular arrhythmia].
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Biomedical subjects
Publications and source records attributed to E Hennig.
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Total heart replacement was performed in 7 calves. All animals were alive at 3 weeks, and four survived more than 2 months up to 121 days. Failure of the pumping equipment was responsible for death in each case. At autopsy increase both in size of the right atrium and of liver weight and evidence of thromboembolism were regular findings.
This is a report on the special regulation problem of the left blood pump after replacement of the natural heart by incorporated extracorporally driven blood pumps in an animal experiment. The consequence of the peripheral self-regulation on the transporting capacity of the bloodpumps considering the driving pressure and the systemic pressure losses has been investigated. Two possible controlling principles and the respective fields of application are discussed on the example of a lung oedema.
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The inotropic and electrophysiological effects of plasma obtained from patients and experimental dogs during cardiogenic shock following acute myocardial infarction were studied. Changes in the isometric contraction and the intracellular action potential were determined in isolated papillary muscles of rabbits. Control plasma collected from normal subjects produced no significant changes in the contraction or the electrical parameters. Plasma from shock patients decreased peak force by 42% and the maximum rate of force development by 38% in comparison to control values; the time to peak of contraction, the relaxation time and the action potential parameters were not significantly altered. Corresponding results were obtained with plasma from dogs before and during experimental cardiogenic shock. Biochemical determinations failed to identify a single specific "myocardial depressant factor" in the plasma of patients and dogs with cardiogenic shock. The results suggest that (1) various humoral factors released during cardiogenic shock may depress the contractile function of cardiac muscle and (2) that the observed negative intropic effect is not due to electrical changes in the cell membrane.