A Correlative Study on Electrophysiologic,Hemodynamic and Metabolic Changes of the Canine Heart in Experimental Pulomonary Embolism

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  • HATANAKA Yoshie
    The Third Department of Internal Medicine, Osaka University Medical School
  • ISHIYAMA Taro
    The Third Department of Internal Medicine, Osaka University Medical School
  • MORITA Yoshiharu
    The Third Department of Internal Medicine, Osaka University Medical School
  • UENO Teiichi
    The Third Department of Internal Medicine, Osaka University Medical School
  • AZUMA Jun-ichi
    The Third Department of Internal Medicine, Osaka University Medical School
  • TANIMOTO Takuji
    The Third Department of Internal Medicine, Osaka University Medical School
  • OGURA Kyoko
    The Third Department of Internal Medicine, Osaka University Medical School
  • TSUKAMOTO Nozomu
    Department of Internal Medicine, Nishinomiya City Central Hospital
  • YAMAMURA Yuichi
    The Third Department of Internal Medicine, Osaka University Medical School

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  • A Correlative Study on Electrophysiologic, Hemodynamic and Metabolic Changes of the Canine Heart in Experimental Pulmonary Embolism
  • Correlative Study on Electrophysiologic

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Experimental pulmonary charcoal embolism was produced in dogs. The changes of energy liberation were observed in the right and left ventricular myocardium in relation to the changes of cardiac dynamics. In some dogs, histamine was administered with or without charcoal embolization in order to study whether or not this agent, well-known to be released from lung tissue in pulmonary embolism, had a modifying effect on the myocardial energy metabolism. The effect of histamine was also observed in other dogs. Twice infusions of each 50ml saline suspension of 1Gm charcoal powder were performed into the right ventricle through catheter. The right ventricular overloading was recognized hemodynamically and electrophysiologically. An hour after the first charcoal infusion, mitochondrial fractions were isolated from the right and left ventricles. Uncoupling of oxidative phosphorylation was proved polarographically. These changes were enhanced with histamine (0.01mg/Kg), and were mitigated with diphenhydramine (0.5mg/Kg). Histamine per se was seemed to have a certain uncoupling effect on the heart mitochondria without remarkable alterations in cardiac dynamics and electrophysiologic findings. It was concluded that oxidative phosphorylation of the heart mitochondria was uncoupled in experimental pulmonary charcoal embolism, and that histamine might be a chemical mediator inducing this change by aggravating myocardial hypoxia through pulmonary vasoconstrictive action and/or by affecting the myocardial cell metabolism directly.

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