The effects of the right and the left ventricular pressure overload on the left ventricular function and metabolism in dogs

The effects of the right and the left ventricular pressure overload on the left ventricular function and metabolism in dogs

126 THE EFFECTS OF THE RIGHT AND THE LEFT VENTRICULAR PRESSURE OVERLOAD ON THE LEFT VENTRICULAR FUNCTION AND METABOLISM IN DOGS. A. Ueda, K.M. Su, F. ...

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126 THE EFFECTS OF THE RIGHT AND THE LEFT VENTRICULAR PRESSURE OVERLOAD ON THE LEFT VENTRICULAR FUNCTION AND METABOLISM IN DOGS. A. Ueda, K.M. Su, F. Okabe, T. Ito, S. Matsumoto, and Y. Ito. The 4th Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Tokyo, Japan The effects of the right ventricular pressure overload and of the left ventricular pressure overload on the left ventricular hemodynamics, metabolism, and coronary circulation were observed in the open chest dogs. The right ventricular pressure overload was produced by the pulmonary artery constriction,and the left ventricular pressure overload was induced by the two types of aortic constriction; simple aortic constriction (A) and aortic constriction with the distal aorto-coronary bypass (B). In the right ventricular pressure overload, cardiac output, LV work, LV max dp/dt/IIP and LV systolic pressure and circumflex coronary flow were decreased but LV edp was slightly increased. As for the LV myocardial metabolism, non-esterified fatty acid (NEFA) uptake was reduced, but the carbohydrate uptake increased. In the left ventricular pressure overload, LV systolic pressure, LV work and coronary flow were increased, but aortic pressure was decreased. The degree of the increase in coronary flow of the group A was higher than that in the group B. NEFA uptake was increased in the group A but was decreased in the group B; however, carbohydrate uptake was increased in the both group A and B. The reason of the difference of NEFA uptake between the group A and B will be discussed.

MONOAMINERGIC METABOLIC ACTIVITY IN EXPERIMENTALLY INFARCTED MYOCARDIUM. 3. Veikb, S. Dolefel, T, Slhdek, E. Urbh-tek, 3. Filkuke, L. KrEek, 9. HartmannovB. Institute of Pathophyaiolog , Faculty of Medicine, Purkinje University, Brno, ESSR. The reuptake of the released noradrenaline is a mechanism, which depends on energy for stabilising the transmitter level within the nonoaminergic nerve terminals. The histochamical fluorescence technique for visualisation of noredreneline has revealed, thet the ligation of the coronary artery induces complete depletion of the intraneurons1 noradranaline during 2 hours within the infarcted area. The treatment of the infarcted tissue with the oxygenated Kreba - Ringer solution in vitro regenerated quickly the fluorescence. The increased oxygen perfusion of the infarcted myocardium, eecured by intraaortic balloon counterpulsation (IABC) in dogs also ragenaratea quickly the fluoreacenca, which indicates the regeneration of the transmitter in the monoaminergic nerve terminals.