88 ADAPTATION AND POTENTIATION OF CATECHOLAMINE-INDUCED CELL INJURY G. Rona, C. Bier, McGill University,
J. Dusek, Montreal,
and M.-C. Canada.
Badonnel,
CARDIAC MUSCLE
Department
of Pathology
The evolution of cardiac muscle cell injury and the repair process are influenced by a number of variables in addition to the intensity of the stimulus applied. Studies were carried out in rats on adaptation and potentiation of catecholamine-induced cardiac muscle cell injury. The potentiation to isoproterenol (ISO)-induced myocardial necrosis was investigated following DOCA administration (Am Heart J 66:389, 1963). The inherent ability of the cardiac muscle cell to adapt to noxious stimuli led to the concept of increased myocardial resistance (Dusek et al Arch Path 89:79, 1970). Increased resistance to IS0 administration can be produced by various preparatory procedures, that were independent from the localization of the preparative necrosis but varied with the time elapsed between the preparative procedure and the challenging insult. Whereas the ultrastructural basis of adaptation is characterized recent experiments disclosed a principally by mitochondrial changes, representing the ultrastructural unique phenomenon, lysis of Z-lines, equivalent of DOCA potentiation. (Supported by Medical Research Council of Canada - Grant MA 3635).
THE EFFECT OF CALCIUM ON CONTRACTILE ACTIVITY, 02-CONSUMPAND LACTATE RELEASE IN ISOLATED -TION, NADH FLUORESCENCE RAT HEARTS. G.Rubanyi and A.G.B.Kovach. Experimental Research Department, Semmelweis Medical University, Budapest, Hungary. Rat hearts were perfused with Krebs-Henseleit medium containing insulin /lO mu/ml/, glucose or pyruvate /lO mM/ and different concentrations of calcium / Ca / a positive ingtropic /0,3-7,8 mM/. Increase of Ca produced effect and an increase of 0 &onsumption regardless of the substrate present. In the pgesence of glucose, elevation by NADH reduction and a significant of Ca was followed incregse of lactate release from the heart. In contrast, with pyruvate as the exogenous substrate, excess Ca duced NADH oxidation and an increase of lactate rel~a~~" but of much less extent than that observed in the presence of glucose. It is concluded that elevation of Ca enhances the flow of reducing equivalents to the respigatory chain by increasing glycolytic flux. Thus calcium would appear capable of adjusting myocardial intermediary metabolism to altered energy requirements of the heart, thereby ensuring adequate ATP production.