Cytosolic free Ca in chick heart cells: Its role in cell injury

02 FURTEER EVIDENCE THAT THROMBOXANE EXACERBATES ARRHYTHMIAS: EFFEmS OF UK38485 DURING CORONARY ARTERY OCCLUSION AND REPERFUSION IN ANAESTHETISED GREYHOUNDS. S.J, Coker, Department of Physiology and Pharmacology, University of Strathclyde, 204 George Street, Glasgow Gl lXW, Scotland, The administration of the thromboxane synthetase inhibitor UK38485, 3 mg/kg i-v. 30 min prior to occlusion of the LAD in chloralose-anaesthetised dogs reduced the number of extrasystoles that occurred in the first 30 min of ischaemia from 832i158 in controls to 1932126 (P
ITS ROLE IN CELL INJURY. E. Murphy and 83 CYTOSOLIC FREE CA IN CHICK HEART CELLS: M. Lieberman. Department of Physiology, Duke University, USA. A new method is described for measuring cytosollc free Ca in freshly disaqqregated heart cells. This method is based on determining the null point, i.e., the extracellular Ca concentration at which no net Ca movement occurs when the plasma Using this technique basal levels of cytosolic membrane permeability is Increased. Addition of ouabain for 30 minutes caused a 5 fold free Ca averaged 230570 nM (n=6). Rotenone, increase in total cell Ca and raised cytosolic free Ca to only l.Z+o.4pM. an inhibitor of oxidative phosphorylation, was used to inhibit the energy-dependent Ca transport processes which maintain the low basal cytosolic free Ca concentration. While addition of rotenone in the presence of 1.25 rnJ+l extracellular Ca elevated cytosolic free Ca to a level on the order of 100 ~JM; in a nominally Ca-free solution, rotenone resulted in a release of Ca from the cells and increased the cytosolic free Ca concentration to only 1.9 PM. The elevations in cytosollc free Ca were correlated supported by NIH-HL 17670, HL29687, with cell injury as measured by LDH release. Association. HL27105, and the N.C. Heart

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OF CULTURED ACULT CARDIAC MYOCYTES. P.M. Piper, F. Schwartz, J.F. idfitter. Zentrum Physiologic, Universitst Gettingen, FRTSpieckermann. Ctiltured adult cardiac myccytes (JMCC 14 (13823, 3971 were used for studying metobolic alterations and enzyme release (Mllt~) during cxycen deficiency. The features of the metabolic process are of intermediate character compared with that cf ischemic and anoxic perfused hearts. However. because these ventriculccytes are mechanically at the time course is prolonged. Concomitantly kith the fall of ATP contents, Trest, tubuli widen ard mitochondria lose their electron-dense granules. Decay of ATP is cowith mitochondrial swelling and shortering of sarcomeres. Enzyme release incident starts with the initial decrease in high-energy phosphates. eoth enzyme release and lactate production slow down with PTP depleticn. After 12C min of anoxia orly I@ percent of cellular MDH activity are released. These findings indicate that early enzyme leakage in oxygen deficiency is due to a gradual protein release from the individual Contrary to massive enzyme cells starting already with minor energetic disturbances. loss at later stages of anoxia, this early leakage seems to be related tc reversible Reaxygenation leads to extensive recovery of CP; A'F is restorer membrane alteraticns. to the levels of total adenine nucleotides. When the ATP level is above 7 umol/~ (tili EC min anoxia), almost conplete ultrastructural restoration is observed. P lower levels it becomes less homogeneous. Supported

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