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Interaction of ouabain with membrane vesicles from human erythrocytes
ATP St.
AND EARLY CONTRACTILE FAILURE. D.J. Hearse, The Rayne Institute, Thomas’ Hospital, London, U.K. The precise mechanism responsible for early contractile failure following the onset of anoxia or ischaemia has attracted speculation and controversy. The simple and attractive hypothesis that ATP deficiency is responsible for this failure has been discussed on the basis of claims that there is only a small reduction in cellular ATP content at a time when contractile activity is severely reduced. Thus, no measurements of tissue high energy phosphate levels have been reported earlier than 10 or 15 seconds following the onset of oxygen deprivation. However during this period, when contractile activity can fall to near zero, there are major changes in the patterns of synthesis, distribution and utilization of ATP, and it is possible that critical, but transient, changes in cellular ATP content may occur. Using an isolated rat heart preparation and high speed freeze clamping techniques, contractile and metabolic changes during the first few seconds of anoxia have been measured and interrelated. The results reveal that ATP content falls by 25% and CP content by 50% during the first 5 seconds of anoxia. During this period contractile activity remains unaltered. In the succeeding 10 seconds contractile activity falls to less than 10% of the control and during this time the rate of fall of ATP and CP is reduced. After 15 seconds of anoxia the cellular high energy phosphate content increases such that by 40 seconds ATP has returned to less than 20% of control. These and other results suggest that ATP depletion in a specific cellular compartment might,well be the primary trigger for early contractile failure.
INTERACTION OF OUABAIN WITH MEMBRANE VESICLES FROM HUMAN ERYTHROCYTES. M. Heller and S. Beck, Myocardial Research Group, Department of Biochemistry, Hebrew University-Hadassah Medical School, Jerusalem, Israel. Two types of binding sites with low and high affinity (i.e. , type I and II, respective&) which are distinguished by the requirement for certain legands (i.e., Mg plus P., cf. Heller and Beck (1978) Biochim. Biophys. Acta 514, 332). seem to be se’parate entities and are probably not interconvertible. Both types are most probably located on the outer surface of the erythrocyte membrane as judged from studies with sealed or leaky rightside out (RO) or inside out (IO) vesicles .
AND EARLY CONTRACTILE FAILURE. D.J. Hearse, The Rayne Institute, Thomas’ Hospital, London, U.K. The precise mechanism responsible for early contractile failure following the onset of anoxia or ischaemia has attracted speculation and controversy. The simple and attractive hypothesis that ATP deficiency is responsible for this failure has been discussed on the basis of claims that there is only a small reduction in cellular ATP content at a time when contractile activity is severely reduced. Thus, no measurements of tissue high energy phosphate levels have been reported earlier than 10 or 15 seconds following the onset of oxygen deprivation. However during this period, when contractile activity can fall to near zero, there are major changes in the patterns of synthesis, distribution and utilization of ATP, and it is possible that critical, but transient, changes in cellular ATP content may occur. Using an isolated rat heart preparation and high speed freeze clamping techniques, contractile and metabolic changes during the first few seconds of anoxia have been measured and interrelated. The results reveal that ATP content falls by 25% and CP content by 50% during the first 5 seconds of anoxia. During this period contractile activity remains unaltered. In the succeeding 10 seconds contractile activity falls to less than 10% of the control and during this time the rate of fall of ATP and CP is reduced. After 15 seconds of anoxia the cellular high energy phosphate content increases such that by 40 seconds ATP has returned to less than 20% of control. These and other results suggest that ATP depletion in a specific cellular compartment might,well be the primary trigger for early contractile failure.
INTERACTION OF OUABAIN WITH MEMBRANE VESICLES FROM HUMAN ERYTHROCYTES. M. Heller and S. Beck, Myocardial Research Group, Department of Biochemistry, Hebrew University-Hadassah Medical School, Jerusalem, Israel. Two types of binding sites with low and high affinity (i.e. , type I and II, respective&) which are distinguished by the requirement for certain legands (i.e., Mg plus P., cf. Heller and Beck (1978) Biochim. Biophys. Acta 514, 332). seem to be se’parate entities and are probably not interconvertible. Both types are most probably located on the outer surface of the erythrocyte membrane as judged from studies with sealed or leaky rightside out (RO) or inside out (IO) vesicles .