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Ischemic Alterations in Mitochondrial Calcium Transport Kinetics

An Indicator of Matrix Sulfhydryl Redox State
  • Jeanie B. McMillin
  • Daniel F. Pauly
  • Kiminori Kajiyama
Part of the GWUMC Department of Biochemistry Annual Spring Symposia book series (GWUN)

Abstract

Cardiac function and energetics are intimately linked to an extracellular source of activator calcium. The levels of cytosolic free calcium available to the contractile proteins are precisely regulated by a variety of ion pump and channel proteins present in the cell membrane and sarcoplasmic reticulum. Low to moderate levels of calcium entry across the sarcolemma results in positive inotropy with increases in systolic pressure. However, further increase in calcium influx has only modest effects on systolic function, and diastolic pressure becomes elevated. High concentrations of cell calcium reduce systolic pressure from its optimal levels and increase diastolic pressure even more. It is now believed that the calcium-dependent “diastolic tonus” results from calcium loading and spontaneous release from the sarcoplasmic reticulum (Lakattaet al., 1986). Therefore, calcium appears to play a central role in aberrant cardiac function. In model studies of cardiac disease, accumulation of cellular calcium following 30 min of ischemia with reflow is also associated with a large change in diastolic pressure and low rates of systolic pressure development (Burtonet al., 1986). Both conditions are diagnostic of a high calcium load. The sequence of events which leads to postischemic calcium entry is not well defined; however, an observed ischemic increase in intracellular sodium is thought to activate sarcolemmal sodium-calcium exchange with large increases in cellular calcium influx (Grinwald, 1982). Decreases in sarcolemmal Na+ ,K+ -ATPase activity in early ischemia (Bersohnet al., 1982) could be the basis for the increases in intracellular Na+ . However, other investigators observed only small changes in activity associated with irreversible cell injury (Schwartzet al., 1973). Calcium overload during reperfusion of reversibly injured, acutely ischemic tissue could explain the prolonged contractile abnormalities which accompany the reperfusion period (McMillin-Woodet al., 1979).

Keywords

Sarcoplasmic Reticulum Calcium Uptake Calcium Channel Antagonist Cellular Calcium Mitochondrial Calcium 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Plenum Press, New York 1989

Authors and Affiliations

  • Jeanie B. McMillin
    • 1
    • 2
  • Daniel F. Pauly
    • 1
    • 2
  • Kiminori Kajiyama
    • 1
    • 2
  1. 1.Department of Medicine, Division of Cardiovascular DiseaseUniversity of Alabama at BirminghamBirminghamUSA
  2. 2.Department of Medicine, Section of Cardiovascular SciencesBaylor College of MedicineHoustonUSA

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