Abstract
Numerous investigators have proposed that calcium overload is a factor in lethal ischemic injury (Nayler, 1981; Farber, 1982; Poole-Wilson et al. 1984; Trump et al., 1984). However the precise role of calcium in ischemic myocardial damage can only be evaluated by applying methods to measure cytosolic free calcium concentration (Cai). Allen and Orchard (1983) using aequorin loaded ventricular muscle, did not find an increase in Cai after 10 minutes of hypoxia. In a later study of aequorin loaded ferret ventricular muscle, Allen and Smith (1985) reported an increase in Cai after 15 minutes of cyanide treatment. Similarly, Cobbald and Bourne (1984) measured Cai in aequorin loaded isolated myocytes, and found a rise in Cai after ~20 minutes of metabolic inhibition. Both the studies of Allen and Smith (1983) and Cobbald and Bourne (1984) showed that the increase in Cai occurred after the development of contracture. Yet, from these studies, it is uncertain whether a relationship exists between the elevation in Cai and lethal cell injury because contracture is not synonymous with necrosis. In this study, we utilize two myocardial preparations to clarify the role of Cai in myocardial cell injury specifically, by establishing whether Cai increases prior to lethal myocardial cell injury.
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Murphy, E., Steenbergen, C., LeFurgey, A., Lieberman, M., London, R.E. (1988). Cytosolic Free Calcium and Myocardial Cell Injury. In: Lemasters, J.J., Hackenbrock, C.R., Thurman, R.G., Westerhoff, H.V. (eds) Integration of Mitochondrial Function. Springer, Boston, MA. https://doi.org/10.1007/978-1-4899-2551-0_38
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DOI: https://doi.org/10.1007/978-1-4899-2551-0_38
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