Book Chapter Details
Mandatory Fields
Allshire AP, Cobbold PH;
1990 Unknown
Pathophysiology of Severe Ischemic Myocardial Injury (Developments in Cardiovascular Medicine, Volume 104)
Causes and effects of changes in cytosolic free calcium in the hypoxic myocardial cell
Kluwer Academic Publishers
Optional Fields
We review cytosolic free calcium (Cai) measurements in hypoxic single cardiomyocytes, isolated heart tissue and intact myocardium.  In single cells the seminal event may be a shortening which is (largely) Cai-independent and probably corresponds to hypoxic contracture of intact tissue.  This shortening is soon followed by a Cai rise and net Ca2+ ingress across the sarcolemma which is sensitive to the Na+ electrochemical gradient, suggesting that na-Ca exchange occurs, and that a Nai imbalance precedes the Cai rise.  Reoxygenation of single cells triggers spontaneous mechanical activity (and oscillation of Ca2+ between cytosol and sarcoplasmic reticulum) analogous to reoxygenation arrhythmias in intact myocardium, and provided that Cai has not risen above several micromolar it is returned to resting levels.  We interpret the Cai-independent shortening as a rigor which activates the myosin ATPase and thereby accelerates ATP depletion so that ATP-linked ion pumps in the cell membranes become thermodynamically limited.  An ensuing Nai rise leads through depressed Na-Ca exchange to a Cai rise.  Such a model highlights rigor-complex mediated activation of myosin S1-ATPase as the fundamental target for interventions to ameliorate ischemic damage to the myocardium.
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