Summary
In ischemic-reperfused myocardium, necrosis of cardiomyocytes may develop not only due to the ischemic conditions but also due to the specific circumstances of reperfusion. Reperfusion-induced hypercontracture is a major cause of lethal reperfusion-injury of myocardium. Hypercontracture of myofibrils is caused by reenergetisation of Ca2+-overloaded cardiomyocytes. Ca2+-overload is due to the preceding ischemic period. Upon reperfusion, Ca2+-overload leads to rapid oscillations of cytosolic Ca2+-concentration. Rapid normalisation of pH favors hypercontracture, prolonged acidosis protects against it. Inhibition of reperfusion-induced Ca2+-oscillations (inhibition of Ca2+-uptake or Ca2+-release by the sarcoplasmic reticulum; inhibition of the reverse mode of the sarcolemmal Na+/Ca2+-exchanger) or of pHi recovery (simultaneous inhibition of the Na+/H+-exchanger and the Na+/HC03 - symporter of sarcolemma) during the vulnerable phase of reperfusion can protect the ischemic-reperfused cardiomyocyte against reperfusion injury.
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Schäfer, C., Piper, HM. (2004). Cell Biology of Acute Reperfusion Injury. In: Dhalla, N.S., Rupp, H., Angel, A., Pierce, G.N. (eds) Pathophysiology of Cardiovascular Disease. Progress in Experimental Cardiology, vol 10. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-0453-5_16
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DOI: https://doi.org/10.1007/978-1-4615-0453-5_16
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