Ischemic reperfusion injury is a sequence of chemical events leading to cellular dysfunction and necrosis. A tissue is undergoing to ischemia can lead to cellular dysfunction by release of various mediators at a site of ischemic region, and when it is ended by the restoration of blood flow, a second series of injurious events ensue producing additional injury. Thus, whenever there is a transient decrease or interruption of blood flow the net injury is the sum of two components; the direct injury occurring during the ischemic period and the indirect or reperfusion injury that follows. In case of reperfusion injury, various consequent event follows like oxidative stress or oxygen paradox, leukocyte-endothelium interactions or platelet mediated reperfusion injury, calcium overload, mitochondrial permeability transition pore (PTP) opening, reperfusion injury salvage kinase (RISK) pathway etc. Complement may be also activated during reperfusion through the antibody-dependent classical pathway, the alternative pathway, or the MBL/MASP pathway.
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