The underlying mechanism of cell injury during ischemia and reperfusion is complex and timesesnsitive. Some processess develop coincidentally with the onset of ischemia and during reperfusion leading to abnormalities in energy metabolism, acid base status, and intracellular ion homeostasis. Other processes develop later and encompass activation of various signalling pathways that have deleterious or beneficial effects on specific effectors, but associated with sustained disruption of energy production contractile dysfunction and activation of apoptotic pathways. Discussion on the various cell mechanisms resposible for cell injury is beyond the scope of this review. However, pertinent to our discussion is the mounting evidence pointing to mitochondria as key target organelles of reperfusion injury.

Key words: cardiac arrest, mito-chondrial injury, cardiopulmonary resuscitation, apoptosis

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