Bcl-2 Protection of Mitochondrial Function Following Chemical Hypoxia/Aglycemia
Neuronal death following cardiac arrest or stroke is a primary cause of delayed morbidity and mortality. In cardiac arrest, neurologic compromise is primarily the result of delayed neuronal death which develops over 24 to 72 h following resuscitation. In the case of stroke, the cells at the core of the lesion die acutely. However, the cells at the penumbra are at risk in subsequent days, and it is their fate that can determine survival or the degree of debilitation of the victim. The mechanisms underlying delayed neuronal death following cerebral ischemia and reperfusion are not fully understood. Amelioration of in vivo damage through the administration of excitatory amino acid antagonists of the NMDA and especially non-NMDA type have met with success. As well, inhibitors of free-radical induced damage such as antioxidants or heavy metal chelators have been found to inhibit delayed neuronal death. However, no treatment has been found to completely prevent the deleterious effects of ischemia/reperfusion, due either to a complex interplay of multiple degradative mechanisms1, or to a lack of appreciation of the sequence and relative importance of events in the death pathway.
KeywordsCerebral Ischemia Neuronal Death Respiratory Control Ratio Respiratory Inhibition Membrane Permeability Transition
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