Pure hypoxic and ischemic brain insults

Hypoxia can be classified into hypoxic, anemic and histotoxic hypoxia, depe nding on whether there is insufficient inspired oxygen, lowered O-2 carryin g capacity in the blood, or deficient utilization in the tissue, respective ly. Histotoxic hypoxia, as in cyanide or sulfide poisoning, was thought to cause tissue necrosis via impaired brain mitochondrial function. However, e xperiments in several laboratories have shown that blood pressure drops are essential to cause necrosis, casting doubt on the capacity of these agents to directly cause tissue necrosis by histotoxicity. The remaining exceptio n is carbon monoxide poisoning, where true histotoxic hypoxia causes necros is in iron-rich brain areas by virtue of CO binding to heme iron. Anemic hy poxia likewise does not cause brain damage. Hypoxic hypoxia, by itself is a lso incapable of causing necrosis, due to compensatory increased cerebral b lood flow, upholding the oxygen extraction fraction by the brain. Hypoxia c an cause coma, however having a basis in synaptic damage, not neuronal cell body necrosis. This is evident from clinical cases of hypoxic coma which r egularly recover after 2 weeks, the time course of synaptic repair. Patient s in pure hypoxic coma (usually young patients, with e.g. anaphylaxis, asth ma, bronchiolitis) must not be mistaken for neocortical death, since neuron al cell body necrosis is absent, and clinically remarkable recovery occurs regularly Global ischemia, in contrast, causes widespread cortical and subc ortical necrosis. If reperfusion is not immediate, a situation of global no -reflow exists termed respirator brain or non-perfused brain.