The hypoxic brain: histological and ultrastructural aspects.
A brief review of structural damage to cerebral cells resulting from experimentally induced hypoxia or ischemia is presented. The histological aspect of the brain is compared in different animal models with respect to the onset and progression of damage. Cell changes detected in the early post-hypoxic period consist of microvacuolation and seem to be fully reversible. Coagulative cell change and edematous cell change which may be considered as the morphologic equivalent of irreversible cell death, develop in a later phase, often as a result of secondary events such as microcirculatory impairment or tissue lactic acidosis. A striking difference in vulnerability exists between cerebral cell types or anatomic brain regions. Possible determinant factors for this phenomenon are discussed. Finally, the special contribution of calcium in cell destructive processes is demonstrated with the aid of ultrastructural calcium distribution studies.
D000136:Acid-Base Equilibrium; D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001921:Brain / Q000098:blood supply / Q000473:pathology; D001925:Brain Damage, Chronic / Q000473:pathology; D001929:Brain Edema / Q000473:pathology; D002545:Brain Ischemia / Q000473:pathology*; D002118:Calcium / Q000378:metabolism; D002196:Capillaries / Q000473:pathology; D006801:Humans; D002534:Hypoxia, Brain / Q000473:pathology*; D009410:Nerve Degeneration; D009474:Neurons / Q000648:ultrastructure; D051381:Rats
D000255:Adenosine Triphosphate; D002118:Calcium