Mitochondrial contributions to @entity3145 in XXXX .

@entity64 @entity2806 @entity63 @entity3145 @entity4674 @entity26 @entity1188 @entity842 @entity224 @entity6710 @entity204 @entity413 @entity855
Tissue @entity1188 , involving @entity204 of essentially all cells within a part of the brain, is a common pathology resulting from @entity64 and an important determinant of the long-term consequences of this disorder. The cell @entity204 that leads to @entity1188 formation is likely to be the result of multiple interacting pathological processes. A range of factors, including the severity of the ischemic insult and whether this is permanent or reversed, determine which mechanisms predominate. Although evaluating mitochondrial properties in intact brain is difficult, evidence for several potentially deleterious responses to @entity2806 or post-ischemic reperfusion have been obtained from investigations using animal models of @entity64 . Marked changes in @entity855 and related energy metabolites develop quickly in response to occlusion of a cerebral artery, as expected from limitations in the delivery of @entity26 and @entity413 . However, these alterations are often only partially reversed on reperfusion despite improved substrate delivery. @entity63 -induced decreases in the mitochondrial capacity for respiratory activity probably contribute to the ongoing impairment of energy metabolism during reperfusion and possibly also to the magnitude of changes seen during @entity63 . Conditions during reperfusion are likely to be conducive to the induction of the permeability transition in mitochondria. There are as yet no well-characterized techniques to identify this change in the intact brain. However, the protective effects of some agents that block formation of the transition pore are consistent with both the induction of the permeability transition during early recirculation and a role for this in the development of @entity3145 . Release of @entity4674 into the cytoplasm of cells has been observed with both permanent and reversed @entity63 and could trigger the @entity204 of some cells by apoptosis, a process which probably contributes to the expansion of the @entity2806 . Mitochondria are also likely to contribute to the widely-accepted role of @entity842 in the development of @entity2806 . These organelles are a probable target for the deleterious effects of this substance and can also act as a source of @entity224 for reaction with the @entity842 to produce the damaging species, @entity6710 . Further characterization of these mitochondrial responses should help to elucidate the mechanisms of cell @entity204 due to @entity2806 and possibly point to novel sites for therapeutic interventions in @entity64 .
