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Ischemia-Induced Ionic Mechanisms of Injury in the Developing Brain

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Brain Injury

Part of the book series: Molecular and Cellular Biology of Critical Care Medicine ((MCCM,volume 2))

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Abstract

Ischemia-induced mechanisms of brain injury are a final common pathway for a variety of acute brain insults. Age at the time of brain insult may also have significant bearing on severity of injury induced. For example, for many years it has been known that, in comparison with adult animals, neonatal animals display a reduced sensitivity to ischemia-induced damage (Fazekas et al. 1941; Adolph 1948; Adolph 1971) and a different distribution of neuropathological sequelae (Brierley et al. 1984). A number of properties of brain tissue may account for these ontogeny-related differences, and in the laboratory, the rat has been used to elucidate potential mechanisms, since its neurochemistry over the first 28-postnatal days has similarities with changes in humans over the first few years of life (Clarke et al. 1970; Benjamins et al. 1981; Clark et al. 1989). This review will therefore focus on the experimental work about ischemia-induced ionic failure and its interrelation with excitatory amino acid- and oxidant-related injury in the developing brain.

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Tasker, R.C. (2001). Ischemia-Induced Ionic Mechanisms of Injury in the Developing Brain. In: Clark, R.S.B., Kochanek, P. (eds) Brain Injury. Molecular and Cellular Biology of Critical Care Medicine, vol 2. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-1721-4_11

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  • DOI: https://doi.org/10.1007/978-1-4615-1721-4_11

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