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Extracellular amino acids and lipid peroxidation products in periventricular white matter during and after cerebral ischemia in preterm fetal sheep
Author(s) -
Fraser Mhoyra,
Bennet Laura,
Van Zijl Pierre L.,
Mocatta Tessa J.,
Williams Christopher E.,
Gluckman Peter D.,
Winterbourn Christine C.,
Gunn Alistair J.
Publication year - 2008
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2008.05313.x
Subject(s) - ischemia , white matter , malondialdehyde , endocrinology , fetus , medicine , lipid peroxidation , hypoxia (environmental) , microdialysis , anesthesia , oxidative stress , chemistry , biology , central nervous system , magnetic resonance imaging , oxygen , pregnancy , genetics , organic chemistry , radiology
It is widely hypothesized that accumulation of excitatory amino acids, and oxygen free radicals during or after exposure to hypoxia–ischemia play a pivotal role in preterm periventricular white matter injury; however, there is limited evidence in the intact brain. In preterm fetal sheep (0.65 gestation; term 147 days) we found no significant increase in extracellular levels of excitatory amino acids measured by microdialysis in the periventricular white matter during cerebral ischemia induced by bilateral carotid occlusion. There was no significant change in 8‐isoprostane or malondialdehyde levels in the early phase of recovery after occlusion. In contrast, there was a significant delayed increase in most amino acids and in malondialdehyde (but not 8‐isoprostane) that was maximal approximately 2–3 days after occlusion. The increase in glutamate was significantly correlated with a secondary increase in cortical impedance, an index of cytotoxic edema, and with white matter damage 3 days post‐insult. In conclusion, no significant accumulation of cytotoxins was found within immature white matter during cerebral ischemia. Although a minority of fetuses showed a delayed increase in some cytotoxins, this occurred many days after ischemia, in association with secondary cytotoxic edema, strongly suggesting that these changes are mainly a consequence of evolving cell death.