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The role of free radicals and eicosanoids in the pathogenetic mechanism underlying ischemic brain edema.

Molecular and chemical neuropathology (1989-04-01)
T Asano, T Koide, O Gotoh, H Joshita, T Hanamura, T Shigeno, K Takakura
ABSTRACT

Results of our consecutive study on the pathogenic mechanism underlying ischemic brain edema are summarized in this paper. Pertinent findings are as follows: (1) there is a close correlation between the influxes of water and sodium following ischemia; (2) the edema fluid can be regarded as the ultrafiltrate of serum; (3) there is a significant increase in the brain content of HETEs following ischemia; (4) the lipoxygenase activity of brain microvessels is increased following ischemia; (5) the lipoxygenase activity as well as the Na+, K+-ATPase activity of brain microvessels are enhanced by a hydroperoxide, 15-HPETE; (6) inhibition of Na+, K+-ATPase of brain microvessels by intraarterial infusion of ouabain resulted in a significant decrease in edema formation; and (7) not the cyclooxygenase, but the lipoxygenase pathway seems to be involved in the enhancement of microvessel Na+, K+-ATPase. Lipoxygenase(s) and Na+-K+-ATPase of brain microvessels, the activities of which are enhanced by an increased level of free radicals and/or hydroperoxides, may play a significant role in the occurrence of ischemic brain edema.

MATERIALS
Product Number
Brand
Product Description

Sigma-Aldrich
15(S)-Hydroperoxy-(5Z,8Z,11Z,13E)-eicosatetraenoic acid, ~100 μg/mL in ethanol, ≥95%