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Published on: January 20, 2023
Ethanol-induced hyponatremia augments brain edema after traumatic brain injury
Ryuichi Katada1, Satoshi Watanabe, Atsushi Ishizaka
1Department of Legal Medicine and Molecular Alcohology, Sapporo Medical University School of Medicine, S-1 W-17, Chuo-ku, Sapporo, Hokkaido 060-8556, Japan. r.katada@sapmed.ac.jp
Abstract:
Alcohol consumption augments brain edema by expression of brain aquaporin-4 after traumatic brain injury. However, how ethanol induces brain aquaporin-4 expression remains unclear. Aquaporin-4 can operate with some of ion channels and transporters. Therefore, we hypothesized that ethanol may affect electrolytes through regulating ion channels, leading to express aquaporin-4. To clarify the hypothesis, we examined role of AQP4 expression in ethanol-induced brain edema and changes of electrolyte levels after traumatic brain injury in the rat. In the rat traumatic brain injury model, ethanol administration reduced sodium ion concentration in blood significantly 24 hr after injury. An aquaporin-4 inhibitor recovered sodium ion concentration in blood to normal. We observed low sodium ion concentration in blood and the increase of brain aquaporin-4 in cadaver with traumatic brain injury. Therefore, ethanol increases brain edema by the increase of aquaporin-4 expression with hyponatremia after traumatic brain injury.
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