Citation

Katada R. Nihon Arukoru Yakubutsu Igakkai Zasshi 2011; 46(5): 424-435.

Affiliation

Department of Legal Medicine and Molecular Alcohology, Sapporo Medical University School of Medicine, S-1 W-17, Chuo-ku, Sapporo, Hokkaido 060-8556, Japan.

Copyright

(Copyright © 2011, Japanese Medical Society of Alcohol and Drug Studies)

DOI

unavailable

PMID

22256591

Abstract

It has been well known that alcohol consumption affects traumatic brain injury. The mechanism of detrimental effect of ethanol on traumatic brain injury has not been clarified. This review focused on the relationship among traumatic brain injury, ethanol and aquaporin-4. We have reported that ethanol increased brain edema after brain contusion and decreased survival rates in rats. It was suggested that increasing brain edema by ethanol after brain contusion may be caused by oxidative stress. Brain edema consists of cytotoxic brain edema, vasogenic brain edema, interstitial brain edema and osmotic edema. Ethanol mainly increases cytotoxic brain edema. Both alcohol consumption and brain contusion cause oxidative stress. Antioxidant treatment decreases cytotoxic brain edema. Aquaporin-4, an water channel, was increased by ethanol 24 hr after traumatic brain injury in rat. The aquaporin-4 inhibitor decreased brain edema after brain contusion and increased survival rates under ethanol consumption. Aquaporin-4 may have strict relation between ethanol and brain edema increasing after brain contusion.

Language: ja