Katada Ryuichi
Department of Legal Medicine and Molecular Alcohology, Sapporo Medical University School of Medicine, S-1 W-17, Chuo-ku, Sapporo, Hokkaido 060-8556, Japan.
Nihon Arukoru Yakubutsu Igakkai Zasshi. 2011 Oct;46(5):424-35.
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.
众所周知，饮酒会影响创伤性脑损伤。乙醇对创伤性脑损伤产生有害影响的机制尚未阐明。本综述聚焦于创伤性脑损伤、乙醇与水通道蛋白4之间的关系。我们曾报道，乙醇会增加大鼠脑挫伤后的脑水肿，并降低其存活率。有人提出，乙醇导致脑挫伤后脑水肿增加可能是由氧化应激引起的。脑水肿包括细胞毒性脑水肿、血管源性脑水肿、间质性脑水肿和渗透性水肿。乙醇主要增加细胞毒性脑水肿。饮酒和脑挫伤都会导致氧化应激。抗氧化治疗可减轻细胞毒性脑水肿。水通道蛋白4是一种水通道，在大鼠创伤性脑损伤后24小时，乙醇会使其增加。水通道蛋白4抑制剂可减轻脑挫伤后的脑水肿，并提高饮酒情况下的存活率。水通道蛋白4可能在乙醇与脑挫伤后脑水肿增加之间存在密切关系。
