@article{ref1,
title="A pre-injury high ethanol intake in rats promotes brain edema following traumatic brain injury",
journal="British journal of neurosurgery",
year="2014",
author="Wu, Weichuan and Tian, Runfa and Hao, Shuyu and Xu, Feifan and Mao, Xiang and Liu, Baiyun",
volume="28",
number="6",
pages="739-745",
abstract="Drinking is a risk factor for traumatic brain injury (TBI), and ethanol can aggravate the outcome by promoting brain edema. The mechanism involved is not fully understood. It has been confirmed that aquaporin-4 (AQP4) and vascular endothelial growth factor (VEGF) play pivotal roles in cytotoxic/vasogenic brain edema individually, and both of these proteins are downstream regulatory factors of hypoxia-inducible factor-1α (HIF-1α). In this study, we used a fluid percussion injury (FPI) model in rats to determine the effects of acute ethanol intake on the expression levels of HIF-1α, AQP4, and VEGF prior to FPI. The animals were sacrificed 1, 2, 3, and 4 days post-injury. We found that the expression levels of HIF-1α and AQP4 were significantly upregulated in the ethanol-pretreated groups, whereas the VEGF expression level was not. In addition, there was a positive correlation between HIF-1α and AQP4. The results of this study indicate that cytotoxic brain edema may play an important role in the early stage of FPI in ethanol-pre-treated animals and that HIF-1α and AQP4 might be involved.<p /> <p>Language: en</p>",
language="en",
issn="0268-8697",
doi="10.3109/02688697.2014.915007",
url="http://dx.doi.org/10.3109/02688697.2014.915007"
}