French S W
Department of Pathology, Faculty of Medicine, University of Ottawa, Ontario, Canada.
Alcohol Alcohol Suppl. 1991;1:57-63.
Organ damage due to alcohol abuse includes especially the CNS and the GI tract. The mechanism of liver injury has been studied in depth. Alterations in membrane fluidity, signal transduction, cytochrome, P-450 induction, oxidative stress, acetaldehyde adducts, eicosanoid metabolism, cytoskeletal function, energy metabolism, O2 consumption, microcirculation, Kupffer cell and ito cell activation, immune injury, and gene expression have been documented. Therapeutic implications of these studies include oxandrolone, PTU and colchicine. Pancreatic injury has been studied in vivo and with isolated acini. Amylase release is enhanced directly by ethanol probably by increasing cytosolic Ca2+. Chronic alcohol feeding decreases the CCK receptor sensitivity and affinity for CCK and the pkc response is reduced as is Ca2+ mobilization. Eicosanoids may mediate the damage to the gastric microcirculation. Inhibitors of leukotriene A4 synthesis reduce the ethanol-induced mucosal damage. Exogenous prostaglandins protect the gastric mucosa from ethanol damage and microvascular stasis. In the CNS, alterations induced by ethanol include changes in membrane fluidity and receptor transduction modulation.
酒精滥用导致的器官损伤尤其包括中枢神经系统和胃肠道。肝脏损伤的机制已得到深入研究。已证实存在膜流动性、信号转导、细胞色素、P - 450诱导、氧化应激、乙醛加合物、类花生酸代谢、细胞骨架功能、能量代谢、氧气消耗、微循环、库普弗细胞和贮脂细胞激活、免疫损伤以及基因表达等方面的改变。这些研究的治疗意义包括使用氧雄龙、丙硫氧嘧啶和秋水仙碱。已在体内和分离的腺泡上对胰腺损伤进行了研究。乙醇可能通过增加胞质Ca2+直接增强淀粉酶释放。长期喂食酒精会降低胆囊收缩素（CCK）受体对CCK的敏感性和亲和力，蛋白激酶C（PKC）反应以及Ca2+动员也会降低。类花生酸可能介导对胃微循环的损伤。白三烯A4合成抑制剂可减轻乙醇诱导的黏膜损伤。外源性前列腺素可保护胃黏膜免受乙醇损伤和微血管淤滞。在中枢神经系统中，乙醇诱导的改变包括膜流动性变化和受体转导调节。
