Tarnasky P R, Livingston E H, Jacobs K M, Zimmerman B J, Guth P H, Garrick T R
Medical Services, Veterans Affairs Medical Center-West Los Angeles, UCLA 90073.
Dig Dis Sci. 1990 Feb;35(2):173-7. doi: 10.1007/BF01536759.
Cold water immersion restraint of the rat results in focal gastric mucosal erosions. The lesions are associated with powerful, prolonged-duration gastric contractions. Phasic gastric contractions may attenuate gastric mucosal blood flow, resulting in ischemia followed by reperfusion. Therefore, the conditions of cold-water-immersion restraint might lead to mucosal injury by an oxyradical-mediated mechanism. To test this hypothesis, we studied the effect of oxyradical inhibition on cold water immersion restraint-induced lesions. In separate groups of rats subjected to cold water immersion restraint (6-10 animals per group), oxyradical inhibition was achieved by chronic feeding of a sodium tungstate diet, oral administration of allopurinol, or intraperitoneal administration of dimethylsulfoxide. None of these regimens significantly attenuated the number of lesions per stomach, the total lesion area, or the percent of corpus mucosa containing lesions. We conclude that oxyradicals do not play a role in the pathogenesis of cold water immersion restraint-induced lesions.
对大鼠进行冷水浸浴束缚会导致局灶性胃黏膜糜烂。这些损伤与强烈且持续时间长的胃收缩有关。阶段性胃收缩可能会使胃黏膜血流减少,导致缺血,随后再灌注。因此,冷水浸浴束缚的条件可能通过氧自由基介导的机制导致黏膜损伤。为了验证这一假设,我们研究了抑制氧自由基对冷水浸浴束缚诱导损伤的影响。在单独几组接受冷水浸浴束缚的大鼠中(每组6 - 10只动物),通过长期喂食钨酸钠饮食、口服别嘌呤醇或腹腔注射二甲基亚砜来抑制氧自由基。这些方案均未显著减少每个胃的损伤数量、总损伤面积或含有损伤的胃体黏膜百分比。我们得出结论,氧自由基在冷水浸浴束缚诱导损伤的发病机制中不起作用。