Gastric mucosal injury in the rat. Role of iron and xanthine oxidase.
Gastric mucosal injury in the rat. Role of iron and xanthine oxidase.
复制标题
大鼠胃粘膜损伤。
DOI：
10.1016/0016-5085(87)90969-3
复制
发表时间：
1987
期刊：
影响因子：
29.4
通讯作者：
Kvietys,PR
中科院分区：
文献类型：
--
作者：
Smith,SM;Grisham,MB;Manci,EA;Granger,DN;Kvietys,PR
最近的研究表明氧自由基与胃粘膜缺血再灌注损伤有关。本研究的目的是：(a)验证黄嘌呤氧化酶是缺血胃中氧自由基来源的假设，(b)确定铁催化的Haber-Weiss反应在产生细胞毒性氧自由基中的重要性。在30分钟的对照期、30分钟的缺血期（出血至25 mmHg动脉压）和60 - 80分钟的再灌注期（再输血）测量胃粘膜5 ' cr标记红细胞的清除率。在未治疗的（对照）大鼠中，仅在再灌注期间观察到51cr标记的红细胞渗漏到胃腔的急剧增加（100倍）。再灌注期结束后，通过大体病变面积和组织学进一步评估胃粘膜损伤情况。大鼠被置于钨酸钠饮食（灭活黄嘌呤氧化酶），或用铁螯合剂脱氧胺或超氧化物歧化酶（超氧化物清除剂）治疗。与未治疗的大鼠相比，这三种干预措施均显著降低了51cr标记红细胞清除率和大体病变面积。然而，组织损伤的组织学评估在治疗和未治疗的动物是相似的。本研究结果支持氧自由基介导出血性休克诱导红细胞外渗的假说。数据还表明，黄嘌呤氧化酶是氧自由基的来源，铁催化的Haber-Weiss反应是该模型中羟基自由基产生的主要原因。
Recent studies have implicated oxygen free radicals in ischemia-reperf usion injury to the gastric mucosa. The aims of the present study were to (a) test the hypothesis that the enzyme xanthine oxidase is the source of the oxygen radicals in the ischemic stomach and (b) determine the importance of the ironcatalyzed Haber—Weiss reaction in,generating the cytotoxic oxygen radicals. Gastric mucosal clearance of 5 'Cr-labeled red blood cells was measured during a 30-min control period, a 30-min ischemic period (hemorrhage to 25 mmHg arterial pressure), and a 60–80-min reperf usion period (reinf usion of shed blood). In untreated (control) rats, a dramatic rise (100-fold) in the leakage of51Cr-labeled red blood cells into the gastric lumen was observed only during the reperf usion period. A f ter the reperf usion period, gastric mucosal damage was further assessed using gross lesion area and histology. Rats were placed on a sodium tungstate diet (to inactivate xanthine oxidase), or treated with either de f eroxamine (an iron chelating agent) or superoxide dismutase (a superoxide scavenger). All three interventions substantially reduced51Cr-labeled red blood cell clearance and gross lesion area relative to untreated rats. However, tissue injury assessed histologically was similar in both treated and untreated animals. The results of this study support the hypothesis that oxygen free radicals mediate the hemorrhagic shock-induced extravasation of red blood cells. The data also indicate that xanthine oxidase is the source of the oxy-radicals and that the ironcatalyzed Haber—Weiss reaction is largely responsible for hydroxyl radical generation in this model.