Wadhwa S S, Perry M A
Am J Physiol. 1987 Aug;253(2 Pt 1):G129-33. doi: 10.1152/ajpgi.1987.253.2.G129.
Gastric mucosal injury caused by local intra-arterial generation of oxygen-derived free radicals was compared with gastric injury caused by 30 min of hemorrhage-induced ischemia (systemic pressure of 30 mmHg) or local ischemia (celiac artery pressure of 30 mmHg). The index of injury was the loss of 51Cr-labeled red cells across the gastric mucosa. Generation of oxygen radicals in the celiac artery caused a rapid increase in mucosal blood loss during the period of radical generation (0.029 +/- 0.013 ml X min-1 X 100 g-1, mean +/- SE), and this loss was maintained after radical production ceased (0.041 +/- 0.018 ml X min-1 X 100 g-1). Local ischemia produced similar mucosal injury; however, this occurred after reperfusion of the stomach (0.038 +/- 0.006 ml X min-1 X 100 g-1) and not during the ischemic episode (0.001 +/- 0.0003 ml X min-1 X 100 g-1). Hemorrhage-induced ischemia produced a threefold greater mucosal blood loss (0.133 +/- 0.048 ml X min-1 X 100 g-1) than local ischemia. The results of this study indicate that oxygen radicals generated enzymatically in the blood supply to the stomach cause mucosal bleeding of similar magnitude to that observed after local ischemia and that gastric ischemia induced by systemic hypotension produces more severe gastric injury than the same level of local hypotension.
将局部动脉内产生氧衍生自由基所引起的胃黏膜损伤，与出血性缺血30分钟（全身血压30 mmHg）或局部缺血（腹腔动脉血压30 mmHg）所引起的胃损伤进行比较。损伤指标是51Cr标记红细胞穿过胃黏膜的损失量。腹腔动脉中氧自由基的产生导致在自由基产生期间黏膜失血量迅速增加（0.029±0.013 ml·min-1·100 g-1，平均值±标准误），并且在自由基产生停止后这种失血仍持续存在（0.041±0.018 ml·min-1·100 g-1）。局部缺血产生了类似的黏膜损伤；然而，这种损伤发生在胃再灌注后（0.038±0.006 ml·min-1·100 g-1），而不是在缺血发作期间（0.001±0.0003 ml·min-1·100 g-1）。出血性缺血所导致的黏膜失血量比局部缺血大三倍（0.133±0.048 ml·min-1·100 g-1）。本研究结果表明，在胃供血中酶促产生的氧自由基引起的黏膜出血程度与局部缺血后观察到的相似，并且全身性低血压诱导的胃缺血比相同程度的局部低血压产生更严重的胃损伤。
