A experimental study on elucidation of developmental mechanism and treatment of stress ulcer from the viewpoint of gastric mucosal barrier.

本实验采用200- 250 g雄性Ulistar大鼠，腹腔结扎1.5h后处死，观察内源性氧自由基清除剂对胃缺血再灌注损伤及组织修复的影响。实验<10>结果表明，再灌注后第7天，胃酸和胃蛋白酶分泌量由31 μ Eg明显下降，胃粘膜血流量由89 ml/min/100 g下降到47 ml/min/100 g，胃粘膜血流量由89 ml/min/100 g下降到47 ml/min/100 g，胃粘膜血流量由89 ml/min/100 g下降到47 ml/min/100 g，胃粘膜血流量由89 ml/min/100 g下降到47 ml/min/100 g。再灌注后第2天，恢复到钳夹前水平，提示外源性辅酶Q_2<10>阴离子水平对应激性溃疡的发生有一定的指示作用，提示氧自由基可能是应激性溃疡的一个重要的促进因素。人工血的预防作用采用大鼠全血减影法检测SFH无基质血红蛋白（SFH stroma free hemoglobin）（2%重量，1.0ml/10 sec），SFH可部分抑制应激性溃疡的形成，这是由于SFH降低了应激性溃疡的光致发光水平，提示SFH有可能作为一种清除剂来抑制溃疡的形成。

The role of endogeuous oxygen-derived free radical scavengers on ischemia-reperfusion injury and tissue Recovery in rat ulcer model corresponding to the gastric histopathology was investigated.Male Ulistar rats weighing 200-250g were haparinized before occlusion of celiac for 1.5h. Acid and pepsin secretion, gastric mucosal blood flow, and CoQ_<10> anion radical level in tissue were measured.Exogenous superoxide dismutase (SOD) and catalase as a scavenger were administered and investigated the preventive effect of stress ulcer.Acid and pepsin output decreased significantly from 31muEg prior to the seventh day after reperfusion.The gastric mucosal blood flow decreased from 89ml/min/100g to 47ml/mim/100g. On the second day after reperfusion, the value retuned to that prior to clamping.CoQ_<10> anion level demonstrated exogenously were effective to present the development of stress ulcer.Based on these data, oxygen-derived free radical was supposed to be a camsative factor of stress ulcer.In preliminary study, Preventive effect of artificial blood (SFH stroma free hemoglogbin) was examined using subtraction of blood from rat (2% of weight 1.0ml/10sec) .SFH prevented partially from the development of stress ulcer due to decrease of chamiluminescence level.We conclude SFH has posibility to prevent ulcer formation as a scavenger.