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

为探讨内源性氧自由基清除剂在大鼠胃溃疡模型缺血再灌注损伤和组织修复中的作用，将体重200~250g的雄性Uistar大鼠制成肝素化模型，阻断大鼠腹腔1.5h。观察胃酸和胃酶分泌、胃粘膜血流量和组织中阴离子自由基水平，外源性超氧化物歧化酶和过氧化氢酶作为清除剂对应激性溃疡的预防作用。胃酸和胃蛋白酶产量从再灌流前的31mlmin/100g降至47ml/mim/100g。在再灌流后第二天，恢复到阻断前的水平。外源性显示的CoQ_&lt；10&gt；阴离子水平有效地反映了应激性溃疡的发展。基于这些数据，氧自由基被认为是应激性溃疡的一个诱因。在初步研究中，通过减去大鼠的血(2%体重1.0ml/10s)来观察人工血(SFH基质去血球蛋白)对应激性溃疡的预防作用。SFH可以部分地阻止由于热发光水平降低而导致的应激性溃疡的发展。我们认为SFH作为一种清除剂有可能预防溃疡的形成。

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.