Nilsson I M, Bergentz S E, Hedner U, Kullenberg K
Thromb Diath Haemorrh. 1975 Nov 15;34(2):409-18.
Gastric juice from 15 normals, 20 patients with gastric ulcer and 14 patients with erosive haemorrhagic gastroduodenitis was investigated in respect of its activity on unheated and heated fibrin plates and its content of FDP and plasminogen or plasmin with immunochemical methods. Gastric juice from normals showed no activity on unheated and heated fibrin plates, and no FDP or plasminogen could be demonstrated. In the patients with gastric ulcer the gastric juice showed little or no fibrinolytic activity on fibrin plates except in 2, who had regurgitation of duodenal juice and neutral pH of the juice. These patients had equally high activity on heated as on unheated plates and no plasmin could be demonstrated. It was shown that this activity was not due to fibrinolysis, but to non-specific proteolytic activity (probably trypsin). The patients with erosive haemorrhage gastroduodenitis exhibited quite a different picture. The gastric juice from these patients showed extremely high activity on fibrin plates, the activity was higher on unheated than on heated plates. The activity was inhibited in vitro by addition of EACA and in vivo after administration of AMCA. The occurence of plasmic could be demonstrated directly immunologically in the gastric juice. By comparsion of plasmin and trypsin in various assays it could further be improved that the gastric juice in these cases contained plasminogen activator and plasmin. The patients with erosive haemorrhagic gastroduodenitis showed no increase in fibrinolysis in the blood, but low values for plasminogen and alpha2-M, and the serum contained FDP. These findings in the blood and gastric juice were interpreted as signs of local fibrinolysis in the stomach and duodenum. There is reason to assume that this gastric fibrinolysis contributes substantially to the bleeding tendency. The effect of administration of AMCA on fibrinolytic activity and the haemorrhage lends support to the assumption of such a mechanism.
对15名正常人、20名胃溃疡患者和14名糜烂性出血性胃十二指肠炎症患者的胃液,就其对未加热和加热纤维蛋白平板的活性以及纤维蛋白降解产物(FDP)、纤溶酶原或纤溶酶的含量,采用免疫化学方法进行了研究。正常人的胃液对未加热和加热的纤维蛋白平板均无活性,且未检测到FDP或纤溶酶原。胃溃疡患者的胃液,除2例十二指肠液反流且胃液pH值呈中性者外,对纤维蛋白平板几乎没有或没有纤溶活性。这2例患者对加热平板和未加热平板的活性相同,且未检测到纤溶酶。结果表明,这种活性并非由纤维蛋白溶解引起,而是由非特异性蛋白水解活性(可能是胰蛋白酶)所致。糜烂性出血性胃十二指肠炎症患者则呈现出截然不同的情况。这些患者的胃液对纤维蛋白平板表现出极高的活性,对未加热平板的活性高于加热平板。体外添加6 - 氨基己酸(EACA)可抑制该活性,体内给予对氨基甲基苯甲酸(AMCA)后也可抑制。可通过免疫方法直接在胃液中检测到纤溶酶的存在。通过在各种检测中比较纤溶酶和胰蛋白酶,进一步证实这些病例的胃液中含有纤溶酶原激活物和纤溶酶。糜烂性出血性胃十二指肠炎症患者血液中的纤维蛋白溶解未见增加,但纤溶酶原和α2 -巨球蛋白(α2 -M)值较低,且血清中含有FDP。血液和胃液中的这些发现被解释为胃和十二指肠局部纤维蛋白溶解的迹象。有理由认为这种胃纤维蛋白溶解在很大程度上导致了出血倾向。给予AMCA对纤维蛋白溶解活性和出血的影响支持了这种机制的假设。