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PGI_2和TXA_2均系前列腺酸的衍生物,胃粘膜细胞可不断合成和释放,具有很强的细胞保护作用。然而,关于它们与胃蛋白酶的适应性细胞保护作用的关系,尚未见报道。本文则采用放射免疫方法,测定了胃粘膜组织 PGI_2和TXA_2的代谢物 6-Keto-PGF_(1α)和TXB_2含量在不同情况下的变化。结果表明,单纯胃蛋白酶225U或胃蛋白酶150U溶于0.1NHCl或75U溶于0.2NHCl中,提前15min灌胃,均可防止由25％NaCl高渗溶液和沸水所致的胃粘膜坏死的发生,这种保护作用呈明显的量效关系。在上述三种配方灌胃后15min,胃粘膜组织PGI_2和TXA_2含量明显升高,约为对照组的2.0—2.15和1.7—2.0倍;且以PGI_2含量的增加占优势;胃蛋白酶浓度与两者含量呈现明显的量效关系。说明胃蛋白酶作为弱刺激对高渗和物理性烫伤所致的胃粘膜损伤均有保护作用,其作用机制是通过诱发内源性PG_s 的合成和释放而实现的,这一现象对解释胃粘膜的自身耐受机制,具有重要的生理意义。
PGI_2 and TXA_2 are prostatole derivatives, gastric mucosal cells can be continuously synthesized and released, with a strong cytoprotective effect. However, there is no report about their relationship with the adaptive cytoprotective effect of pepsin. In this paper, radioimmunoassay was used to determine the changes of 6-Keto-PGF_ (1α) and TXB_2 contents in PGI_2 and TXA_2 of gastric mucosa under different conditions. The results showed that the simple pepsin 225U or pepsin 150U dissolved in 0.1NHCl or 75U dissolved in 0.2NHCl, 15min early oral administration, can prevent 25% NaCl hypertonic solution and boiling water caused by gastric mucosal necrosis, which The protective effect is obvious dose-effect relationship. PGI_2 and TXA_2 in gastric mucosa significantly increased at 15min after the above three kinds of intragastric administration, which were about 2.0-2.15 and 1.7-2.0 times higher than that of the control group, and the content of PGI_2 was dominant. The concentration of pepsin and both The content showed a significant dose-effect relationship. Pepsin as a weak stimulation of hypertonic and physical injury caused by gastric mucosal injury have a protective effect, its mechanism is through the induction of endogenous synthesis and release of PG_s achieved, the phenomenon of gastric mucosa to explain the Self-tolerance mechanism, has important physiological significance.