脾气虚证胃粘膜超微结构及其发病机理的研究

目的:了解脾气虚证的胃粘膜病理形态及其发病机理。方法:慢性胃病24例,进行胃粘膜超微结构研究,超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量,及餐后/空腹血清胃液素检测。结果:脾气虚证其壁细胞线粒体、主细胞酶原颗粒、G细胞分泌颗粒的面数密度,及餐后/空腹血清胃液素比值均明显低于对照组肝胃不和证(P<0.01)。同时,线粒体结构亦有明显损伤。此外,脾虚证胃粘膜MDA含量高于对照组(P<0.05),而SOD活性则低于对照组(P<0.05)。结论:提示脾气虚证胃蛋白酶储备不足,G细胞分泌储备力差。线粒体质和量的改变,可能是脾气虚证病理形态改变的主要环节。脾气虚证的发病过程有氧自由基参与。

Ultrastructure of gastric mucosa and pathogenesis in spleen - energy deficiency

AIM The pathologic changes of gastric mucosa and pathogenesis in spleen-energy deficiency were observed.METHODS Gastric mucosa ultrastructure,superoxide dismutase(SOD)activity,malonyl dialdehyde(MDA,TBA method)value as well as post prandial/fast serum gastrin levels were studied in 24 chronic gastropathy patients with spleen-energy deficiency or liver-spleen incoordination.RESULTS The quantitative and area density of mitochondria in parietal cells,zymogen granules in principal cells,secretory granlues in G cells and postprandial/fast gastrin ratio in spleen-energy deficiency group were all significantly lower than that in control and liver-spleen incoordination groups(P< 0.01).Marked injury was found in mitochondria.Otherwise,their gastric mucosa MDA value was higher in spleen-energy deficiency group than that in control group(P < 0.05),but the SOD activity was lower in spleen-energy deficiency group. CONCLUTIONS Patients with spleen-energy deficiency have insufficient pepin reserve as well as both poor secretory deposit and low secretory function in G cells.Mitochondria structure injury may be the key link of pathological and structure changes of spleen-energy deficiency.Oxigen free radicals participate in the pathogenesis of spleen-energy deficiency syndrome.