论文部分内容阅读
目的：从细胞和细胞膜酶分子水平探讨慢性胃炎中医脾胃虚实证病理生理特征。方法：测定１０２ 例慢性胃炎患者和３０ 例正常人红细胞［Ｃａ２＋ ］ｉ、ＡＴＰ含量、膜Ｃａ２＋ －Ｍｇ２＋ －ＡＴＰａｓｅ活性和２４ ｈ 尿１７－羟皮质类固醇排出量。结果：湿热证细胞内外Ｃａ２＋ 转换率加快，膜Ｃａ２＋ －Ｍｇ２＋ －ＡＴＰａｓｅ活性和细胞内ＡＴＰ合成量呈代偿性亢进；脾胃气虚Ｃａ２＋ 转换率有所下降，膜Ｃａ２＋ －Ｍｇ２＋ －ＡＴＰａｓｅ活性明显低于湿热，组织细胞代谢的代偿功能有所降低；脾肾气虚组织细胞代谢功能已完全失代偿，Ｃａ２＋ 在细胞内有明显滞留现象。结论：上述变化与肾上腺皮质功能有密切关系。
Objective: To explore the pathophysiological characteristics of spleen - stomach deficiency syndrome of chronic gastritis from the level of cellular and membrane enzyme molecules. Methods: The levels of [Ca2 +] i, ATP, membrane Ca2 + -Mg2 + -ATPase activity and 24-hour urinary 17-hydroxycorticosteroid excretion in 102 chronic gastritis patients and 30 normal subjects were determined. Results: The rate of Ca2 + conversion inside and outside of damp-heat syndrome cells was accelerated, and the membrane Ca2 + -Mg2 + -ATPase activity and intracellular ATP synthesis were compensatory hyperthyroidism. The conversion rate of Ca2 + in spleen-qi deficiency was decreased and the activity of Ca2 + -Mg2 + -ATPase was significantly lower , The compensatory function of tissue metabolism decreased; spleen and kidney Qi metabolic function of tissue cells have been completely decompensated, Ca2 in the cells were significantly retained phenomenon. Conclusion: The above changes are closely related to adrenocortical function.