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[氯化铵过量、运动不足及应激影响下酸碱平衡的代偿性变化]

[Compensatory changes in the acid-base balance under the influence of excess ammonium chloride, hypodynamia and stress].

作者信息

Pakhomova V O, Biloklits'ka H F, Pakhomova O O, Rozanov V A, Protunkevych O O, Hruzova I L, Mel'nychuk D O

机构信息

Medical Academy After Diploma Formation, Ministry of Public Health of Ukraine, Kiev.

出版信息

Fiziol Zh (1994). 1999;45(5):68-75.

PMID:10687066
Abstract

Two variants of alternative integrative compensatory mechanisms of metabolic reactions in organism developing at the compensated shifts of acid-base balance under the influence of different risk factors have been discovered by the authors. Compensated metabolic acidosis appears with the excess of salt ammonia in the animals ration, at the immobilization stress, hypodynamia, deafferentation and surgical stress. The start reaction of acidosis is lipolysis activation and nonacidified products accumulation at the reactions of tricarboxylic acid cycle are (TAC) inhibited. The compensatory mechanism directed to bind hydrogen ions and prevent pH shifts is activity of glyconeogenesis reactions, transamination, increase the contents ammonia, as well as by increases of restored combinations. Carbohydrates excess in the ration, emotional stress (anxiety expectation) lead to the metabolic alkalosis development at which low hydrogen ion formation and their rapid use in the activated process of peroxide lipids oxidation is compensated with the increase of organic acids formation in glycolysis and TAC as well as by the increase of oxidation properties in tissues. Besides adaptive physiological meaning, the described mechanisms may be the reason for a number of pathological state appearance. The discovery in population and prevention of endogenic risk factors prevention is principle new basis of modern integrated system of human and animals common diseases prevention.

摘要

作者发现了两种在不同风险因素影响下,机体在酸碱平衡代偿性变化时代谢反应的替代性综合代偿机制变体。当动物日粮中盐氨过量、处于固定应激、运动不足、去传入神经作用和手术应激时,会出现代偿性代谢性酸中毒。酸中毒的起始反应是脂解激活,三羧酸循环(TAC)反应中未酸化产物积累受到抑制。旨在结合氢离子并防止pH值变化的代偿机制是糖异生反应、转氨基作用的活性增加,氨含量增加以及还原组合增加。日粮中碳水化合物过量、情绪应激(焦虑预期)会导致代谢性碱中毒,此时低氢离子形成及其在过氧化脂质氧化激活过程中的快速利用,通过糖酵解和三羧酸循环中有机酸形成的增加以及组织氧化特性的增加得到代偿。除了适应性生理意义外,所描述的机制可能是许多病理状态出现的原因。在人群中发现并预防内源性危险因素是人类和动物常见疾病预防现代综合系统的重要新基础。

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