Loginov A S, Vysotskaia R A
Vestn Ross Akad Med Nauk. 1995(12):32-8.
The paper summarizes the results of in-depth study of the prostaglandin system in healthy individuals and in patients with chronic hepatic diseases. Radioimmunological, gas chromatographic, enzyme immunoassays, and other biochemical studies have first provided evidence for the relationship between the impaired endogenous biological synthesis of prostaglandins (PG) E, F2 alpha, I2, thromboxane A2, the development of metabolic and hormonal disorders and the severity of hepatic failure in chronic hepatitis and cirrhosis of varying etiology, which leads to the conclusion that PGs play an important role in the regulation of liver function and in the pathogenesis of chronic damages. Previously unknown biochemical mechanisms of decreased PGE, PGF2 alpha, and PGI2 in this diseased organ have been revealed, which trigger the deficiency of their precursors (essential fatty acids), the impairment of lipid metabolism and the activity decline of prostaglandin synthetase and adenylate cyclase, etc. A concept on the multiplicity of the biochemical mechanisms responsible for systemic PG action, whose impairments are essential in the pathogenesis of chronic hepatic diseases has been forwarded. The findings are discussed by comparing recent data published in the literature on this problem.
本文总结了对健康个体和慢性肝病患者前列腺素系统深入研究的结果。放射免疫分析、气相色谱分析、酶免疫分析及其他生化研究首次证实,在不同病因的慢性肝炎和肝硬化中,前列腺素(PG)E、F2α、I2、血栓素A2的内源性生物合成受损、代谢和激素紊乱的发生以及肝衰竭的严重程度之间存在关联,这得出PG在肝功能调节和慢性损伤发病机制中起重要作用的结论。已揭示出患病器官中PGE、PGF2α和PGI2减少的此前未知的生化机制,这些机制引发其前体(必需脂肪酸)缺乏、脂质代谢受损以及前列腺素合成酶和腺苷酸环化酶活性下降等。提出了一个关于负责全身PG作用的生化机制多样性的概念,其损害在慢性肝病发病机制中至关重要。通过比较文献中关于该问题的最新数据对这些发现进行了讨论。