肾综合征出血热发病机理中花生四烯酸代谢和部分免疫因素的作用
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摘要
本文从临床角度对肾综合症出血(HFRS)热患者炎性介质-花生四烯酸(AA)的代谢及其产物和几个有关的因素进行了系统观察，同时对HFRS患者和感染大鼠的杀伤细胞和自然杀伤细胞功能及体内汉滩病毒(HTN)结构蛋白和相应抗体水平进行研究，探讨其在HFRS发病机理中的作用和意义。
肾综合症出血热是以发热、循环衰竭、出血、肾功衰竭为主要临床特征的急性传染病。花生四烯酸及其代谢产物与感染性疾病关系密切，尤其在休克、肾功衰竭及炎症的发生中起重要病理介导作用。采用酸滴定、放射免疫和荧光分析技术，观察了HFRS患者的磷脂酶A_2(PLA_2)、血栓素A_2(TXA_2)、前列环素(PGI_2)和丙二醛(MDA)水平，结果表明，HFRS病程各期TXA_2水平升高、PGI_2水平下降(发热期PGI_2已明显)和TXA_2／PGI_2(T／P)比值升高(T＞P，倒置)；PLA_2活性和MDA水平也在各病期有明显改变。上述变化在发热期开始已明显，并与病情呈平行改变，与病的轻重、有无休克及与临床病型和患者的血小板数量、尿蛋白量、BUN值等不同程度地相关；还发现PLA_2、MDA和TXA_2的变化呈正楣关。提示，本病的早期已出现广泛的血管内皮细胞损伤和AA代谢紊乱；并参与了本病的血管损伤、休克的发生、出血和肾功能衰竭等的病理过程。
采用体外诱导的方法观察了HFRS患者血小板转化外源性AA生成TXA_2的能力和转化外源性AA前后脂质过氧化物水平变化以及血小板内环核苷酸含量变化规律。结果表明本病各期血小板转化外源性AA
Hemorrhagic fever with renal syndrome(HFRS) is a severe infectious disease with high mortality in China. However, the pathogenesis of the disease remains unclear. So far most people are of the belief that the direct viral attack and immunopathogenesis are considered as the main mechanism of HFRS. It is the absence of clear evidence for virus cytopathology in fatal cases of HFRS and the coincidence of the humoral immune response with disease that have led to regarding immunopathogenesis as the main cause of this disease. But the data reported so far have not given a comprehensive explanation of the mechanism of the disease. Metabolic disorder of some inflammatory medium during the course of HFRS has also been regarded as a pathophysiological basis for this disease. It has been beleived that there are some obvious disorders of arachidonic acid(AA) metabolism, to which the pathologic course of HFRS correlated. Little is known, however, about the mechanism of this metabolism derangement, about the relation between arachidonic acid and about the pathologic damage in HFRS.
The present study was undertaken to investigate the relationship between AA and its metabolic products to the pathogenesis of this disease and to explore the immunopathogenesis of HFRS.
1. High levels of circulating PLA_2 have been implicated on the pathogenesis of profound systemic hypotension in infectious disease. In attempting to detect similar mechanisms in HFRS, the plasma samples form pateints were assayed by acidimetric for PLA_2 activity. The results showed that the activity of PLA_2 in the febrile phase of HFRS was slightly elevated, but there was no significant difference compared with that of normal control. However, in the oliguric stage the activity of PLA_2 became remarkably higher and it was the highest in the hypotensive stage in comparison with that of normal control. It restored to normal levels in the diuretic and convalescent stages. It was also found that these variations corresponded well with the serum BUN level, proteinuria contents, platelets counts, cAMP/cGMP level in platelets and plasma TXA_2, indicating that the elevated PLA_2 levels were related well with clinical manifestations. The results suggest that circulating PLA_2 was involved in the
肾综合症出血热是以发热、循环衰竭、出血、肾功衰竭为主要临床特征的急性传染病。花生四烯酸及其代谢产物与感染性疾病关系密切，尤其在休克、肾功衰竭及炎症的发生中起重要病理介导作用。采用酸滴定、放射免疫和荧光分析技术，观察了HFRS患者的磷脂酶A_2(PLA_2)、血栓素A_2(TXA_2)、前列环素(PGI_2)和丙二醛(MDA)水平，结果表明，HFRS病程各期TXA_2水平升高、PGI_2水平下降(发热期PGI_2已明显)和TXA_2／PGI_2(T／P)比值升高(T＞P，倒置)；PLA_2活性和MDA水平也在各病期有明显改变。上述变化在发热期开始已明显，并与病情呈平行改变，与病的轻重、有无休克及与临床病型和患者的血小板数量、尿蛋白量、BUN值等不同程度地相关；还发现PLA_2、MDA和TXA_2的变化呈正楣关。提示，本病的早期已出现广泛的血管内皮细胞损伤和AA代谢紊乱；并参与了本病的血管损伤、休克的发生、出血和肾功能衰竭等的病理过程。
采用体外诱导的方法观察了HFRS患者血小板转化外源性AA生成TXA_2的能力和转化外源性AA前后脂质过氧化物水平变化以及血小板内环核苷酸含量变化规律。结果表明本病各期血小板转化外源性AA
Hemorrhagic fever with renal syndrome(HFRS) is a severe infectious disease with high mortality in China. However, the pathogenesis of the disease remains unclear. So far most people are of the belief that the direct viral attack and immunopathogenesis are considered as the main mechanism of HFRS. It is the absence of clear evidence for virus cytopathology in fatal cases of HFRS and the coincidence of the humoral immune response with disease that have led to regarding immunopathogenesis as the main cause of this disease. But the data reported so far have not given a comprehensive explanation of the mechanism of the disease. Metabolic disorder of some inflammatory medium during the course of HFRS has also been regarded as a pathophysiological basis for this disease. It has been beleived that there are some obvious disorders of arachidonic acid(AA) metabolism, to which the pathologic course of HFRS correlated. Little is known, however, about the mechanism of this metabolism derangement, about the relation between arachidonic acid and about the pathologic damage in HFRS.
The present study was undertaken to investigate the relationship between AA and its metabolic products to the pathogenesis of this disease and to explore the immunopathogenesis of HFRS.
1. High levels of circulating PLA_2 have been implicated on the pathogenesis of profound systemic hypotension in infectious disease. In attempting to detect similar mechanisms in HFRS, the plasma samples form pateints were assayed by acidimetric for PLA_2 activity. The results showed that the activity of PLA_2 in the febrile phase of HFRS was slightly elevated, but there was no significant difference compared with that of normal control. However, in the oliguric stage the activity of PLA_2 became remarkably higher and it was the highest in the hypotensive stage in comparison with that of normal control. It restored to normal levels in the diuretic and convalescent stages. It was also found that these variations corresponded well with the serum BUN level, proteinuria contents, platelets counts, cAMP/cGMP level in platelets and plasma TXA_2, indicating that the elevated PLA_2 levels were related well with clinical manifestations. The results suggest that circulating PLA_2 was involved in the
引文
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