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血液透析过程中补体激活和中性粒细胞聚集的变化

Complement activation and neutrophil aggregation changes during haemodialysis.

作者信息

Kubatiev A, Rudko I, Ermolenko V

机构信息

Department of General Pathology and Pathophysiology, National Centre of Postgraduate Medical Training, Moscow, Russia.

出版信息

Int J Clin Pharmacol Res. 1993;13(6):293-9.

PMID:8088929
Abstract

Complement activation (plasma levels of the anaphylatoxins C3a and C5a), the aggregation of polymorphonuclear neutrophils (PMN) on 12-O-tetradecanoyl-4 beta-phorbol-13-acetate (TPA) 2.5 microM, A23187 5 microM, arachidonic acid 0.1 mM and TPA-induced thromboxane A2 production by PMN were examined in 10 uraemic patients at times 0, 15 and 240 min after the onset of haemodialysis with Cuprophan (CU) and polyacrylonitrile (PAN) membranes. The rise in plasma C3a and C5a was intense during haemodialysis with CU, but mild with PAN. PMN aggregation in uraemic patients was lower (as compared to normal controls) independently of the agonist used. At 15 min of haemodialysis with CU, PMN aggregation increased and decreased at 240 min, while during haemodialysis on PAN no significant changes in PMN aggregation were noticed. TPA-induced TxA2 synthesis by PMN was decreased in uraemic patients. It was normalized after haemodialysis with PAN, but not with CU. Apparently the mechanisms underlying PMN aggregation and TxA2 synthesis during haemodialysis may not be entirely dependent on complement activation. Evidently, dialysable plasma factors may be responsible for the abnormal PMN function in uraemic patients. Thus, removal of these factors by haemodialysis with an appropriate membrane may improve the PMN functions.

摘要

在10例尿毒症患者中,于使用铜仿膜(CU)和聚丙烯腈膜(PAN)进行血液透析开始后0、15和240分钟时,检测补体激活(过敏毒素C3a和C5a的血浆水平)、多形核中性粒细胞(PMN)在2.5微摩尔12 - O - 十四烷酰佛波醇 - 13 - 乙酸酯(TPA)、5微摩尔A23187、0.1毫摩尔花生四烯酸作用下的聚集情况以及PMN经TPA诱导产生血栓素A2的情况。在使用CU进行血液透析期间,血浆C3a和C5a显著升高,而使用PAN时升高程度较轻。与正常对照组相比,尿毒症患者中PMN的聚集较低,且与所使用的激动剂无关。在使用CU进行血液透析15分钟时,PMN聚集增加,在240分钟时减少,而在使用PAN进行血液透析期间,未观察到PMN聚集有显著变化。尿毒症患者中PMN经TPA诱导的TxA2合成减少。使用PAN进行血液透析后其恢复正常,但使用CU则未恢复正常。显然,血液透析期间PMN聚集和TxA2合成的潜在机制可能并不完全依赖于补体激活。显然,可透析的血浆因子可能是尿毒症患者PMN功能异常的原因。因此,使用合适的膜进行血液透析去除这些因子可能会改善PMN功能。

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