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溶血磷脂胆碱在缺血性心律失常中的作用X(PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
1998年第3期
页码:
137-139
栏目:
论著
出版日期:
1998-05-01

文章信息/Info

Title:
Effects of lysophosphatidylcholine in ischemic arrhythmia
作者:
杜友爱
温州医学院生理学教研室 325000
Author(s):
Du Youai
Department of Physiology, Wenzhou Medical College, Wenzhou 325000
关键词:
溶血磷脂胆碱　心肌缺血　电生理
Keywords:
lysophosphatidylcholine　myocardium ischemia　electrophysiology
分类号:
-
DOI:
-
文献标识码:
-
摘要:
用台氏液加溶血磷脂胆碱(LPC) 3×10-4 mol/L 灌流离体绵羊心室小梁肌, 其0期去极化最大速率(Vmax)、静息电位(RP)、动作电位幅值(APA)、动作电位复极达APA 50% 和APA 90% 的时程(APD50, APD90) 分别下降39. 8% , 10.4% , 14.5% , 21.3% 和14.8% (n= 12, P < 0.01) ; 用“模拟缺血溶液”和LPC 3×10-4mol/L灌流, 其Vmax , RP, APA , APD50, APD90分别下降78.0% , 22.7% , 2.0% , 35.4% 和21.0%。实验中对“模拟缺血溶液”中各种成分对LPC 效应的影响进行分析, 发现其主要因素是酸中毒。结果表明: LPC是心肌缺血中心律失常的重要因素之一, 缺血诱导的酸中毒更加重了LPC对心肌细胞的毒性作用。
Abstract:
The sheep ventricular myocardial trabeculae were immersed in Tyrode′s solution with lysophosphatidylcholine (LPC) 3×10-4mol/L. The maximal depolarized rate at O phase (Vmax) ,the resting potential (RP) , the action potential ampiltude (APA) , and the action potential duration at 50% and 90% of APA(APD50, APD90 )were reduced 39.8% , 10.4% , 14.5% , 21.3%and 14.8% , respectively (n=12, P < 0.01). When the sheep ventricular myocardial trabeculae were immersed in the simulated ischemic solution with LPC 3×10-4mol/L , the Vmax , RP, APA ,APD50, and APD90 were reduced 78.0% , 22.7% , 26.0% , 35.4% and 21.0% , respectively.When the influence of every componen t in the simulated ischemic solution on the effects of LPC was analysed, the main factor was found to be acidosis. These results indicated that LPC was one of the important factors of early cardiac arrhythmia caused by myocardial ischemia and the acidosis induced by ischemia increased the toxic effects of LPC on the myocardial cells.inversion in the future was forecast.

参考文献/References

［1］Corr PB. Potential arrhythmogenic electrophysiological derangements in canine purkinje fibers induced by lysophosphoglycerides. Circ Res, 1997; 44: 822.

［2］Arnsdorf MF, Sawicki GJ. The effects of lysophosphatidylcholine, a toxic metabolite of ischemia, on the components of cardiac excitability in sheep Purkinje fibers. Circ Res, 1981; 49: 16.

［3］Clarkso CW , Ten Eick RE. On the mechanism of lysophosphatidylcholine induced depolarization of cat ventricular myocardium. Circ Res, 1983; 52: 543.

［4］Kiyosue T , Arita M. Effects of lysophosphatidylcholine of resting potassium conductance of isolated guinea pig ventricular cells. Eure J Physiol, 1986; 406: 296.

［5］Akita H, Michael H. Electrophysiological effects of intracellular lysophosphoglycerides and their accumulation in cardiac lymph with myocardial ischemia in dogs. J Clin Invest, 1986; 78: 271.

［6］Snyder DW , William A. Lysophospholycerides in ischemia myocardium effluents and potentiation of their arrhythmogenic effects. Am J Physiol, 1981; 241:H700.

［7］Gilmour RF, Zipes DP. Different electrophysiological responses of canine endocardium and epicardium to combined hyperkalemia, hypoxic and acidosis. Circ Res,1980; 46: 814.

备注/Memo

备注/Memo:
(收稿1997-07-14　修回1997-12-22)X国家自然科学基金资助项目（No.39470311)
更新日期/Last Update: 1998-05-01