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|本期目录/Table of Contents|

外源性磷酸肌酸对缺血豚鼠心室肌细胞L型钙通道电流的影响

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2010年第2期
页码:
168-171,175
栏目:
基础研究
出版日期:
2010-03-04

文章信息/Info

Title:
Effect of exogenous phosphocreatine on L-type calcium current in ischemic ventricular myocytes
作者:
时向民1; 李天德2; 王玉堂2; 单兆亮2; 杨庭树1
解放军总医院:1.南楼心内科，2.普通心内科，北京 100853
Author(s):
Shi Xiang-min1;  Li Tian-de1;  Wang Yu-tang2;  Shan Zhao-liang2;  Yang Ting-shu1
1.Cardiology Department, South Building, 2.Department of Cardiology, General Hospital of PLA, Beijing 100853, China
关键词:
豚鼠; 膜片钳;  L型钙电流; 缺血; 磷酸肌酸
Keywords:
guinea pig;  patch clamp;  L-type calcium current;  ischemia heart failure;  phosphocreatine
分类号:
R542.2;R331.38
DOI:
-
文献标识码:
A
摘要:
目的: 观察不同浓度外源性磷酸肌酸（exogenous phosphocreatine,PCr）对豚鼠缺血心室肌细胞L型钙通道（ICa·L）电流的影响，探讨其治疗缺血性心力衰竭的电生理学机制。方法: 单个心室肌细胞经酶解从豚鼠左心室获得，采用膜片钳全细胞模式记录ICa·L电流，通过灌注模拟缺血液并充以95%N2+5%CO2的混合气体建立缺血模型，将PCr加入模拟缺血液中分别配成5,10,20,30 mmol/L浓度。将细胞分成6组，分别予模拟缺血液，含有5,10,20,30 mmol/L浓度PCr的模拟缺血液，台氏液灌流，后者充以95%O2+5%CO2的混合气体。10 min后记录各组的峰电流及电流密度。结果: 与台氏液组相比，模拟缺血液组ICa·L峰电流密度降低(80.6±5.2)%（P<0.05），含有5,10,20,30 mmol/L浓度PCr的模拟缺血液组ICa·L峰电流密度分别降低(53.8±6.7)%（P<0.05）；(41.8±8.2)%（P<0.05）；(38.1±7.4)%（P<0.05）；(36.6±9.7)%（P<0.05）。10,20,30 mmol/L3种浓度对ICa·L峰电流密度的影响无统计学差别。结论: PCr能明显增加缺血时受抑制的ICa·L峰电流及电流密度，这可能是其治疗缺血性心力衰竭的电生理学机制。PCr在低浓度 (0~10 mmol/L)对ICa·L电流及电流密度的影响呈现明显的量效关系，浓度大于10 mmol/L量效关系不明显。
Abstract:
AIM: To explore the effect of exogenous phosphocreatine (PCr) with different concentration on L-type calcium (ICa·L) current in ischemic ventricular myocytes of guinea pig and to investigate its underlying electrophysiological mechanism for the treatment of ischemic heart failure. METHODS: Ventricular myocytes were isolated enzymatically from left ventricular of guinea pig. Peak ICa·L current were recorded using patch clamp techniques in the whole-cell configuration when myocytes had been superfused with normal Tyrode solution, simple ischemic solution, ischemic solution containing PCr with different concentration of 5, 10, 20, 30 mmol/L for 10 min, respectively. RESULTS: Peak ICa·L current density of myocytes superfused with simple simulated ischemic solution was remarkably inhibited by (80.6±5.2)% compared with myocytes superfused with normal Tyrode solution (P<0.05). Ischemic solution containing PCr of 5, 10, 20, 30mmol/L inhibited Peak ICa·L current density by (53.8±6.7)%(P<0.05); (41.8±8.2)%(P<0.05); (38.1±7.4)%(P<0.05); (36.6±9.7)% (P<0.05), respectively. There was no statistical significance among PCr of 10, 20, 30 mmol/L. CONCLUSION: PCr could reverse the inhibition of ICa·L current under ischemic condition, which could be the ionic basis for the treatment of ischemic heart failure. 0-10 mmol/L PCr exerted a significant dose-effect relationship, which no longer existed as concentration >10 mmol/L.

参考文献/References

［1］ Liu Q, Robert L. Stimulation of cardiac L-type calcium channels by extracellular ATP［J］. Am J Physiol Cell Physiol, 2001, 280(5):C1107-C1113.

［2］ Soball S, Conrad A, Eistert A, et al. Uptake of creatine phosphate into heart mitochondria: A leak in the creatine shuttle［J］. Biochem Biophys Acta, 1997, 1320(1):27-33.

［3］ Ferraro S, Codella C, Palumbo F, et al. Hemodynamic effects of creatine phosphate in patients with congestive heart failure: a double-blind comparison trial versus placebo［J］. Clin Cardiol, 1996, 19(9):699-703.

［4］ Hamil OP. Twenty odd years of stretch-sensitive channels［J］. Pflugers Arch, 2006, 453（3）:331-351.

［5］ Treinys R, Jurevicius J. L-type Ca2+ channels in the heart: structure and regulation［J］. Medicina, 2008, 44(7):491-499.

［6］ Kubalová Z. Inactivation of L-type calcium channels in cardiomyocytes. Experimental and theoretical approaches［J］. Gen Physiol Biophys, 2003, 22(4):441-454.

［7］ Grzyb K, Skorkowski EF. Creatine kinase isoenzymes--characterization and functions in cell［J］. Postepy Biochem, 2008, 54(3):274-283.

［8］ Conway M, Allis J, Ouwerkerk R, et al. Detection of phosphocreatine to ATP ratio in failing hypertrophied human myocardium by 31p magnetic resonance spectroscopy［J］. Lancet, 1991, 338(8773):973-976.

［9］ Pastoris O, Dossena M, Vercesi L, et al. Biochemical changes induced in the myocardial cell during cardioplegic arrest supplemented with creatine phosphate［J］. J Cardiothorac Vasc Anesth, 1991, 5(5):475-480.

［10］Saks V, Dzhaliashvili I, Strumia E, et al. Molecular and cellular aspects of the cardioprotective mechanism of phosphocreatine［J］. Biokhimiia, 1992, 57(12):1763-1784.

备注/Memo

备注/Memo:
收稿日期：2009-5-27.通讯作者：王玉堂，主任医师，主要从事心脏电生理基础与临床研究Email：wyt301@sina.com 作者简介：时向民，副主任医师，博士Email:shixm301cardiac@hotmail.com
更新日期/Last Update: 2010-03-05