我们的网站为什么显示成这样？

可能因为您的浏览器不支持样式，您可以更新您的浏览器到最新版本，以获取对此功能的支持，访问下面的网站，获取关于浏览器的信息：

|本期目录/Table of Contents|

高、低剂量极化液对缺血/ 再灌注心肌细胞凋亡及相关基因的影响(PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2004年第5期
页码:
427-430
栏目:
基础研究
出版日期:
2004-09-01

文章信息/Info

Title:
Comparative study of the effects of high dose and low dose GIK on cardiomyocyte apoptosis and apoptosis related genes during myocardial ischemic and reperfusion
作者:
高　晖1; 张　清1; 贾国良1; 张荣庆1; 马兰香2; 赵新国2; 王　岚2
1. 第四军医大学西京医院心血管内科, 陕西西安710032 ; 2.武警陕西总队医院心血管内科,陕西西安710054
Author(s):
GAO Hui1; ZHANG Qing1; JIA Guo-liang1; ZHANG Rong-qing1; MA Lan-xiang2; ZHAO Xin-guo2; WANG Lan2
11Department of Cardiology , Xijing Hospital , Fourth Military Medical University , Xi’an , Shaanxi 710032 , China; 21Department of Cardiology , Shaanxi Provincial Corps Hospital , Chinese People’s Armed Police Forceds , Xi’an , Shaanxi 710054 , China
关键词:
胰岛素;  再灌注损伤;  心肌缺血;  细胞凋亡;  超微结构
Keywords:
insulin ;  Myocardial ischemia reperfusion ;  apoptosis ;  ultrastructure
分类号:
R542. 2
DOI:
-
文献标识码:
A
摘要:
目的: 探讨高、低两种剂量葡萄糖- 胰岛素- 钾极化液(GIK) 对缺血/ 再灌注(MI/ R) 心肌超微结构,细胞凋亡 及其相关基因的影响。方法: 制备兔MI/ R 模型,分别用生理盐水,低剂量极化液(LGIK) ,高剂量极化液(HGIK) 干 预分组。检验心肌组织SOD 活性,原位末端标记(TUNEL) 法测定凋亡心肌细胞,免疫组化SP 法测定Bcl-2 , Fas 的 含量,在电镜下观察心肌细胞的超微结构。结果:与对照组比较,HGIK组SOD 活性增加( P < 0. 01) ,凋亡指数(AI) 和Fas 含量减少( P < 0. 01) , Bcl-2 含量增加( P < 0. 01) 。心肌细胞超微结构表现为损伤减轻。LGIK亦可增加SOD 活性和Bcl-2 含量( P < 0. 05) ,减少AI 和Fas( P < 0. 05) 含量。结论: GIK具有抗缺血/ 再灌注损伤的作用,其机制可 能是通过调节Bcl-2 和Fas 介导的心肌缺血/ 再灌注细胞凋亡而实现。高剂量GIK对缺血/ 再灌注心肌细胞的保护 作用显著大于低剂量GIK( P < 0. 05) 。
Abstract:
AIM: To study the effect of different doses of glucose-insulin-potassium (GIK) cocktail on cardiac myocyte apoptosis and ultrastructure following myocardial ischemia/ reperfusion (MI/ R) . METHODS: Rabbits were subjected to 45 min myocardial ischemia , followed by reperfusion for 3 h. Anesthetized rabbits were randomly treated with continuous infusion of saline , LGIK (100 g/ L Glucose ,20 U/ L Insulin and 20 mmol/ L KCl) , HGIK (300 g/ L Glucose , 50 U/ L Insulin and 80 mmol/ L KCl) , 5 min before the reperfusion and throughout the 3 h reperfusion. The animals were sacrificed and the heart was harvested for SOD and ultrastructure examination(electron microscope) . Apoptosis was identified by TUNEL and apoptosis index (AI)was obtained. The expressions of Fas ,Bcl-2 protein were measured by immunohistochemical technique. SOD was assayed spectrophocometrically and myocardial ultrastructure was examined. RESULTS : Compared with the vehicle treated rabbits , the HGIK-treated rabbits showed protection against MI/ R injury as evidenced by marked decrease of AI and the content of Fas protein ( P < 0. 01) , significantly increased the content of Bcl-2 protein and activity of SOD( P < 0. 01) . The ultrastructure of myocardium showed attenuated injury. AI and the content of Fas protein of the LGIK-treated rabbits were reduced ( P < 0. 05) , and the content of Bcl-2 protein and activity of SOD were improved( P < 0. 05) . CONCLUSION: GIKcan protect myocardiumfrom MI/ R injury by modulating the expressions of Fas and Bcl22 protein and inhibit apoptosis following myocardial MI/R and the high dose of GIKplay a more important role in protecting myocardial ischemia reperfusion than that of the low dose of GIK.

参考文献/References

[1 ] Broomhead CJ , Colvin MP. Glucose , insulin and the cardiovascular system[J ] . Heart , 2001 , 85 : 495 - 496.

[2 ] Gao F , Shi DW, Wang XM, et al . Effects of glucose-insulin-potassium cocktail on cardiac myocyte death and post-ischemic recovery cardiac functional recovery : the critical role of insulin[J ] . Chin J Intern Med ,2003 ,42 (3) :146 - 152.

[3 ] Gao F , Gao E , Yue TL , et al . Nitric oxide mediates the antiapoptotic effect of insulin in myocardial ischemia-reperfusion : the roles of PI3-Kinase , Akt and endothelial nitric oxide synthase phosphorylation[J ] . Circulation , 2002 , 105 : 1497 - 502.

[4 ] 范　谦,张　博,王跃民,等1 胰岛素对缺血/ 再灌注心肌的保护作用[J ]1 心脏杂志,2002 ,14(1) : 1 - 3.

[5 ] Diza R , Paolasso EA , Piegas LS , et al . Metabolic modulation infarction : remarkable results from a new prospective , randomized trial [J ] .Circulation , 1998 , 98 :2223 - 2226.

[6 ] Sodi2pallares D. Testelli M. Fishelder F. Effects of an intravenous infusion of a potassium2insulin2glucose solution on the electrocardiographic signs of myocardial infarction [J ] . Am J Cardiol , 1962 , 9 : 166 - 181.

[7 ] Opie LH. The glucose hypothesis : relation to acute myocardial ischemia [J ] . J Mol Cell Cardiol , 1970 , 1 : 107 - 115.

[ 8 ] Fath-Ordoubadi F , Beatt KJ . Glucose-insulin-potassium therapy for treatment of acute myocardial infarction : an overview of randomized placebo controlled trials[J ] . Circulation , 1997 , 96 : 1152 - 1156.

[9 ] Diza R , Paolasso EA , Piegas LS , et al . Metabolic modulation infarction : remarkable results from a new prospective , randomized trial [J ] .Circulation , 1998 , 98 :2223 - 2226.

[10 ]Apstein CS , Glucose-insulin-potassium for acute myocardial infarction : remarkable results from a new prospective , randomized trial [J ] . Circulation , 1998 ,98 : 2223 - 2226.

[11 ]Ceremuzynski L , Budai A , Czepiel A , et al . Low dose glucose - insulin - potassiumis ineffective in acute myocardial infarction : results of a randomized multicenter Pol-GIK trial [ see comments ] [J ] . Cardiovasc Drugs Ther , 1999 , 13 :191 - 200.

[12 ]Stanley AWJr ,Moraski RE , Russell RO , et al . Effects of glucose-insulin-potassium on myocardial substrate availability and utilization in stable carbohydrate , lipid and oxygen arterial-coronary sinus differences in patients with coronary artery disease [J ] . Am J Cardiol , 1975 ,36 :929 - 937.

[13 ]Von Harsdorf R , Li PF ,Dietz , et al . Signaling pathways in reactive oxygen species-induced cardiomyocyte apoptosis[J ] . Circulation ,1999 ,99 :2934 - 2941.

[14 ] Schwartz SM. Cell death and the casoase cascade [ J ] . Circulation ,1998 ,97 :227 - 229.

[15 ]Colucci WS. Apoptosis in the heart [J ] . New Engl J Med , 1996 ,335 :1224 - 1226.

[16 ]Nguyen M, Philip EB , Paul AW, et al . Role of membrane anchor domain of Bcl-2 in suppression of apoptosis carsed by EIB-defective adnovirus[J ] . J Biol Chem ,1994 ,269 :16521 - 16524.

[17 ]Marchetti P , Castedo M, Susin SA , et al . Mitochondrial permeability transition is a central coordination event of apoptosis[J ] . J EXP Med ,1996 ,184 :1155 - 1160.

[18 ]张海峰,马新亮,高　峰,等. 从极化液到胰岛素的作用机制的认识[J ] . 中华医学杂志,2003 ,83 :257 - 259.

[19 ]Sack MN , Yellon DM. Insulin therapy as an adjunct to reperfusion after acute coronary ischemia : a proposed direct myocardial cell survival effect independent of metabolic modulation[J ] . J Am Coll Cardiol , 2003 ,41(8) :1404 - 1407.

备注/Memo

备注/Memo:
收稿日期：2003-8-1
更新日期/Last Update: 2004-09-01