缺血后处理对缺血-再灌注心肌的保护作用及其与线粒体ATP敏感性钾通道的关系()
《中国胸心血管外科临床杂志》[ISSN:1007-4848/CN:51-1492/R]
- 期数:
- 2009年第16卷第6期
- 页码:
- 466-471
- 栏目:
- 基础研究论著
- 出版日期:
- 2009-12-25
文章信息/Info
- Title:
- The Protective Effects of Ischemic Postconditioning on Ischemiareperfusion Myocardium and the Relationship with Mitochondrial Adenosine Triphosphate Sensitive K+ Channels
- 文章编号:
- 1007-4848 (2009)06-0466-06
- 作者:
- 任静华 陈玉培
- 重庆医科大学附属第二医院 麻醉科， 重庆 400010
- Author(s):
- REN Jing-hua; CHEN Yu-pei.
- Department of Anesthesiology, Affiliated Second Hospital, Chongqing University of Medical Science, Chongqing 400010, P.R.China
- 关键词:
- ; 缺血后处理; 心肌保护; 缺血再灌注损伤; 线粒体三磷酸腺苷敏感性钾通道.
- Keywords:
- ; Ischemic postconditioning; Myocardial protection; Ischemiareperfusion injury; Mitochondrial adenosine triphosphate sensitive K+ channel
- 分类号:
- R654.1
- DOI:
- -
- 文献标识码:
- A
- 摘要:
- 目的 探讨缺血后处理（IPo）的心肌保护作用及与心肌线粒体三磷酸腺苷（ATP）敏感性钾通道(mitoKATP)的关系，为药物后处理的研发提供依据。 方法 40只Wistar大鼠，建立大鼠离体心脏Langendorff灌注模型，采用随机数字表法分为5组，每组8只，正常对照组（NC组）：用K-H液持续灌注100 min，不做任何处理；缺血-再灌注（I/R）组：全心缺血40 min，再灌注60 min；IPo组：全心缺血40 min，再灌注10 s，缺血10 s，反复6次，然后持续再灌注58 min；5-羟基癸酸（5-HD）组：全心缺血40 min后，先用含5-HD(100 μmol/L)的KH液再灌注15 min，再用不含5-HD的K-H液再灌注45 min；IPo+5-HD组：全心缺血40 min后，先用含5-HD（100 μmol/L）的K-H液再灌注10 s，缺血10 s，反复6次，再用含5-HD的K-H液持续灌注13 min，然后用不含5-HD的K-H液再灌注45 min。观察比较各组心功能、冠状动脉流量（CF）、冠状动脉流出液中心肌肌钙蛋白I（cTnI）含量、心肌梗死（AMI）面积和心肌细胞超微结构改变。 结果 再灌注末IPo组左心室发展压（74.3±3.3 mm Hg vs.57.1±3.3 mm Hg,t=13.00, P=0.000）、+dp/dtmax（1 706.6±135.6 mm Hg/s vs. 1 313.3±96.2 mm Hg/s, t=6.28,P=0.000）、－dp/dtmax（1 132.8±112.1 mm Hg/s vs. 575.7±67.7 mm Hg/s,t=13.48, P=0.000）、CF（6.49±0.30 ml/min vs. 3.70±0.24 ml/min,t=28.60, P=0.000）与I/R组比较均升高；左心室舒张期末内压（10.9±1.7 mm Hg vs.26.2±1.5 mm Hg, t=－19.21, P=0.000),冠状动脉流出液中cTnI含量（0.62±0.01 ng/ml vs. 0.71±0.01 ng/ml，t=－12.00, P=0.000）均降低，AMI面积与I/R组比较减少20.8％（P<0.05）。IPo+5-HD组对心肌的保护作用与IPo组相似，但作用轻于IPo组。电子显微镜观察结果表明，IPo和IPo+5HD可减轻I/R引起的心肌纤维和线粒体损伤。 结论 IPo对I/R心肌有保护作用，其作用与mitoKATP的激活有关。
- Abstract:
- Objective To investigate the protective effects of ischemic postconditioning (IPo) on ischemiareperfusion (I/R) myocardium and the relationship with mitochondrial adenosine triphosphate (ATP) sensitive K
+ channels (mitoKATP) and provide evidences to the development of druginduced postconditioning. Methods Langendorff models were established in 40 Wistar rats which were divided into 5 groups by random number table with 8 rats in each group. Normal control group(NC group): the rat hearts were continuously reperfused by KrebsHenseleit bicarbonate buffer (K-HB) for 100 min without any other treatment; I/R group: the rat hearts underwent a 40-min global ischemia followed by a 60-min reperfusion; IPo group: after a 40-min global ischemia, the process of 10-second reperfusion followed by a 10-second ischemia was repeated 6 times, then there was a continuous 58min reperfusion; 5-hydroxydecanoic acid(5-HD) group: after a 40min global ischemia, hearts with 5HD(100 μmol/L) K-HB were reperfused for 15min and then perfused without 5HD for 45min；IPo+5-HD group: after a 40-min global ischemia, the process that the isolated hearts with 5-HD(100 μmol/L) KHB were reperfused for 10second followed by a 10second ischemia was repeated 6 times, then the hearts with 5-HD(100 μmol/L) KHB were continuously [CM(159mm]perfused for 13-min followed by reperfusion without 5-HD(100 μmol/L) K-HB for 45-min. The cardiac function,coronary flow(CF), cardiac troponin I(cTnI) content in coronary effluent, the area of acute myocardial infarction (AMI) and myocardial ultrastructure were observed. Results Left ventricular developed pressure(74.3±3.3 mm Hg vs. 57.1±3.3 mm Hg,t=1300, P=0.000),+dp/dtmax(1 706.6±135.6 mm Hg/s vs. 1 313.3±96.2 mm Hg/s,t=6.28,P=0.000),－dp/dtmax(1 132.8±112.1 mm Hg/s vs. 575.7±67.7 mm Hg/s,t=13.48, P=0.000) and CF(6.49±0.30 ml/min vs. 3.70±0.24 ml/min,t=28.6,P=0.000) in IPo group were higher than those in I/R group. Left ventricular enddiastolic pressure(10.9±1.7mm Hg vs. 26.2±1.5 mm Hg,t=－19.21, P=0000)and cTnI content in coronary effluent (0.62±0.01 ng/ml vs. 0.71±0.01 ng/ml, t=-12.00,P=0.000) were lower than those in I/R group; the area of AMI decreased 20.8％ compared with that in I/R group (P<0.05). The myocardial protective effect in IPo+5HD group was similar with that in IPo group, but lower than that in IPo group. The electron microscope showed that IPo and IPo+5HD could reduce myocardial fiber damage and mitochondrial damage caused by I/R. Conclusion IPo can protect I/R myocardium, which is achieved mainly by activating mitoK-ATP channels.
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更新日期/Last Update: 2009-12-29