《中国康复理论与实践》

《中国康复理论与实践》 ›› 2002, Vol. 8 ›› Issue (07): 423-425.

• 基础研究 • 上一篇    下一篇

老年大鼠心肌再灌注时ICAM-1表达变化规律及艾司洛尔的影响

何坪1;司良毅2   

  1. 1.重庆市全科医学教育中心 重庆市 400050;2.第三军医大学西南医院老年病科 重庆市 400038
  • 收稿日期:2002-05-15 出版日期:2002-07-25 发布日期:2002-07-25

Changes of ICAM-1 expression of myocardial ischemic reperfusion injury in old rats and cardiac protective effect of Esmolol

HE Ping,SI Liang-yi   

  1. Chongqing General Family Medicine Education Center,Chongqing 400050,China
  • Received:2002-05-15 Published:2002-07-25 Online:2002-07-25

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摘要： 目的探讨细胞间粘附分子-1(ICAM-1)表达与老年大鼠心肌缺血再灌注损伤(IRI)的关系,并观察艾司洛尔(ES)对IRI的影响。方法大鼠116只,分设缺血再灌注(IR)组,IR+ES组和假手术对照组,并分设缺血1h,再灌注3、6、12、24h时相点,取缺血心肌用原位杂交和免疫组织化学方法检测ICAM-1 mRNA及其蛋白质表达水平,用酶法测定中性粒细胞(PMNs)浸润数 ,硫代巴比妥酸比色法测定心肌组织丙二醛(MDA),用黄嘌呤过氧化物酶法测定过氧化物岐化酶(SOD)活性,TTC染色法测定梗死范围。结果心肌IR时,ICAM-1表达、MDA含量、PMNs浸润数均明显增高,SOD活性明显降低;ICAM-1蛋白表达水平、PMNs浸润与心肌梗死范围呈显著正相关,但ICAM-1 mRNA、MDA、SOD与梗死范围无明显相关性。IR+ES组上述指标于再灌注时虽也明显增高,但比IR组明显减轻。结论心肌IR时,ICAM-1参与介导了PMNs对组织细胞的粘附、浸润和IRI的发生、发展;ES可通过抑制ICAM-1的表达而产生心肌保护作用。

关键词: 细胞粘附分子, 心肌缺血, 再灌注损伤, 艾司洛尔

Abstract: ObjectiveTo investigate the changes of expression of intercellular adhesion molecule 1 (ICAM-1) on myocardial ischemic reperfusion injury(IRI) in old rats and the cardiac protective effect of Esmolol(ES). Methods116 rats were divided into three groups: IR group, IR+ES group and Sham group. The ischemic samples were observed in ischemia and 3,6,12,24 hours after IR. The myocardial levels of expression of ICAM-1 mRNA were evaluated by method of IN Situ Hybridization and the protein were evaluated by immunocytochemistry. The content of infiltration of polymorphonuclear neutrophils(PMNs), malomdialdehyde(MDA), superoxides dismutase(SOD) and the myocardial infarction area were measured too. ResultsAfter IR, myocardial levels of expression of ICAM-1 mRNA, protein,MDA and PMNs were increased significantly; SOD was decreased significantly. Between the levels of expression of ICAM-1 protein and PMNs, infarction area of myocardium, a close correlation were observed(P<0.05). In IR+ES group, all of the indicators were increased after IR, but the levels of increase in IR+ES group were more significantly modification as compared with IR group(P<0.05-0.01).Conclusions The findings indicate that PMNs could induce myocardial IRI after IR, which result from the ICAM-1 mediated PMNs adhesion.ES is able to decrease myocardial IRI by blocking the expression of ICAM-1 partially.

Key words: cell adhesion molecules, myocardial ischemia, reperfusion injury, Esmolol