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 1 1 6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、1 2、2 4h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 1mRNA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 1mRNA、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
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 1mRNA 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 1mRNA, 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.
出处
《中国康复理论与实践》
CSCD
2002年第7期423-425,420,共4页
Chinese Journal of Rehabilitation Theory and Practice
基金
20 0 1年度重庆市医学科研项目 ( 0 1 1 0 0 8)