细胞间粘附分子—1表达水平对心肌再灌注损伤的影响及N—乙 …

探讨细胞间粘附分子表达与中性粒细胞浸润与心肌血再灌注损伤的关系并观察Ｎ－乙酰半胱氨酸对ＩＲＩ的保护效果。方法大鼠１１６只,分设：（１）缺血再灌注（ＩＲ）组;（２）ＩＲ＋ＮＡＣ组;（３）假手术对照组,并分庙再灌注１、３、６、１２、２４ｈ时相点。取缺血心肌用原位杂交和免疫组织检测ＩＣＡＭ－１ｍＲＮＡ及其蛋白表达水平,用酶法测定ＰＭＮｓ浸润数,ＴＴＣ染色法测心肌梗死范围,结果心肌再灌注时,ＩＣＡＭ－１表

Influenceof expression of intercellular adhesion molecule-1 on myocardial ischemic reperfusioninjury and cardiac protective effect of N-acetylcysteine

Objective　To investigate the influence ofexpression of intercellular adhesion molecule-1(ICAM-1) on myocardial ischemic reperfusioninjury (IRI), myocardial infiltration of polymorphonuclear neutrophils(PMNs) andinfarction size, and the cardiac protective effect of N-acetylcysteine(NAC). Methods　One hundred and sixteen rats weredivided into three groups IR, IR+NAC and sham-group. The ischemic myocardial samples werestudied at 1,3, 6,12, 24 hours after ischemic reperfusion (IR). The levels of expressionof ICAM-1 mRNA were evaluated by in situ hybridization and the protein byimmunocytochemistry. The numbers of infiltrated PMNs were measured with MPO enzyme markermethod and the myocardial infarction area was evaluated by TTC staining method. Results　After IR, myocardial levels ofexpression of ICAM-1 mRNA were increased significantly and reached a peak at 6 h; but theICAM-1 protein peaked during 12-24 h. Number of PMNs and infarction size also increasedand peaked after reperfusion 12-24 h. Close positive correlation (P<0.05) was foundbetween the levels of expression of ICAM-1 protein, PMNs infarction area of themyocardium. In IR+NAC group, all of the indices were increased after IR, but the levels ofincrease in IR+NAC group were significantly lower (P<0.05 or 0.01) as compared withgroup IR (P<0.05-0.01). Conclusion　The findings indicate that PMNs adhesion and infiltrationinduced by ICAM-1 is implicated in the development of myocardial IRI. NAC could protectthe myocardium from IRI by partially blocking the expression of ICAM-1.