肾缺血预处理后急性心肌梗死大鼠炎症反应的变化及机制  

Effects of Renal Ischemic Preconditioning on Inflammatory Response in Rats After Acute Myocardial Infarction

作　　者：康素娴[1] 张冬会[2] 卢亚敏[2] 赵晓云[2] 邢邯英[2] 张萍[2] 李小慧[2] 

机构地区：[1]河北省老年病医院,河北石家庄050011 [2]河北省人民医院

出　　处：《中国微循环》2009年第6期508-513,共6页Journal of Chinese Microcirculation

摘　　要：目的观察肾缺血预处理后急性心肌梗死大鼠心肌梗死面积和早期炎症反应变化,探究其在心肌保护中的作用机制。方法将72只健康雄性成年SD大鼠随机分为三大组,①对照组(NC,n=8);②急性心肌梗死组(AMI,n=32);③肾缺血预处理组(RIP,n=32);各组大鼠分别在急性心肌梗死后2、4、6、12h四个时间点处死取材。术中以MS-4000生物信号采集处理系统监测并记录大鼠Ⅱ导联心电图,确定心肌梗死模型成功。Even’s蓝-TTC染色推测心肌梗死面积;HE染色观察心肌病理变化。双抗体夹心(ELISA)法测定血清白介素8(IL-8)和白介素10(IL-10)的含量;RT-PCR测定缺血区心肌组织IL-10mRNA和IL-8mRNA表达情况。结果RIP组12h梗死部位重量(IS)和缺血危险区(AAR)重量比值(IS/AAR)(46.18±6.15)%较AMI组(66.44±19.24)%明显减小(P<0.05)。RIP组与AMI组比较,心梗后2、4、6h浸润白细胞数目无明显差异(P>0.05),仅在12h时减少(P<0.05),外周血白细胞计数在12h有明显差异(P<0.05),血清IL-8浓度各时间点无明显差异(P>0.05)。血清IL-10含量仅见4h升高差异明显(P<0.05)。缺血心肌IL-8mRNA表达普遍降低,其中在6h和12hIL-8mRNA明显降低(P<0.05)。缺血心肌IL-10mRNA表达普遍降低,但同时间点间无明显差异(P>0.05)。结论经肾缺血预处理后12h急性缺血心肌中浸润的白细胞减少,急性心肌梗死面积缩小,全身炎症反应减轻,提示肾缺血预处理对急性心肌缺血有保护作用。Objective To observe the infarction areas and the change of leukocyte cell and leukocyte factor in AMI rat with remote ischemic preconditioning and explore its effect on ischemic myocardium. Methods Seventy-two healthy male SD drats were divided into three groups. ① normal control group（NC, n = 8）, ②acute myocardial infarction group（AMI, n = 32） ③ renal ischemic preconditioning group （ RIP, n = 32）. All the rats in AMI and RiP groups were sacrificed at 2, 4, 6, 12 hours after AMI. During the course, we recorded their Ⅱ lead ECG. Myocardial infarction size was examined with Evans and TFC staining. Counting the numbers of peripheral blood leukocyte, pathological change and the leukocyte infiltration numbers in myocardium were detected by HE -staining section. Using ELISA to determine the serum level of IL-8 and IL-IO and RT-PCR to investigate the expression of IL-8 and IL-10 mRNA. Results Compared with AMI group, the infarction size and IS/AAR of RiP group at 12h diminished obviously（46. 18 ± 6.15% vs 66.44 ± 19.24%, P 〈 0.05）. Compared group RIP with group AMI, histopathoogical aspects showed different damage at 12h （P 〈 0.05 ）, the former is better than the later. Compared with group AMI, the leukocytes infiltration count reduced at 12h （P 〈0.05） in group RIP. The concentration of serum IL-8 at each time had no difference（ P 〉 0.05）. Only at 4h, the concentration of serum IL-10was significantly higher than the group of AMI（P 〈0.01）. The expression of IL-8 mRNA was significantly lower than that of AMI at 2h,6h. （P 〈0.05）, the expression of IL-10 mRNA showed no difference （ P 〉 0.05）. Conclusion RIP can decrease the myocardiurn area and inflammatory response goes smoothly. All of those suggest RIP protects AMI.

关 键 词：缺血预处理 急性心肌梗死 白介素-10 白介素-8 大鼠 

分 类 号：R543.31[医药卫生—心血管疾病]