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目的观察衰老大鼠心肌对缺血再灌注损伤的敏感性,并探讨其可能的机制。方法成年和老年雄性Wistar大鼠各12只,分为4组：成年假手术组、成年缺血再灌注组、老年假手术组和老年缺血再灌注组,每组6只,进行缺血30 min再灌注3 h。脱氧核糖核苷酸末端转移酶介导的缺口末端标记(TUNEL)法检测心肌细胞凋亡,比色法检测心肌组织半胱胺酸蛋白酶蛋白-3 (caspase-3)活性,化学发光法测定心肌组织总一氧化氮(NOx)含量,ELISA法检测心肌过氧亚硝基(ONOO~-)含量。结果老年组缺血再灌注引起心肌细胞凋亡的程度明显高于成年组,凋亡指数分别为(14．6±1.7)%、(19．0±2．1)%,差异有统计学意义(P＜0．05)；caspase-3活性：成年组为(340±32)μmol/mg,老年组为(436±35)μmol/mg,差异有统计学意义(P＜0．05)；心肌组织中NOx含量：成年缺血再灌注组、老年缺血再灌注组分别为成年假手术组的(2．1±0．2)、(4．4±0．5)倍,差异有统计学意义(P＜0．05)；ONOO~-含量：成年缺血再灌注组和老年缺血再灌注组分别为(4．68±0．15)nmol/g、(7．25±0．18)nmol/g,差异有统计学意义(P＜0．05)。结论老年大鼠对心肌缺血再灌注损伤的敏感性增加,可能的原因是老年鼠心脏中NO的毒性衍生物ONOO~-含量增加,从而导致功能蛋白的硝基化。
Objective To observe the sensitivity of myocardium to ischemia-reperfusion injury in aging rats and to explore its possible mechanism. Methods Twelve adult male and female Wistar rats were divided into 4 groups: adult sham operation group, adult ischemia reperfusion group, aged sham operation group and aged reperfusion group, 6 in each group, with ischemia 30 min reperfusion 3 h. The apoptosis of cardiomyocytes was detected by TUNEL method. The activity of caspase-3 in myocardial tissue was detected by colorimetric assay. Tissue total nitric oxide (NOX) content was detected by enzyme linked immunosorbent assay (ELISA). Results The degree of myocardial cell apoptosis induced by ischemia reperfusion in aged group was significantly higher than that in adult group (14.6 ± 1.7%, 19.0 ± 2.1%, respectively), the difference was statistically significant (P <0.05). The activity of caspase-3 was (340 ± 32) μmol / mg in adult group and 436 ± 35 μmol / mg in elderly group (P <0.05) The content of NO in myocardial tissue was (2.1 ± 0.2) and (4.4 ± 0.5) times higher than that in adult sham-operated group (P <0.05). ONOO ~ - content was (4.68 ± 0.15) nmol / g, (7.25 ± 0) in the adult and reperfusion groups, respectively. 18) nmol / g, the difference was statistically significant (P <0.05). Conclusions The sensitivity of senile rats to myocardial ischemia reperfusion injury may be increased due to the increase of ONOO ~ -, which is a toxic derivative of NO in aged rat hearts, resulting in the nitration of functional proteins.