CAJ | 학술논문

目的探讨肢体缺血-再灌注损伤后心肌的氧化损伤机制及HO-1的保护作用,为研究肢体缺血-再灌注损伤所致的心肌损伤的预防提供实验依据.方法应用止血带构造SD大鼠双后肢IR模型,实验动物随机(随机数字法)分为正常对照组和缺血4 h再灌注2 h,4 h,6 h,8 h,16 h,24 h共7组,分别取心肌和血液标本检测MDA,SOD,MPO,心肌形态学及心肌组织中HO-1 mRNA的表达.方差分析方法进行统计学处理.结果 (1)血浆及心肌IR各组MDA均较对照组明显升高(P<0.05),且于IR 4 h达高峰.血浆及心肌IR各组SOD均较对照组明显降低(P<0.05),且血清SOD于IR4 h达最低值,心肌SOD于IR 8 h达最低值.血浆及心肌IR各组MPO均较对照组明显升高(P<0.05),且血清MPO于IR 4 h达高峰,心肌MPO于IR 6 h达高峰.(2)在肢体缺血4 h再灌注4-6 h组,心肌形态学损伤最重.(3)与对照组比较,IR2 h组HO-1 mRNA表达差异无统计学意义(P>0.05),其余各组HO-1 mRNA表达均显著上调(P<0.05)且于IR 16 h达高峰.结论心肌局部组织的自由基和中性粒细胞聚集活化是LIR心肌损伤的机制且能上调HO-1 mRNA的表达,HO-I在心肌组织的高表达能减轻心肌组织的损伤.
목적 탐토지체결혈-재관주손상후심기적양화손상궤제급HO-1적보호작용,위연구지체결혈-재관주손상소치적심기손상적예방제공실험의거.방법 응용지혈대구조SD대서쌍후지IR모형,실험동물수궤(수궤수자법)분위정상대조조화결혈4 h재관주2 h,4 h,6 h,8 h,16 h,24 h공7조,분별취심기화혈액표본검측MDA,SOD,MPO,심기형태학급심기조직중HO-1 mRNA적표체.방차분석방법진행통계학처리.결과 (1)혈장급심기IR각조MDA균교대조조명현승고(P<0.05),차우IR 4 h체고봉.혈장급심기IR각조SOD균교대조조명현강저(P<0.05),차혈청SOD우IR4 h체최저치,심기SOD우IR 8 h체최저치.혈장급심기IR각조MPO균교대조조명현승고(P<0.05),차혈청MPO우IR 4 h체고봉,심기MPO우IR 6 h체고봉.(2)재지체결혈4 h재관주4-6 h조,심기형태학손상최중.(3)여대조조비교,IR2 h조HO-1 mRNA표체차이무통계학의의(P>0.05),기여각조HO-1 mRNA표체균현저상조(P<0.05)차우IR 16 h체고봉.결론 심기국부조직적자유기화중성립세포취집활화시LIR심기손상적궤제차능상조HO-1 mRNA적표체,HO-I재심기조직적고표체능감경심기조직적손상.
Objective To study the mechanism of oxidative damage in myocardial tissue after limb ischemia reperfusion (IR), and the protective effects of heme oxygenase-1 on myocardial injury in experimental rats. Method The models of bilateral hind limbs ischemia and reperfusion in rats were established by using tourniquets applied to the roots of both hind limbs until palm blanched and pulseless for 4 hours. A total of 56 SD rats were randomly (random number) divided into 7 groups, namely one normal control group ( n = 8) and 6 ischemia-reperfusion groups as per different lengths of reperfusion time, e. g. 2 hrs, 4 hrs, 8 hrs, 16 h rs and 24 hr ( n = 8 each). The experimental rats were sacrificed after different lengths of reperfusion time. Specimens of myocardium and blood were taken for assays of malonaldehyde (MDA), superoxide dismutase (SOD) and myeloperoxidase (MPO), and pathological changes of myocardium were observed, and the expressions of HO-1 mRNA in myocardium were detected. Data were analyzed with ANOVA. Results (1) Compared with the control group, the levels of serum MDA and myocardial MDA of rats were increased in all IR groups and were higher (P < 0.05), and the levels of MDA reached the peak after reperfusion for 4 hours. The levels of serum SOD and myocardial SOD in rats of all IR groups were decreased and lower than those in rats of the control group ( P < 0.05), and the levels of serum SOD dropped away to the lowest point after reperfusion for 4 hours, and the levels of myocardial SOD fell off to the bottom after reperfusion for 8 hours. The levels of serum MPO and myocardial MPO were significantly increased in rats of all IR groups compared with the control group (P < 0.05). The levels of serum MPO reached peak after reperfusion for 4 hours, and the levels of myocardial MPO were increased to the highest spot after reperfusion for 6 hours. (2) The pathological changes in myocardium showed the most severe damage after reperfusionfor 4-6 hours.(3) After reperfusion for 2 hours, there were no significant differences in the expression of HO-1 mRNA between IR groups and control group (P >0.05), and after reperfusion for 4 hours and over, the expressions of HO-1 mRNA were markedly increased in IR groups and reached peak after reperfusion for 16 hours in comparison with the control group (P < 0.05). Conclusions The activation of neutrophils and free radicals may play a primarily adverse role in myocardial injury after limb IR, and the increase in the expression of HO-1 mRNA lessens the harm effects of IR on myocardium.