摘要
目的探讨含血Plegisol液微流量持续灌注对热缺血猪心的心肌保护作用及其机制。方法12个离体猪心,随机分为实验组(n=6,热缺血10min,4℃含血微流量连续灌注8h,移植期间温血连续灌注)和对照组(n=6,热缺血10rain,4℃Plegisol液单纯浸泡8h),进行原位心脏移植。所有猪心恢复跳动再灌注24h后观察各组心肌组织的病理变化;分别测定心肌组织中超氧化物歧化酶(SOD)活性、丙二醇(MDA)含量及B细胞淋巴瘤/白血病-2(bcl-2)和半胱氨酰天冬氨酸特异性蛋白酶(Caspase)-3的蛋白表达。结果实验组和对照组比较,病理检查显示对照组冠状动脉内皮及心肌组织损伤较实验组重。与对照组比较,实验组心肌组织SOD活性[(7.88±0.41)u/(nlg·蛋白)]显著增高(P〈0.05),MDA含量[(9.97±1.05)nmol/(mg·蛋白)]显著降低(P〈0.05);实验组心肌组织中bcl-2mRNA和蛋白的表达(0.651±0.052,0.506±0.048)水平较对照组(0.337±0.026,0.271±0.022)显著增多(P〈0.01);而实验组Caspase-3mRNA和蛋白的表达水平(0.343±0.027,0.215±0.019)较对照组(0.782±0.059、0.629±0.054)显著下降(P〈0.01)。结论含血Plegisol液微流量持续灌注保护热缺血猪心的机制可能与减轻离体猪心的冠状动脉内皮及心肌水肿程度、减轻再灌注的氧化损伤及抑制心肌细胞的凋亡作用有关。
Objective To study the myocardial protective effect of micro-flow perfusion with blood Plegisol solution on warm ischemic pig heart and the mechanism. Methods Twelve isolated pig hearts were subjected to orthotopic heart transplantation and randomly divided into experimental group ( n = 6, warm is- chemia for 10 rain, 4~C blood the micro-flow continuous infusion for 8 h, and warm-blooded continuous perfusion during transplantation) and control group (n = 6, wark ischemia for 10 rain, and immersion with 4℃ Plegisol liquid alone for 8 h). The pathological changes of myocardial tissue in all pig hearts after reperfusion were observed. The superoxide dismutase (SOD) activity and malondialdehyde (MDA) content in myocardial tissue were measured by xanthine oxidase and thiobarbituric acid method. Immunohistochem- istry was used to detect B lymphoeytes/leukemia-2 (bel-2) and Caspase-3 protein expression. Results In control group, coronary endothelial and myocardial tissue injury was more serious than in experimental group. As compared with control group, myocardial tissue SOD activity [ (7. 88 -± 0. 41 ) U/( mg. pro- rein) ] was significantly increased, and MDA content [ (9. 97 ± 1.05 ) nmol/(mg.protein) ] was signifi- cantly reduced in experimental group ( P 〈 0. 05 ). The expression levels of bel-2 mRNA and protein in ex- perimental group (0. 651 ±0. 052 and 0. 506 ±0. 048) were significantly increased as compared with con- trol group (0. 337 ±0. 026 and 0. 271 ±0. 022) , and those of Caspase-3 mRNA and protein in experimen- tal group (0. 343 ± 0. 027 and 0. 215± 0. 019 ) were significantly decreased as compared with control group [ (0. 782 ±0. 059 and 0. 629 ±0. 054) ,P 〈0. 011. Conclusion The mechanism by which micro-flow per- fusion with blood Plegisol solution protects warm ischemic pig heart may be related to the alleviation of the isolated pig heart coronary endothelial and myocardial edema, reduction of the reperfusion oxidative damage and the inhibition of cardiac apoptosis.
出处
《中华实验外科杂志》
CAS
CSCD
北大核心
2013年第7期1490-1492,共3页
Chinese Journal of Experimental Surgery
基金
河南省科技创新人才计划资助项目(104200510007)
关键词
微流量持续灌注
热缺血
心肌保护
Micro-flow infusion
Warm ischemic
Myocardial protective