摘要
目的探讨失血性休克再灌注心脏损伤变化及左旋精氨酸的保护作用。方法健康SD大鼠30只,随机均分成正常对照组(NC组)、失血性休克再灌注组(HS组)和左旋精氨酸治疗组(L-Arg组)。实验结束时,取血进行心功能检测,并测定超氧化物歧化酶(SOD)和黄嘌呤氧化酶(XOD)活性。结果与NC组相比较,HS组和L-Arg组血浆CK含量均明显升高,HS组心脏组织SOD活性显著下降,XO活性明显增高,而L-Arg组心脏组织的SOD活性无显著下降,XO活性亦无显著升高;L-Arg组血浆CK含量和XO活性明显低于HS组,而SOD活性明显高于HS组。结论大鼠失血性休克复苏后,心功能下降,氧自由基参与心脏的损伤过程,L-Arg通过抑制氧自由基的产生,减轻脂质过氧化反应发挥对心脏的保护作用。
Objective To observe the protective effect of L - arginine on heart resuscitation injury after hemorrhagic shock in rats and explore the mechanism of injury in hemorrhagic shock resuscitation rats. Methods 30 SD rats were randomly divided into 3 group： normal control （NC） group （n = 10）, hemorrhagic shock resuscitation （HS） group （n = 10） and L - arginine （L - Arg） group （n = 10）. The CK content in plasm and the SOD, XO in heart tissue were detected. Results In HS group and L - Arg group, plasm CK content increased remarkably compared to NC group; In HS group, the SOD activity in heart tissue reduced and XO activity increased remarkably compared with the NC group.However, in L - Arg group, the SOD activity in heart tissue has not reduced and XO activity increased with frace compared with the NC group. In L - Arg group, plasm CK content and XO activity were markedly lower than those in HS group, while SOD and activity were significandy higher than that in HS group. Conclusion： The heart function decreases after resuscitation in hemorrhagic shock of rats; the oxygen free radicals can cause heart injury; L - Arginine has protective effects on HS heart injury because of blocking the generation of OFR, elevating the ability of antioxidization and its anti - lipid peroxidation reaction.
出处
《医学研究通讯》
2005年第11期34-35,共2页
Bulletin of Medical Research
