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目的探讨失血性休克再灌注心脏损伤氧自由基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,取心脏组织测定超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-PX)和黄嘌呤氧化酶(XO)活性。结果与 NC 组相比较,HS 组心脏组织 SOD、GSH-PX 活性显著下降,XO 活性明显增高,而 L-Arg 组心脏组织的 SOD、GSH-PX 活性无显著下降,XO 活性亦无显著升高;L-Arg 组 XO 活性明显低于 HS 组,而 SOD、GSH-PX 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,增加冠脉血流量,减轻脂质过氧化反应,有助于减轻心肌缺血再灌注损伤,从而起到保护心脏的作用。
Objective To investigate the changes of oxygen free radicals and the protective effects of L-arginine in heart injury induced by hemorrhagic shock and reperfusion. Methods Thirty healthy SD rats were randomly divided into normal control group (NC group), hemorrhagic shock reperfusion group (HS group) and L-arginine treatment group (L-Arg group). At the end of the experiment, the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-PX) and xanthine oxidase (XO) were measured in heart tissue. Results Compared with NC group, the activity of SOD and GSH-PX in heart tissue of HS group decreased significantly and the activity of XO increased obviously. However, the activity of SOD and GSH-PX in heart tissue of L-Arg group did not decrease significantly and the activity of XO did not increase significantly The activity of XO in L-Arg group was significantly lower than that in HS group, while the activity of SOD and GSH-PX was significantly higher than that in HS group. Conclusions After hemorrhagic shock resuscitation, heart function is decreased and oxygen free radicals are involved in the process of heart injury. L-Arg helps to reduce the production of oxygen free radicals, increase coronary blood flow, relieve lipid peroxidation, Myocardial ischemia-reperfusion injury, which play a role in protecting the heart.