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作 者:潘景业[1] 孙英刚[2] 李长[1] 全世超[1] 金可可[1] 张艳杰[1] 陈洁[1]
机构地区:[1]温州医学院附属第一医院,325000 [2]济南军区总医院,250031
出 处:《医学研究通讯》2005年第12期9-10,共2页Bulletin of Medical Research
摘 要: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 observe the protective effect of L-arginine on heart after resuscitation injury for hemorrhagic shock in rats and explore the mechanism of injury in hemorrhagic shock resuscitation rats. Methods 30 SD rats were randomly divided into 3 groups: normal control (NC) group (n = 10), hemorrhagic shock resuscitation (HS) group (n = 10) and L-arginine (L-Arg) group (n = 10). The SOD, GSH-PX and XO activity in heart tissue were detected.Results In HS group, the SOD and GSH - PX activity in heart tissue were reduced and XO activity increased remarkably compared with that in NC group. However, in L-Arg group, the SOD and GSH - PX activity in heart tissue didn't reduce clearly and XO activity didn't inerease remarkably compared with that in NC group. In L - Arg group, the XO activity was markedly lower than that in HS group, while SOD and GSH - PX activity were significantly 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 effect on HS heart injury because of blocking the generation of OFR, elevating the ability of antioxidization and its anti - lipid peroxidation reaction.
分 类 号:R541[医药卫生—心血管疾病] R605.971[医药卫生—内科学]
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