论文部分内容阅读
本研究动态观察了20只失血性休克家兔(非保护组和川芎嗪保护组)血浆、组织超氧化物歧化酶(SOD)活性及丙二醛(MDA)含量的变化。结果发现,休克时,两组血浆SOD活性均明显下降(均P<0.01),MDA含量均显著增高(均P<0.01);休克再灌注时,非保护组血浆SOD继续下降(P<0.01),MDA持续上升(P<0.01),而川芎嗪保护组血浆SOD明显回升,至再灌注3h时恢复至休克前水平,MDA显著回降,至再灌注3h时仍未恢复(P<0.05),况且两组差异非常显著(P<0.05和P<0.01)。另外,川芎嗪保护组心、肝、肾、肠组织SOD活性(503±108U/mg pro、603±84U/mg pro、638±124U/mg pro、643±133U/mg pro)明显高于非保护组(P<0.05,424±86
This study dynamically observed the plasma and tissue superoxide dismutase (SOD) activity and malondialdehyde (MDA) content in 20 hemorrhagic shock rabbits (non-protective group and ligustrazine-protected group). The results showed that the plasma SOD activity in the two groups were significantly decreased (all P <0.01) and the content of MDA was significantly increased in both groups (all P <0.01) (P <0.01), and the plasma SOD in the ligustrazine-protected group increased significantly, returned to pre-shock level at 3h after reperfusion, MDA decreased significantly, but not recovered at 3h after reperfusion (P <0.05) Moreover, the differences between the two groups were significant (P <0.05 and P <0.01). In addition, the activity of SOD in heart, liver, kidney and intestine of ligustrazine-protected group was significantly higher than that of non-protected group (503 ± 108U / mg pro, 603 ± 84U / mg pro, 638 ± 124U / mg pro, 643 ± 133U / mg pro) Group (P <0.05, 424 ± 86