一氧化氮在失血性休克再灌注损伤中的作用及牛磺酸的影响

目的:探讨一氧化氮(NO)在失血性休克再灌注损伤中的作用及牛磺酸的影响。方法:新西兰种兔24只随机分为3组(n=8):对照组、休克组、牛磺酸治疗组。采用失血性休克-再灌注损伤模型。连续观察休克前、休克1.5h、再灌注1h、2h、3h时血浆一氧化氮合酶(NOS)活性、一氧化氮代谢产物(NO^-₂／NO^-₃)含量、超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量、乳酸脱氢酶(LDH)活性的动态变化。结果:①休克组再灌注各时限血浆NOS活性、NO^-₂／NO^-₃含量、MDA含量、LDH活性显著高于休克前及休克1.5h;SOD活性显著低于休克前及休克1.5h。②休克组再灌注3h时心、肺组织NOS活性、NO^-₂／NO^-₃含量、MDA含量显著高于对照组;SOD活性显著低于对照组。③牛磺酸(40mg·kg^-1, iv)可减轻再灌注各时限上述指标的变化。④血浆、心肺组织中NO^-₂／NO^-₃含量与MDA含量均呈正相关。结论:NO介导了休克再灌注损伤, 大量释放的NO参与休克再灌注损伤的脂质过氧化反应, 牛磺酸的拮抗作用可能与减少NO的生成、抗脂质过氧化有关。

Role of nitric oxide in hemorrhagic shock/reperfusion and the effect of taurine

AIM:To investigate the effect of nitric oxide (NO) and taurin on hemorrhagic shock/reperfusion injury.METHODS:Twenty-four rabbits were divided randomly into 3 groups (n=8): control group and shock group and taurine group. The model of hemorrhagic shock/reperfusion was used. The activities of nitric oxide synthase (NOS), superoxide dismutase(SOD), lactate dehydrogenase(LDH)and the contents of malondialdehyde(MDA), nitric oxide pvoducts( NO^-₂／NO^-₃) in plasma were observed before shock and shock 1.5 h, reperfusion 1 h , 2 h and reperfusion 3 h. RESULTS:①During shock/reperfusion, the activities of NOS, LDH and the contents of MDA, NO^-₂／NO^-₃ were significantly higher, but the activity of SOD was significantly lower in plasma of shock group than that of before shock and shock 1.5 h. ②At 3 h reperfusion, the activity of NOS and the contents of MDA, NO^-₂／NO^-₃ were significantly higher, but the activity of SOD was significantly lower in the lung and heart of shock group than that of control group. ③ Taurine(40 mg·kg^-1, iv) attenuated all the changes above mentioned at total time points of reperfusion. ④ A close correlation was shown between MDA content and NO^-₂／NO^-₃ content in plasma, lung and in heart. CONCLUSION:These results suggeste that NO may be involved in oxidant-mediated shock/reperfusion, antagonistic effect of taurine on hemorrhagic shock/reperfusion injury may be related to decreasing the generation of NO and anti-lipoperoxidation.