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

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

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2 4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 (4 0mg·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。

AIM: To investigate the effect of nitric oxid e (NO) and taurin on hemorrhagic shock /reperfusion injury. METHODS: Twenty-four rabbit s 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 ni tric 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,reper fusion 1 h ,2 h and reperfusion 3 h. RESULTS: ①During shock/reperfusion, the ac tivities of NOS,LDH and the contents of MDA,NO - 2/NO - 3 were significan tly highe r, 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,bu t the act ivity of SOD was significantly lower in the lung and heart of shock group than t hat of control group. ③ Taurine(40 mg·kg -1 ,iv) attenuated all the c hanges 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 i n heart. CONCLUSION: These results suggeste that NO may be involved in oxida nt-mediated shock/reperfusion, antagonistic effect of taurine on hemorrhagic shock/reperfusi on injury may be relate d to decreasing the generation of NO and anti-lipoperoxidation.