肝血流阻断后硝普钠对胰腺组织SOD活性及MDA含量的影响

Effects of sodium nitroprusside on pancreatic SOD and MDA after hepatic vascular occlusion

目的 观察家兔肝血流阻断后硝普钠对胰腺组织自由基和脂质过氧化反应的影响。方法 门静脉高压模型家兔 2 4只 (部分门静脉结扎法 ) ,随机分为对照组 (Control,C组 )、硝普钠组 (SNP ,S组 )、左旋硝基精氨酸甲酯组 (L -NAME ,L组 ) ,每组 8只 ,戊巴比妥钠静脉麻醉下行气管切开后 ,股动脉切开插管监测血压。行肝门阻断(包括门静脉、肝固有动脉和胆总管 ) 60min后恢复肝血流 ,L组和S组于肝门阻断前 10min分别静脉注射L -NAME(10mg·kg- 1 )和SNP(5 .0 μg·kg- 1 ·min- 1 ,直到肝血流开放后 5min ,共持续 75min) ,C组不给任何药物 ;于肝血流恢复 60min后测量各组胰腺组织超氧化物歧化酶 (SOD)活性及丙二醛 (MDA)含量。结果 与C组相比 ,S组胰腺组织SOD明显升高 ,MDA含量明显减少 (P <0 .0 5 ) ;在L组 ,SOD活性明显降低 (P <0 .0 5 ) ,MDA含量显著增多 (P <0 .0 5 )。L组与S组相比 ,SOD活性显著降低 ,MDA含量显著增多 (P <0 .0 1)。结论 肝血流阻断后 ,SNP作为一氧化氮 (NO)供体 ,可以增加缺血胰腺SOD活性 ,减少MDA产生 ,对胰腺有保护作用。

Objective To investigate the effects of sodium nitroprusside on the activity of superoxide dismutase (SOD) and the level of malondialdehyde (MDA) in pancreatic tissues after hepatic vascular occlusion in the rabbits with portal hypertension.?Methods Twenty-four rabbits of portal hypertension model (produced by partial ligature of the portal vein, weighing 2.0 to 2.5 kg) were randomly divided into control group (C), sodium nitroprusside group (SNP,S) and N-nitro-L-arginine methyl ester group (L-NAME, L) ( n =8 each). Intravenous anesthesia with pentobarbital, tracheal intubation and monitoring of blood pressure were made as routine. The hepatic portal (including the portal vein, proper hepatic artery and choledochus) was occluded for 60 min. Ten min before the occlusion, L-NAME (10 mg·kg -1 ) was given to each rabbits in group L, SNP ( 5.0 μg·kg -1 ·min -1 ,continued for 75 min) in group S, and 0.9% saline in group C. The values of SOD and MDA in pancreatic tissue were measured after the liver was reperfused for 60 min.?Results Compared with those in group C, the pancreatic levels of SOD activity and MDA in group S were increased and decreased respectively ( P <0.05). In group L, the level of SOD activity was decreased and the level of MDA was increased ( P <0.05), with the level of SOD activity being lower and the level of MDA being higher than that in in group S ( P <0.01).?Conclusion During hepatic vascular occlusion, SNP, as a NO donor, increases the SOD activity, decreases the MDA production in the ischemic pancreas, and hence protects it.