胃动素在重症急性胰腺炎并发内毒素血症中的作用

The effects of Motilin on severe Acute Pancreatitis with Endotoxemia

目的采用牛磺脱氧胆酸钠诱发香猪重症急性胰腺炎 (SevereAcutePancreatitis,SAP)模型 ,观察胃动素在香猪重症急性胰腺炎并发内毒素血症中的作用。方法用 8只贵州小香猪 ,雌雄不拘 ,各受试动物术前禁食 12h ,禁水 6h后 ,无菌手术行门静脉、左颈外静脉插管 ,经胰管逆行加压(80cmH2 O)推注 5 %牛磺脱氧胆酸钠 (0 5ml kg体重 )复制SAP模型。分别于制模前 ,制模后 1h、6h、12h、2 4h、4 8h、72h、96h同时采门静脉血和中心静脉血 ,分离血浆 ,检测血浆中内毒素和胃动素浓度。结果SAP诱发后 1h ,门静脉、中心静脉血浆内毒素浓度即开始同步升高至 4 8h达峰值 ,之后下降 ,但至 96h时仍处于较高水平 ,与制模前相比差异非常显著 (P <0 0 1) ;且门静脉内毒素浓度在各时间点(除制模前、制模后 1h外 )均高于中心静脉血浆内毒素浓度 (P <0 0 1)。SAP诱发后 1h ,门静脉、中心静脉血浆胃动素浓度随着时间进行性下降 ,至 96h时分别降至最低 ,且中心静脉血浆胃动素浓度在制模后 12h和 2 4h两个时间点显著低于门静脉血浆胃动素浓度 (P <0 0 1)。结论门静脉、中心静脉血浆中内毒素浓度分别与门静脉 (门 )、中心静脉 (中 )血浆中胃动素浓度呈明显的负相关 (门 :r =- 0 92 0 ,P <0 0 1;中 :r=- 0 893,P <0 0 1) ,提示胃?

Objective To investigate the effects of motilin on severe acute pancreatitis(SAP) with endotoxemia induced by sodium dexytaurocholate in miniature pigs. Methods 8 GuiZhou Miniature pigs were fasted over night and prohibited water drink for six hours , then were performed laparotomyand portal vein, vena cava paracentesis in sterile conditions. All experimental animals were injected 5% sodium deoxycholate (0.5ml/kg) into the pancreatic duct at constant pressure (80cmH 2O) for making model . Results After 1h of SAP, the concentration of plasma endotoxin in portal vein and vena cava were gradually increased, the reched peak value at 48h. As compared with pre-model, thy were higher significantly to 96h( P <0.01). The concentration of plasma endotoxin in portal vein were higher than those of vena cava at all times except pre-model and post-model. After 1h of SAP, the concentration of plasma motilin in portal vein and vena cava were progressively decreased and were the lowest at 96h. The concentration of plasma motilin in vena cava were lower significantly than those of portal vein at 12h and 24h after model( P <0.01). Conclusion The concentration of plasma endotoxin in portal vein and vena cava were negative correlation with those of plasma motilin and the diminution of motilin was correlation with enterogenous endotoxemia.