摘要
目的 探讨内源性一氧化氮 (NO)对急性坏死性胰腺炎大鼠胰腺微血管通透性的影响。方法 以 5 %牛磺胆酸钠溶液胰胆管注射 ( 1ml/kg)制成大鼠急性坏死性胰腺炎模型 ,以工具药L 硝基精氨酸 (L NNA)为内源性NO的阻断剂 ,以EvansBlue的漏出代表微血管的通透性 ,观察内源性NO对胰腺组织损伤程度、胰腺内EvansBlue漏出等的影响。结果 牛磺胆酸钠胰胆管注射造成大鼠胰腺组织明显坏死和炎性细胞浸润 ,以及血清淀粉酶浓度升高、胰腺湿 /干重比率增加和明显的胰腺组织内EvansBlue积聚。以L NNA( 12 5mg/kg)阻断内源性NO后 ,胰腺组织坏死和炎性细胞浸润进一步加重 ,并使血清淀粉酶浓度升高 ,胰腺湿 /干重比率增加 ,EvansBlue的漏出率也较之单纯胰腺炎组大鼠明显增加。结论 内源性NO具有胰腺保护作用 ,其保护机制可能与维持胰腺微血管的完整性有关。
Objective To investigate the effects of endogenous nitric oxide (NO) on pancreatic microvascular permeability in rats with acute necrotizing pancreatitis (ANP). Methods ANP was induced in rats with retrograde infusion of 5% sodium taurocholate into the pancreatobiliary duct (1 ml/kg body weight). NG nitro L arginine (L NNA) was used as the inhibitor of endogenous NO and pancreatic microvascular permeability was determined by measurement of extravasation of Evans Blue to investigate the effects of endogenous NO on pancreatic injury and Evans Blue extravasation. Results Sodium taurocholate infusion induced evident pancreatic acinar necrosis and infiltration of inflammatory cells. Meanwhile, both serum amylase and pancreas wet/dry weight ration were increased and a marked accumulation of Evans Blue in pancreatic tissue was observed. Pretreatment with the NO inhibitor, L NNA (12 5 mg/kg body weight), significantly intensified acinar necrosis and infiltration of inflammatory cells and increased serum amylase, pancreas wet/dry weight ration and Evans Blue extravasation. Concurrent administration of L arginine, the substrate for NO synthesis, markedly reversed all of the above effects of L NNA. Conclusions Endogenous NO can protect the pancreas and its ability to maintain the pancreatic microvascular integrity may be involved in its protective mechanisms.
出处
《中华肝胆外科杂志》
CAS
CSCD
2001年第3期168-170,共3页
Chinese Journal of Hepatobiliary Surgery
