摘要
目的 探讨内源性一氧化氮 (NO)对大鼠实验性急性坏死性胰腺炎的作用及其与胰腺血流的关系。方法 经胰胆管内注射 5 %牛磺胆酸钠溶液 (1ml/kg)制成Wistar大鼠急性坏死性胰腺炎模型。以L 硝基精氨酸 (L NNA)为内源性NO的阻断剂 ,观察内源性NO对胰腺损伤程度的影响 ;不同时相胰腺炎大鼠胰腺血流量的改变 ;内源性NO对损伤状态下大鼠胰腺血流量的影响。结果 经胰胆管注射牛磺胆酸钠可造成大鼠胰腺组织明显的水肿和坏死 ,部分大鼠发生胰腺实质内出血。正常大鼠的胰腺血流量为 (5 10± 84)PU ,胰腺炎大鼠在 2h即出现胰腺血流量明显下降〔(32 0± 6 5 )PU ,vs正常组P <0 0 1〕 ,4h仍处于较低水平〔(2 98± 113)PU ,vs正常组P <0 0 1〕。L NNA使胰腺坏死明显加重 ,胰腺实质内出血发生率增高 ,并使胰腺炎大鼠的胰腺血流量下降更加显著〔(183± 6 9)PU ,vs 4h胰腺炎组P <0 0 5〕。NO底物L 精氨酸能逆转L NNA的作用。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血流量有关。
Objective To investigate the effect of endogenous nitric oxide (NO) on murine acute necro tic pancreatitis and pancreatic blood flow.[WT5”HZ] Methods [WT5”BZ]Acute necrotic pancreatitis in rats was induced by retrograde injection of sodium taurocholate (5%) into the pancreatobiliary duct (1?ml/kg body weight), pancreatic blood flow [CM(43]was determined, and the effect of endogenous NO on pancreatic injury and pancreatic blood flow was evaluated after N G nitro L arginine (L NNA), an inhibitor of endogenous NO, was given.[WT5”HZ] Results [WT5”BZ] Sodium taurocholate[CM(43] administration induced severe pancreatic tissue edema and acinar necrosis, and the intrapancreatic hemorrahage occurred in some animals. The pancreatic blood flow of normal rats was 510±84 PU(Perfusion Unit). 2 hours after the induction of pancreatitis, pancreatic blood flow significantly decreased from normal level of 510±84 PU (perfusion unit) to 320±65 PU, P <0 001), lasting for at least 4 hours (298±113 PU, vs normal P <0 001). Pretreatment by NO inhibitor, L NNA(12 5mg/100g body weight), significantly worsened acinar necrosis, and caused intrapancreatic hemorrahage in increased number of rats. L NNA also resulted in a further decrease of pan[CM(43]creaticblood flow in rats suffering from pancreatitis, P <0 05. Concurrent administration ofL arginine greatly reversed all of the above effects of L NNA.[WT5”HZ] Conclusion [WT5”BZ] Endogenous NO effected pancreatic protection, and its ability to maintain the pancreatic blood flow may be involved in its protective mechanisms.
出处
《中华普通外科杂志》
CSCD
2000年第10期606-608,共3页
Chinese Journal of General Surgery
基金
北京市卫生局重点学科基金
