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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 experimental acute necrotizing pancreatitis in rats and its relationship with pancreatic blood flow. Methods Acute necrotic pancreatitis model of Wistar rats was made by intra-pancreatic bile duct injection of 5% sodium taurocholate solution (1ml / kg). The effect of endogenous nitric oxide (NO) on the degree of pancreatic injury was observed with L-nitroarginine (LNANA) as a blocker of endogenous NO. Changes of pancreatic blood flow in rats with different phases of pancreatitis were observed. Endogenous NO On the damage of pancreatic blood flow in rats. Results Pancreatic duct injection of sodium taurocholate can cause significant edema and necrosis of the pancreas in rats. Some rats developed intraparenchymal hemorrhage of the pancreas. The pancreas blood flow in normal rats was (5 10 ± 84) PU, pancreatic blood flow decreased significantly at 2h (32 ± 6 5) PU, P <0.01 compared with normal group, 4h Still at a lower level (2 98 ± 113) PU, vs normal group P 0 01). L NNA significantly aggravate pancreatic necrosis, increased incidence of pancreatic parenchymal hemorrhage, and pancreatic blood flow in pancreatitis decreased more significantly 〔(183 ± 6 9) PU, 4h pancreatitis group P <0 0 5〕. The NO substrate, L-arginine, reverses the effect of LNA. Conclusion Endogenous NO has pancreatic protective effect and its protective mechanism may be related to the maintenance of pancreatic blood flow.