Closa D, Hotter G, Prats N, Bulbena O, Roselló-Catafau J, Fernández-Cruz L, Gelpí E
Molecular Pathology Unit, Centro de Investigación y Desarrollo, CSIC, Barcelona, Spain.
Inflammation. 1994 Oct;18(5):469-80. doi: 10.1007/BF01560694.
The role of nitric oxide in eicosanoid and oxygen-free radical production in the early stages of sodium taurocholate-induced acute necrotizing pancreatitis has been studied. Male Wistar rats were divided into three groups: group I: control group, a volume of 0.1 ml/100 g body wt saline solution was injected at low pressure in the pancreatic duct; group II: acute pancreatitis was induced by administration of 3.5% sodium taurocholate; and group III: intravenous administration of NG-nitro-L-arginine methyl esther (a nitric oxide synthase inhibitor) 5 min before induction of acute pancreatitis as stated for group II. At 5 and 60 min after induction of pancreatitis, blood and pancreas tissue samples were taken for assays. Increases in 6-keto PGF1 alpha, TXB2, PGE2, PGF2 alpha, and 12-HETE were observed in the pancreatic tissue. Lipoperoxidation was also enhanced and remained unaltered after nitric oxide inhibition. The fact that nitric oxide synthase inhibition could only reverse the increases in 6-keto PGF1 alpha and TXB2 levels indicates that in acute pancreatitis endothelial and platelet eicosanoid generation is mediated through an nitric oxide-dependent mechanism. In contrast, nitric oxide appears to be not related with oxygen free radical damage associated with acute pancreatitis.
已对一氧化氮在牛磺胆酸钠诱导的急性坏死性胰腺炎早期类花生酸和氧自由基产生中的作用进行了研究。雄性Wistar大鼠分为三组：第一组：对照组，以低压向胰管内注射0.1 ml/100 g体重的盐溶液；第二组：通过给予3.5%牛磺胆酸钠诱导急性胰腺炎；第三组：在按照第二组所述诱导急性胰腺炎前5分钟静脉注射NG-硝基-L-精氨酸甲酯（一种一氧化氮合酶抑制剂）。在诱导胰腺炎后5分钟和60分钟，采集血液和胰腺组织样本进行检测。在胰腺组织中观察到6-酮-前列腺素F1α、血栓素B2、前列腺素E2、前列腺素F2α和12-羟基二十碳四烯酸增加。脂质过氧化也增强，且在一氧化氮抑制后保持不变。一氧化氮合酶抑制只能逆转6-酮-前列腺素F1α和血栓素B2水平升高这一事实表明，在急性胰腺炎中，内皮细胞和血小板类花生酸的产生是通过一氧化氮依赖性机制介导的。相比之下，一氧化氮似乎与急性胰腺炎相关的氧自由基损伤无关。
