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目的:观察败血症休克大鼠主动脉外膜L-精氨酸(L-Arg)转运,一氧化氮合酶(NOS)活性和一氧化氮(NO)生成的变化。方法:雄性Wistar大鼠盲肠结扎并穿孔复制败血症休克模型。测定大鼠主动脉外膜亚硝酸盐(NOx)含量、一氧化氮合酶(NOS)活性及L-精氨酸(L-Arg)转运;RT-PCR方法测定诱导型一氧化氮合酶(iNOS)mRNA水平。结果:严重感染休克大鼠呈现严重的血流动力学紊乱,心功能抑制。败血症休克大鼠表现为严重的低血糖和高乳酸血症。血管外膜iNOS的mRNA水平均明显高于假手术组(均P<0.01),主动脉外膜NOx生成、NOS活性及L-Arg转运速率显著高于假手术组(P<0.01)。结论:败血症休克时血管外膜L-Arg/NOS/NO系统激活在败血症休克发病中可能起重要作用。
Objective: To observe the changes of L-arginine (L-Arg) transporter, nitric oxide synthase (NOS) activity and nitric oxide (NO) production in the aorta of septic shock rats. Methods: The cecum of male Wistar rats were ligated and punctured to replicate the septic shock model. The content of nitric oxide (NO), nitric oxide synthase (NOS) and L-arginine (L-Arg) transport in the adventitia of rat aorta were measured. The inducible nitric oxide synthase iNOS) mRNA levels. Results: Severe septic shock rats showed severe hemodynamic disorders and cardiac function. Septic shock rats showed severe hypoglycemia and hyperlactic acidosis. The mRNA level of iNOS in vascular adventitia was significantly higher than that in sham operation group (all P <0.01). The aorta NO production, NOS activity and L-Arg transport rate were significantly higher than those in sham operation group (P <0.01). Conclusion: Activation of L-Arg / NOS / NO system in septic shock may play an important role in the pathogenesis of septic shock.