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目的 用合成的硝基精氨酸 赖氨酸三肽 (以下简称新化合物 )在大鼠感染性休克模型上检测其对血压的影响 ,并对其作用机制作一探讨。方法 :1.盲肠结扎穿孔法 (CLP)建立大鼠感染性休克模型 ,检测新化合物对血压、血清一氧化氮 (NO)的影响。 2 .大鼠腹腔巨噬细胞培养 ,检测新化合物对诱导型一氧化氮合酶 (iNOS)的抑制程度。 3 .大鼠离体主动脉条孵育 ,检测新化合物对结构型一氧化氮合酶 (cNOS)的抑制程度。结果 :1.新化合物 ( 0 0 1mmol/kg)明显升高感染性休克大鼠血压至接近假手术组水平 ;注射新化合物、NG- 硝基 左旋精氨酸(L NNA)可使大鼠血清NO水平下降 ,新化合物较L NNA作用更明显。 2 .新化合物 ( 10 4mol/L)可显著抑制大鼠腹腔巨噬细胞产生NO (P <0 0 1) ,较L NNA作用增强 (P <0 0 1)。 3 .与L NNA相比 ,新化合物 ( 1 5× 10 4mol/L)对大鼠主动脉壁cNOS的抑制程度减小 (P <0 0 5)。结论 :硝基精氨酸 赖氨酸三肽对感染性休克大鼠血压有优越的升高作用 ,其机制在于选择性地抑制iN OS
OBJECTIVE: To investigate the effect of nitric arginine lysine tripeptide (hereinafter referred to as new compound) on the blood pressure in septic shock model of rats and its mechanism of action. The model of septic shock was established by cecal ligation and puncture (CLP), and the effects of new compounds on blood pressure and serum nitric oxide (NO) were detected. The rat peritoneal macrophages were cultured to detect the inhibitory effect of new compounds on inducible nitric oxide synthase (iNOS). The rat aortic strips were incubated to detect the inhibitory effect of the new compounds on structural nitric oxide synthase (cNOS). The new compound (0 0 1mmol / kg) significantly increased the blood pressure in septic shock rats close to the level of the sham-operated group; injection of a new compound, NG-nitro-L-arginine NO level decreased, the new compound L LNA effect more obvious. The new compound (10 4mol / L) can significantly inhibit the NO production in rat peritoneal macrophages (P <0.01), and enhance the effect of LNA (P <0.01). Compared with LNA, the inhibitory effect of the new compound (15 × 10 4 mol / L) on the cNOS in rat aortic wall decreased (P <0.05). CONCLUSIONS: The nitro-arginine lysine tripeptide has an excellent effect on increasing blood pressure in septic shock rats by selectively inhibiting iNOS