Interplay between nitric oxide and VIP in CCK-8-induced phasic contractile activity in the rabbit sphincter of Oddi

AIM: The sphincter of Oddi (SO) plays an important role in delivery of bile into the duodenum. To establish whether vasoactive intestinal polypeptide (VIP) and nitric oxide (NO) were involved in phasic contractile activity of the rabbit SO stimulated by cholecystokinin-octapeptide (CCK-8). METHODS: Isolated SO muscle rings were cleaned of fat and mounted horizontally on two small L-shaped hooks one of which was connected to a force transducer for the measurement of isometric tension.The experiments were carried out in a thermostatically controlled (37±0.2℃) organ bath (5 mL) containing Krebs solution.The organ fluid was gassed with 95% O2 and 50 mL/L CO2 to keep the pH at 7.40±0.05. Contractile responses to CCK-8 (1 μmol/L) were evaluated in the presence and absence of NG-nitro-L-arginine (LNNA), an inhibitor of NO synthase (100 μmol/L), and (p-chloro-D-Phe6-Leu17)-VIP (VlPa, 30 μmol/L), a VIP receptor antagonist. RESULTS: CCK-8 stimulated the phasic activity of the SO. NO synthase inhibition increased the frequency and amplitude of contractions with a slight increase in developed tension. Pre-incubation with VlPa also attenuated this CCK-8 effect. The combined application of LNNA and VlPa abolished the phasic activity of the muscle rings with a marked increase in tension in response to CCK-8. CONCLUSION: VIP and NO together contribute to an increase in phasic activity of SO.

附子合用螺内酯对NOS抑制型高血压模型小鼠的影响

目的:观察附子合用螺内酯对一氧化氮合酶(NOS)抑制型高血压模型小鼠的影响。方法:雄性ICR小鼠随机分为五组,即正常对照组、L-NNA模型组、L-NNA+附子组、L-NNA+螺内酯组、L-NNA+附子+螺内酯组。采用持续7d灌胃给予L-NNA 700mg/(kg.d)方法建立小鼠高血压模型。各组持续7d分别给予1%羧甲基纤维素钠(CMC-Na)溶液,L-NNA,L-NNA+附子水煎液4g/(kg.d),L-NNA+螺内酯36mg/(kg.d),L-NNA+附子水煎液4g/(kg.d)+螺内酯36mg/(kg.d)。测定各组小鼠给药7d后的血压,血清中NO含量,心、肝、肾匀浆中NO和MDA的含量。结果:与对照组比较,模型组小鼠死亡率明显升高,给予附子、螺内酯及二者合用后,死亡率明显降低;与对照组相比,模型组小鼠血压明显升高(P<0.01),血清和心、肝、肾组织中NO含量降低(P<0.01),MDA含量升高(P<0.01),各治疗组小鼠血压明显降低(P<0.01),血清和心、肝、肾组织中NO含量明显升高(P<0.01),MDA含量显著降低(P<0.01)。结论:附子、螺内酯均能升高NOS抑制型高血压模型小鼠体内NO含量,降低MDA含量,起到降压和保护组织免受氧化损伤的作用,且二者合用有明显的协同作用。

施万细胞和一氧化氮合酶抑制剂对大鼠脊髓损伤后背核神经元存活及其轴突再生的影响

目的 探讨施万细胞 (SCs)和一氧化氮合酶 (NOS)抑制剂L NNA联合应用能否促进脊髓损伤后背核神经元存活及其轴突再生。 方法 2 0只成年大鼠分为对照组、SCs组、L NNA组和SCs +L NNA组。在SCs +L NNA组动物T1 1脊髓段半横断后在损伤处植入施万细胞 ,术后腹腔内注射L NNA。 结果 脊髓半横断后 30d ,对照组L1脊髓段损伤侧背核神经元数量减少 ,其胞体皱缩 ,NOS表达阳性。SCs组存活的神经元增加的同时其NOS表达增强 ,胞体也发生皱缩。L NNA组和SCs+L NNA组存活的神经元也增加 ,但NOS表达降低 ,其胞体皱缩得到改善。各组中仅在SCs+L NNA组L1脊髓损伤侧背核观察到有被FG标记的神经元胞体 ,提示其再生轴突穿越损伤区到达头端脊髓组织。 结论 SCs和L NNA都可促进脊髓半横断背核受损伤神经元的存活 ;两者联合应用能更好地促进受损伤背核神经元存活及其轴突再生。