静脉和侧脑室注射内吗啡肽-1对大鼠血清一氧化氮含量和一氧化氮合酶活性的影响

Effects of intravenous and intracerebroventricular injections of endomorphin-1 on serum nitric oxide content and nitric oxide synthase activity of rats

目的:观察大鼠静脉和侧脑室注射内吗啡肽-1(EM-1)降低动脉血压中血清一氧化氮(NO)含量和一氧化氮合酶(NOS)活性的变化及其作用。方法:Wistar大鼠20只,随机分为外周静脉给药组14只和侧脑室给药组6只。静脉和侧脑室注射EM-1及其阻断剂Cyprodime,静脉注射NOS抑制剂L-NNA,分别测定大鼠动脉血压、血清NO含量和NOS活性的变化。结果:大鼠静脉注射EM-1后动脉血压降低及血清NO含量和NOS活性升高(P<0.01和P<0.01),可被Cyprodime和L-NNA阻断;侧脑室注射EM-1后动脉血压降低,血清NO含量和NOS活性均无明显变化(P>0.05)。结论:静脉注射EM-1可能通过μ阿片受体激活血管内皮NOS,促进NO释放降低动脉血压。侧脑室注射EM-1可能通过中枢μ阿片受体降低动脉血压,与NO无关。

Objective ： To observe the effects of intravenous and intracerebroventricular injections of endomorphin-1 （ EM-1 ） on serum nitric oxide（NO） content and nitric oxide synthase （NOS） activity of rats. Methods：Twenty Wistar rats were randomly divided into two groups ：intravenous injection group（ n = 14）and intracerebroventricular injection group（ n = 6 ）. The right femoralartery was cannulated with polyethylene tubing to record arterial pressure. Variations of arterial pressure, NO content and NOS activity were observed after intravenous or intracerebroventricular injection of EM-1 in rats. The effects of intravenous injection of various blockers cyprodime, N-ω- nitrolarg/nine,on the varitation MAP, NO content and NOS activity caused by EM-1 were observed. Results： Intravenous injection of EM-1 produce depressor on mean arterial pressure （ P 〈 0.01 ） in anesthetized rats. NO content and NOS activity in serum were much higher than those in control group（ P 〈 0.01 ）. While intravenous injection L-NNA and cyprodime could partially antagonize the effects; intracerebroventricular injection of EM-1 produced depressor on mean arterial pressure（ P 〈 0.01 ） in anesthetized rats. NO content and NOS activity in serum were no more than those in control group （ P 〉 0.05 ）. Conclusions ： Intravenous injection of EM-1 produces depressor on mean arterial pressure may be most associated with the release of nitric oxide from vascular endothelium. While intracerebroventricular injection of EM-1 produces depressor on MAP may be most associated with central opioid receptor.