异丙酚舒张离体大鼠肺内动脉的作用及机制

Relaxation of isolated rat intrapulmonary arteries induced by propofol

目的:观察异丙酚对预收缩离体大鼠肺内动脉张力的影响及其作用机制。方法:分离SD雄性大鼠肺内动脉,制备血管条,采用微血管张力测定技术,分别测定异丙酚对离体血管高钾(60 mmol/L KCl)和血栓素A2的类似物U46619(100 nmmol/L)诱导收缩反应的张力影响。结果:异丙酚可以明显舒张高钾预收缩的血管环,呈浓度依赖性(EC50=41.50μmmol/L);异丙酚也可以浓度依赖性地舒张U46619预收缩的血管环(EC50=63.38μmmol/L),无明显内皮依赖性;不同浓度异丙酚(10、30、100和300μmmol/L)孵育后,钙离子反应曲线明显右移;在L-型钙通道拮抗剂硝苯地平(nifedipine,1μmmol/L)存在的条件下,异丙酚仍可以舒张U46619预收缩的血管(EC50=89.03μmmol/L)。结论:异丙酚可舒张高钾及U46619预收缩的肺内动脉,且不依赖于内皮,其部分机制可能与抑制电压门控性钙内流与受体操纵钙内流有关。

AIM： To observe the relaxation effect of propofol on isolated rat intrapulmonary arterial rings precontracted by different constrictors.METHODS： Intrapulmonary arterial rings were prepared from male Sprague-Dawley rats and were mounted in a Multi Myograph system.The effects of propofol were tested on the rings precontracted with both receptor-independent（high K＋-containing solution,60 mmol/L） and receptor-dependent（U46619,100 nmol/L） constrictors.RESULTS： Propofol induced dose-dependent relaxation of the arterial rings precontracted by high K＋-containing solution（EC50=41.50 μmmol/L）.Propofol also induced relaxation of the rings precontracted by U46619 in an endothelium-independent way.Propofol at a concentrations of 10,30,100 or 300 μmol/L significantly inhibited the Ca2＋-induced contractions of pulmonary arterial rings exposed to high K＋-containing and Ca2＋-free solution in a dose-dependent manner.Nifedipine at a concentration of 1 μmol/L inhibited L-type Ca2＋ channel after vessel contraction was induced by high K＋-containing solution.Accumulative addition of propofol still relaxed the vessels re-contracted by U46619.CONCLUSION： Propofol relaxes high K＋-containing solution-and U46619-precontracted vessels in an endothelium-independent way.The possible mechanism may be partially involved in the inhibition of calcium influx through voltage-operated calcium channel and receptor-operated calcium channel.