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作 者:张光燕[1,2] 邓春玉[3] 邝素娟[2] 马珏[2] 崔建修[2]
机构地区:[1]南方医科大学,广东广州510515 [2]广东省医学科学院广东省人民医院麻醉科,广东广州510080 [3]广东省医学科学院广东省人民医院医学研究中心,广东广州510080
出 处:《中国病理生理杂志》2011年第11期2225-2228,共4页Chinese Journal of Pathophysiology
基 金:广东省科技计划基金资助项目(No.2008B030301357);广东省自然科学基金资助项目(No.10151008004000010)
摘 要: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.
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