Kamitani K, Yamazaki M, Yukitaka M, Ito Y, Momose Y
Department of Anaesthesiology, Faculty of Medicine, Toyama Medical and Pharmaceutical University, Japan.
Br J Anaesth. 1995 Oct;75(4):457-61. doi: 10.1093/bja/75.4.457.
We have investigated the effect of propofol on isolated rabbit mesenteric arteries and veins. Isometric tension was measured in rings of arteries (with or without endothelium) or veins in organ chambers. The preparation was stimulated with noradrenaline 10(-6) mol litre-1, K+ 50 mmol litre-1 and caffeine 20 mmol litre-1 in the presence or absence of propofol. Propofol potentiated noradrenaline-induced contractions at lower concentrations (3 x 10(-5) mol litre-1) and attenuated them at greater concentrations (10(-4) and 3 x 10(-4) mol litre-1) in arteries with endothelium. Propofol inhibited noradrenaline-induced contractions in arteries without endothelium. In contrast, propofol produced venodilatation in a concentration-dependent manner (10(-5) to 3 x 10(-4) mol litre-1) of significantly greater magnitude than that in arteries. Propofol inhibited K+-induced contraction of both arteries and veins. It decreased the relaxation induced by acetylcholine (3 x 10(-8), 10(-7) and 3 x 10(-7) mol litre-1) of noradrenaline-induced contractions of arteries. Propofol did not affect caffeine-induced contractions after pretreatment with increased Ca2+. We conclude that propofol has a more potent vasodilator effect on veins than on arteries. Vasoconstriction induced by propofol may be associated with inhibition of endothelium-derived relaxing factor, whereas vasodilatation induced by propofol may be associated with block of voltage-gated influxes of extracellular Ca2+.
我们研究了丙泊酚对离体兔肠系膜动脉和静脉的作用。在器官浴槽中，测量动脉环（有或无内皮）或静脉环的等长张力。在有或无丙泊酚存在的情况下，用10⁻⁶摩尔/升去甲肾上腺素、50毫摩尔/升钾离子和20毫摩尔/升咖啡因刺激标本。在有内皮的动脉中，丙泊酚在较低浓度（3×10⁻⁵摩尔/升）时增强去甲肾上腺素诱导的收缩，而在较高浓度（10⁻⁴和3×10⁻⁴摩尔/升）时减弱这种收缩。丙泊酚抑制无内皮动脉中去甲肾上腺素诱导的收缩。相反，丙泊酚以浓度依赖性方式（10⁻⁵至3×10⁻⁴摩尔/升）产生静脉扩张，其程度明显大于动脉。丙泊酚抑制动脉和静脉中钾离子诱导的收缩。它减弱了乙酰胆碱（3×10⁻⁸、10⁻⁷和3×10⁻⁷摩尔/升）对去甲肾上腺素诱导的动脉收缩的舒张作用。在用增加的钙离子预处理后，丙泊酚不影响咖啡因诱导的收缩。我们得出结论，丙泊酚对静脉的血管舒张作用比对动脉更强。丙泊酚诱导的血管收缩可能与内皮源性舒张因子的抑制有关，而丙泊酚诱导的血管舒张可能与电压门控性细胞外钙离子内流的阻断有关。
