Park W K, Lynch C, Johns R A
Department of Anesthesiology, University of Virginia Health Sciences Center, Charlottesville 22908.
Anesthesiology. 1992 Nov;77(5):956-63. doi: 10.1097/00000542-199211000-00019.
This study was performed to determine if direct arterial dilating actions of propofol contribute to the drug's hypotensive actions. The effects of propofol were compared with those of thiopental on isolated vascular ring preparations from rat thoracic aorta and pulmonary artery. Thoracic aortic ring responses were evaluated in the presence and absence of endothelium, indomethacin, and N omega-nitro-L-arginine methyl ester (LNAME; a specific inhibitor of endothelium-derived relaxing factor-nitric oxide [EDRF/NO] synthase). Pulmonary artery responses were investigated with intact endothelium. After the induction of active isometric force by a predetermined EC50 dose of phenylephrine for each ring, effects of propofol (30, 100, 300 microM) and thiopental (10, 30, 100 microM) were examined. Propofol caused significant vasodilation in endothelium-intact, endothelium-denuded, and LNAME-treated aortic rings. In the endothelium-intact aortic and pulmonary artery rings, the initial vasodilation due to 30 and 100 microM propofol showed gradual and partial recovery over 15 min; 300 microM propofol caused sustained vasodilation. Endothelium-denuded rings and LNAME-pretreated endothelium-intact rings showed constant and sustained vasodilation with all propofol concentrations. Propofol also caused marked vasodilation in pulmonary arteries. In contrast, thiopental had no vasodilating effect in aortic or pulmonary artery preparations. In control experiments, propofol vehicle (Intralipid) also had no effect on vascular rings. Indomethacin pretreatment induced a dose-dependent vasoconstriction by thiopental in endothelium-intact rings and decreased the vasodilation due to propofol.(ABSTRACT TRUNCATED AT 250 WORDS)
本研究旨在确定丙泊酚的直接动脉扩张作用是否对该药物的降压作用有影响。将丙泊酚的作用与硫喷妥钠对大鼠胸主动脉和肺动脉的离体血管环标本的作用进行比较。在有或无内皮、吲哚美辛和N-ω-硝基-L-精氨酸甲酯（LNAME；内皮源性舒张因子-一氧化氮[EDRF/NO]合酶的特异性抑制剂）的情况下评估胸主动脉环反应。对完整内皮的肺动脉反应进行研究。在用苯肾上腺素的预定半数有效浓度（EC50）剂量对每个环诱导产生主动等长力后，检测丙泊酚（30、100、300微摩尔）和硫喷妥钠（10、30、100微摩尔）的作用。丙泊酚在有内皮、去内皮和经LNAME处理的主动脉环中均引起显著血管舒张。在有内皮的主动脉和肺动脉环中，30和100微摩尔丙泊酚引起的初始血管舒张在15分钟内逐渐部分恢复；300微摩尔丙泊酚引起持续血管舒张。去内皮环和经LNAME预处理的有内皮环在所有丙泊酚浓度下均表现出持续稳定的血管舒张。丙泊酚在肺动脉中也引起明显血管舒张。相比之下，硫喷妥钠在主动脉或肺动脉标本中无血管舒张作用。在对照实验中，丙泊酚溶媒（脂肪乳剂）对血管环也无作用。吲哚美辛预处理在内皮完整的环中诱导硫喷妥钠产生剂量依赖性血管收缩，并降低丙泊酚引起的血管舒张。（摘要截短于250字）
