Department of Anesthesiology and Pain Medicine, Jeju National University School of Medicine, Jeju, Korea.
Korean J Anesthesiol. 2011 Jul;61(1):55-62. doi: 10.4097/kjae.2011.61.1.55. Epub 2011 Jul 17.
The intravenous administration of indigo carmine has been reported to produce transiently increased blood pressure in patients. The goal of this in vitro study was to examine the effect of indigo carmine on phenylephrine-induced contractions in an isolated rat aorta and to determine the associated cellular mechanism with particular focus on the endothelium-derived vasodilators.
The concentration-response curves for phenylephrine were generated in the presence or absence of indigo carmine. Phenylephrine concentration-response curves were generated for the endothelium-intact rings pretreated independently with a nitric oxide synthase inhibitor, N(ω)-nitro-L-arginine methyl ester (L-NAME), a cyclooxygenase inhibitor, indomethacin, and a low-molecular-weight superoxide anion scavenger, tiron, in the presence or absence of indigo carmine. The fluorescence of oxidized dichlorofluorescein was measured in rat aortic vascular smooth muscle cells cultured in the control, indigo carmine alone and tiron plus indigo carmine.
Indigo carmine (10(-5) M) increased the phenylephrine-induced maximum contraction in the endothelium-intact rings with or without indomethacin, whereas indigo carmine produced a slight leftward shift in the phenylephrine concentration-response curves in the endothelium-denuded rings and L-NAME-pretreated endothelium-intact rings. In the endothelium-intact rings pretreated with tiron (10(-2) M), indigo carmine did not alter phenylephrine concentration-response curves significantly. Indigo carmine (10(-5) M) increased the fluorescence of oxidized dichlorofluorescein in the vascular smooth muscle cells, whereas tiron abolished the indigo carmine-induced increase in oxidized dichlorofluorescein fluorescence.
Indigo carmine increases the phenylephrine-induced contraction mainly through an endothelium-dependent mechanism involving the inactivation of nitric oxide caused by the increased production of reactive oxygen species.
静脉注射靛胭脂已被报道会使患者的血压短暂升高。本体外研究的目的是检测靛胭脂对分离大鼠主动脉中去氧肾上腺素诱导收缩的影响，并确定相关的细胞机制，特别关注内皮衍生的血管扩张剂。
在存在或不存在靛胭脂的情况下生成去氧肾上腺素的浓度-反应曲线。在存在或不存在靛胭脂的情况下，分别用一氧化氮合酶抑制剂 N(ω)-硝基-L-精氨酸甲酯 (L-NAME)、环氧化酶抑制剂吲哚美辛和低分子量超氧阴离子清除剂替罗非班预处理内皮完整的环，生成去氧肾上腺素的浓度-反应曲线。在对照、单独靛胭脂和替罗非班加靛胭脂培养的大鼠主动脉血管平滑肌细胞中测量氧化二氯荧光素的荧光。
靛胭脂（10(-5) M）增加了内皮完整环中去氧肾上腺素诱导的最大收缩，无论是否存在吲哚美辛，而靛胭脂使内皮剥脱环和 L-NAME 预处理的内皮完整环中的去氧肾上腺素浓度-反应曲线向左轻微移动。在替罗非班（10(-2) M）预处理的内皮完整环中，靛胭脂对去氧肾上腺素浓度-反应曲线没有显著影响。靛胭脂（10(-5) M）增加了血管平滑肌细胞中氧化二氯荧光素的荧光，而替罗非班则消除了靛胭脂诱导的氧化二氯荧光素荧光增加。
靛胭脂主要通过一种内皮依赖性机制增加去氧肾上腺素诱导的收缩，该机制涉及由活性氧物质增加引起的一氧化氮失活。
