Effects of norepinephrine on endothelium-dependent vasodilation of forearm resistance vessels.
Effects of norepinephrine on endothelium-dependent vasodilation of forearm resistance vessels.
复制标题
去甲肾上腺素对前臂阻力血管内皮依赖性血管舒张的影响。
DOI：
10.1038/clpt.1993.35
复制
发表时间：
1993
影响因子：
6.7
通讯作者：
Kubo,SH
中科院分区：
文献类型：
--
作者：
Rector,TS;Bank,AJ;DeBruyn,VH;Garr,MD;Kraemer,MD;Kubo,SH
背景：心力衰竭患者前臂阻力血管内皮依赖性扩张减弱。交感神经系统的激活可能通过血管收缩和一氧化氮的化学失活而导致这种异常。方法和结果：在12名正常人中，同时动脉内注射去甲肾上腺素(25，50和100 ng/min)对同等剂量的内皮依赖性血管扩张剂乙酰甲胆碱(0.3和1.5µg/min)和非内皮依赖性血管扩张剂硝普钠(1和5µg/min)的前臂血流反应的影响。注射去甲肾上腺素使平均血浆去甲肾上腺素水平从基线时的255pg/ml分别增加到460、629和1089pg/ml。前臂基础血流量在最高剂量时从2.9降至1.6ml/min/100ml(p<；0.01)。同时输注去甲肾上腺素(分别为4.4、4.2和4.3ml/min/100ml)对低剂量乙酰甲胆碱(4.5ml/min/100ml)的平均反应无显著影响，而对大剂量乙酰甲胆碱(8.9ml/min/100ml)的反应较低(分别为7.2、6.7和7.4ml/min/100ml)，但无统计学意义。乙酰甲胆碱引起的血管扩张对去甲肾上腺素的敏感性并不比硝普钠敏感。下体负压(−80 mm Hg)也能显著降低前臂血流量，增加血浆去甲肾上腺素水平，但对乙酰甲胆碱和硝普钠引起的血管扩张无明显影响。结论：下体负压或去甲肾上腺素引起的交感神经刺激对前臂血管内皮依赖性扩张无明显拮抗作用。这些数据表明，交感神经的激活并不能完全解释心力衰竭患者出现的内皮依赖性的异常血管扩张。《临床药理学与治疗学》(1993年)53,374-379；DOI：10.1038/clpt.1993.35
Background: Endothelium‐dependent dilation of forearm resistance vessels is attenuated in patients with heart failure. Activation of the sympathetic nervous system could cause this abnormality by way of vasoconstriction and chemical inactivation of nitric oxide.Methods and results: The effects of concurrent intra‐arterial norepinephrine infusions (25, 50 and 100 ng/min) on forearm blood flow responses to equipotent doses of an endothelium‐dependent vasodilator, methacholine (0.3 and 1.5 µg/min), and an endothelium‐independent vasodilator, nitroprusside (1 and 5 µ/min), were studied in 12 normal subjects. Norepinephrine infusions increased the mean plasma norepinephrine from 255 pg/ml at baseline to 460, 629, and 1089 pg/ml, respectively. Basal forearm blood flow was reduced from 2.9 to 1.6 ml/min/100 ml of forearm volume at the highest dose(p <0.01). The average response to the lowest dose of methacholine (4.5 ml/min/100 ml) was not significantly reduced by concurrent infusion of norepinephrine (4.4, 4.2, and 4.3 ml/min/100 ml, respectively), whereas the response to the higher dose of methacholine (8.9 ml/min/100 ml) tended to be lower (7.2, 6.7, and 7.4 ml/min/100 ml, respectively) but did not attain statistical significance. Methacholine induced vasodilation was not more sensitive to norepinephrine than nitroprusside responses. Lower body negative pressure (− 80 mm Hg) also significantly reduced baseline forearm flow and increased plasma norepinephrine but did not effect either methacholine or nitroprusside induced vasodilation.Conclusion: Sympathetic stimulation induced by infusion of norepinephrine or lower body negative pressure is not a potent antagonist to endothelium‐dependent vasodilation of the forearm vasculature. These data suggest that sympathetic activation does not completely explain the abnormal endothelium‐dependent vasodilation seen in patients with heart failure.Clinical Pharmacology and Therapeutics(1993)53,374–379; doi:10.1038/clpt.1993.35