Blankestijn P J, Man in't Veld A J, Tulen J, van den Meiracker A H, Boomsma F, Moleman P, Ritsema van Eck H J, Derkx F H, Mulder P, Lamberts S J
Department of Internal Medicine I, Erasmus University Rotterdam, The Netherlands.
Lancet. 1988 Dec 17;2(8625):1386-9. doi: 10.1016/s0140-6736(88)90585-5.
In a double blind, crossover study 6 h infusions of adrenaline (15 ng/kg/min; 1 ng = 5.458 pmol), noradrenaline (30 ng/kg/min; 1 ng = 5.911 pmol), and a 5% dextrose solution (5.4 ml/h), were given to ten healthy volunteers in random order 2 weeks apart. By means of intra-arterial ambulatory monitoring the haemodynamic effects were followed for 18 h after the infusions were stopped. Adrenaline, but not noradrenaline, caused a delayed and protracted pressor effect. Over the total postinfusion period systolic and diastolic arterial pressure were 6 (SEM 2)% and 7 (2)%, respectively, higher than after dextrose infusion (ANOVA, p less than 0.001). Thus, "stress" levels of adrenaline (230 pg/ml) for 6 h cause a delayed and protracted pressor effect. These findings are strong support for the adrenaline-hypertension hypothesis in man.
在一项双盲交叉研究中，将肾上腺素（15纳克/千克/分钟；1纳克 = 5.458皮摩尔）、去甲肾上腺素（30纳克/千克/分钟；1纳克 = 5.911皮摩尔）和5%葡萄糖溶液（5.4毫升/小时）以随机顺序给予10名健康志愿者，每次输注间隔2周，持续6小时。通过动脉动态监测，在输注停止后跟踪血流动力学效应18小时。肾上腺素而非去甲肾上腺素引起了延迟且持久的升压效应。在整个输注后期间，收缩压和舒张压分别比输注葡萄糖后高6（标准误2）%和7（2）%（方差分析，p < 0.001）。因此，6小时的“应激”水平肾上腺素（230皮克/毫升）会引起延迟且持久的升压效应。这些发现有力地支持了人类肾上腺素 - 高血压假说。
