Mason R T, Allen K J, Coghlan J P, Denton D A, Fei D T, Graham W F, Stewart K W, Scoggins B A
Prostaglandins Leukot Med. 1984 Oct;16(1):57-68. doi: 10.1016/0262-1746(84)90086-6.
The aim of this study was to determine the effect of ACTH-induced hypertension on the hemodynamic dose-response curves to intravenous infusion of prostacyclin (PGI2) in conscious sheep. PGI2 was infused for 10 minutes at doses of 0.05-0.50 micrograms/kg per min and hemodynamic dose-response curves were performed before, during and after ACTH-induced hypertension. Prior to ACTH administration prostacyclin infusions produced dose dependent decreases in mean arterial pressure (MAP), calculated total peripheral resistance (CTPR) and stroke volume (SV). These changes were accompanied by an increase in cardiac rate (CR) and cardiac output (CO). After five days of ACTH treatment MAP had risen from 72 +/- 1 to 91 +/- 2 mm Hg and infusions of PGI2 produced similar effects on MAP to those seen prior to ACTH. However the effects on CTPR, CO, SV and CR were all potentiated relative to normotensive animals. Three days after ACTH administration had ceased and basal pressure had returned to normotensive levels, the responses of CR, CO and SV to PGI2 infusions were similar to those seen prior to ACTH. However the exaggerated fall in CTPR seen during ACTH treatment was still present and this resulted in a very large decrease in MAP. These studies suggest that in this model of steroid-induced hypertension the resistance vessels are more sensitive to PGI2 and that the blood pressure response to PGI2 is regulated by different mechanisms to those seen prior to ACTH.
本研究的目的是确定促肾上腺皮质激素（ACTH）诱导的高血压对清醒绵羊静脉输注前列环素（PGI2）时血流动力学剂量反应曲线的影响。以0.05 - 0.50微克/千克每分钟的剂量输注PGI2 10分钟，并在ACTH诱导高血压之前、期间和之后进行血流动力学剂量反应曲线测定。在给予ACTH之前，输注前列环素可使平均动脉压（MAP）、计算得出的总外周阻力（CTPR）和每搏量（SV）呈剂量依赖性降低。这些变化伴随着心率（CR）和心输出量（CO）的增加。ACTH治疗五天后，MAP从72±1毫米汞柱升至91±2毫米汞柱，输注PGI2对MAP产生的影响与ACTH治疗前相似。然而，相对于血压正常的动物，对CTPR、CO、SV和CR的影响均增强。停止给予ACTH三天且基础血压恢复至正常血压水平后，CR、CO和SV对PGI2输注的反应与ACTH治疗前相似。然而，ACTH治疗期间CTPR出现的过度下降仍然存在，这导致MAP大幅下降。这些研究表明，在这种类固醇诱导的高血压模型中，阻力血管对PGI2更敏感，并且对PGI2的血压反应受不同于ACTH治疗前的机制调节。
