Mason R T, Coghlan J P, Congiu M, Denton D A, Fei D T, Whitworth J A, Scoggins B A
Prostaglandins Leukot Med. 1985 May;18(2):261-9. doi: 10.1016/0262-1746(85)90026-5.
The present experiments examine the hemodynamic effects of an intravenous infusion of prostacyclin on the development of ACTH-induced hypertension in conscious sheep. Prostacyclin was infused at either 0.01 microgram/kg min-1 for 9 days or 0.25 microgram/kg min-1 for 4 days. At 0.01 microgram/kg min-1 prostacyclin had no effect on blood pressure in normotensive sheep or on the development of ACTH hypertension. Infusion at 0.25 microgram/kg min-1 increased heart rate, cardiac output and plasma renin concentration and decreased stroke volume and peripheral resistance in normotensive sheep. Despite these effects it did not prevent development of ACTH-induced hypertension. It is unlikely on the basis of these results that glucocorticoid-induced inhibition of vasodepressor prostacyclin and resulting increase in pressor responsiveness to circulating agonists is the primary cause of ACTH induced hypertension in sheep.
本实验研究了静脉输注前列环素对清醒绵羊促肾上腺皮质激素（ACTH）诱导的高血压发展过程中的血流动力学影响。前列环素以0.01微克/千克·分钟 -1 的速度输注9天或0.25微克/千克·分钟 -1 的速度输注4天。以0.01微克/千克·分钟 -1 的速度输注时，前列环素对正常血压绵羊的血压或ACTH高血压的发展没有影响。以0.25微克/千克·分钟 -1 的速度输注可增加正常血压绵羊的心率、心输出量和血浆肾素浓度，并降低每搏输出量和外周阻力。尽管有这些作用，但它并不能阻止ACTH诱导的高血压的发展。基于这些结果，糖皮质激素诱导的血管舒张抑制性前列环素的抑制以及由此导致的对循环激动剂的升压反应性增加不太可能是绵羊ACTH诱导的高血压的主要原因。
