Isenring P, Lebel M, Falardeau P, Grose J H
Department of Medicine, Laval University, Quebec, Canada.
Prostaglandins Leukot Essent Fatty Acids. 1996 Jan;54(1):59-63. doi: 10.1016/s0952-3278(96)90082-4.
The main objective of this study was to investigate the role of eicosanoids in modulating the effect of norepinephrine (NE) on blood pressure and renal hemodynamics during NE administration. Eight healthy volunteers were randomly assigned to three (1 week apart) infusion periods (180 min) with either dextrose 5% or NE, with or without indomethacin pretreatment. Pressor doses of NE induced marked alterations in renal hemodynamics and concomitant increases in eicosanoid excretion rates. The production of the vasodilatory prostacyclin (PGI2), as reflected in the excretion rate of the stable metabolites 6-keto-prostaglandin (PG)F1(alpha) and 2,3-dinor-6-keto-PGF1(alpha), was 2.7 times higher than that of the constrictor thromboxane (TX)A2, which was measured as the stable derivative TXB2. Indomethacin pretreatment blunted the NE-induced augmentation in eicosanoid excretion and resulted in further increases in arterial pressure and in renal vascular resistance. These results demonstrate that PGI2 attenuates the systemic and the renal hemodynamic vasoconstrictor effect of NE in normotensive control normal subjects.
本研究的主要目的是探讨在给予去甲肾上腺素（NE）期间，类二十烷酸在调节NE对血压和肾血流动力学影响中的作用。八名健康志愿者被随机分为三个（间隔1周）输注期（180分钟），分别输注5%葡萄糖或NE，并进行或不进行吲哚美辛预处理。升压剂量的NE可引起肾血流动力学的显著改变，并伴随类二十烷酸排泄率增加。作为稳定代谢产物6-酮-前列腺素（PG）F1α和2,3-二去甲-6-酮-PGF1α排泄率所反映的血管舒张性前列环素（PGI2）的生成量，比作为稳定衍生物血栓素（TX）B2所测定的缩血管性血栓素（TXA2）高2.7倍。吲哚美辛预处理减弱了NE诱导的类二十烷酸排泄增加，并导致动脉压和肾血管阻力进一步升高。这些结果表明，在血压正常的对照正常受试者中，PGI2可减弱NE的全身和肾血流动力学血管收缩作用。
