Harrison G L, Moore L G
Cardiovascular Pulmonary Research Laboratory, University of Colorado Health Sciences Center, Denver 80262.
Am J Obstet Gynecol. 1989 Jan;160(1):258-64. doi: 10.1016/0002-9378(89)90132-4.
Pregnant women show a reduced pressor responsiveness to angiotensin II, but the mechanism responsible in unclear. We sought to determine whether reduced pressor responsiveness was due to decreased vasoreactivity and the involvement of increased vasodilator prostaglandin production in decreases observed. We found that pregnancy decreased systemic vascular resistance and the systemic vascular resistance response to angiotensin II infusion but not to phenylephrine hydrochloride infusion in awake, unstressed guinea pigs. The decreased systemic vascular resistance response to angiotensin II in the pregnant animals was accompanied by a reduced pressor response. Contractility to phenylephrine hydrochloride and norepinephrine was reduced in aortic rings isolated from pregnant, compared with nonpregnant, guinea pigs. Treatment with meclofenamate, a prostaglandin synthesis inhibitor, did not restore vasoreactivity in either the pregnant animal or the isolated vessel to levels observed in the nonpregnant state. We concluded that pregnancy reduced systemic vascular resistance and vasoreactivity but that mechanisms other than increased vasodilator prostaglandin production were likely responsible.
孕妇对血管紧张素II的升压反应性降低,但其机制尚不清楚。我们试图确定升压反应性降低是否是由于血管反应性降低以及血管舒张性前列腺素生成增加在观察到的降低中所起的作用。我们发现,在清醒、未应激的豚鼠中,妊娠会降低全身血管阻力以及对血管紧张素II输注的全身血管阻力反应,但对盐酸去氧肾上腺素输注的反应则不会降低。妊娠动物对血管紧张素II的全身血管阻力反应降低伴随着升压反应的减弱。与未妊娠的豚鼠相比,从妊娠豚鼠分离的主动脉环对盐酸去氧肾上腺素和去甲肾上腺素的收缩性降低。用前列腺素合成抑制剂甲氯芬那酸治疗,并未使妊娠动物或分离血管的血管反应性恢复到未妊娠状态下观察到的水平。我们得出结论,妊娠会降低全身血管阻力和血管反应性,但可能是由血管舒张性前列腺素生成增加以外的机制所致。