Ferris T F, Weir E K
J Clin Invest. 1983 Apr;71(4):809-15. doi: 10.1172/jci110834.
Captopril, 5 mg/kg, administered to pregnant rabbits caused a reduction in mean arterial pressure (MAP) from 106+/-2 to 87+/-2 mmHg (P<0.01) without change in cardiac output or renal blood flow. Uterine blood flow fell from 31.9+/-2.5 to 21.3+/-3.4 ml/min (P<0.01) as uterine vein prostaglandin E series level (PGE) decreased from 127+/-23 ng/ml to 26+/-8 ng/ml (P<0.01). Saralasin also caused a reduction in MAP from 110+/-5 to 92+/-4.3 (P<0.01), a reduction in uterine blood flow from 28.8+/-1.6 to 21.8+/-1.7 ml/min (P<0.01) as uterine vein PGE decreased from 121.3+/-14.4 to 63.5+/-14.2 ng/ml (P<0.01). Plasma renin activity (PRA) was higher in the uterine vein, 11+/-3 ng/ml per h, than peripheral vein, 6+/-1.6 ng/ml per h, (P<0.05), before Captopril and rose in the uterine vein to 90+/-19 ng/ml per h (P<0.01) as peripheral vein PRA rose to 62+/-15 ng/ml per h (P<0.05) after Captopril. After saralasin uterine vein PRA rose from 4.6+/-1.5 to 14.8+/-6.3 ng/ml per h (P<0.05) and peripheral vein PRA rose from 3.7+/-1 to 6.5+/-2.1 (P<0.05). Reducing MAP with MgSO(4) from 98+/-4 to 70+/-2 (P<0.01) caused a significant fall in cardiac output from 695+/-33 to 588+/-49 (P<0.01) without change in renal or uterine blood flow. Uterine vein PGE concentration also did not change significantly following MgSO(4); 80+/-22 ng/ml before and 60+/-27 ng/ml (NS) during the administration of MgSO(4). Chronic administration of Captopril in doses of either 2.5 or 5.0 mg/kg per d from the 15th d of gestation caused an 86% fetal mortality at the lower and a 92% fetal mortality at the higher dose of the drug. These experiments point to the importance of uterine PGE synthesis in maintenance of uterine blood flow and fetal survival during pregnancy and suggest that uterine PGE synthesis is dependent upon angiotensin II. Synthesis of uterine renin and PGE may be necessary for maintenance of uterine blood flow and fetal survival during pregnancy.
给怀孕兔子注射5毫克/千克的卡托普利，可使平均动脉压（MAP）从106±2毫米汞柱降至87±2毫米汞柱（P<0.01），而心输出量或肾血流量无变化。子宫血流量从31.9±2.5毫升/分钟降至21.3±3.4毫升/分钟（P<0.01），同时子宫静脉前列腺素E系列水平（PGE）从127±23纳克/毫升降至26±8纳克/毫升（P<0.01）。沙拉新也可使MAP从110±5降至92±4.3（P<0.01），子宫血流量从28.8±1.6毫升/分钟降至21.8±1.7毫升/分钟（P<0.01），子宫静脉PGE从121.3±14.4降至63.5±14.2纳克/毫升（P<0.01）。在注射卡托普利前，子宫静脉血浆肾素活性（PRA）高于外周静脉，分别为11±3纳克/毫升每小时和6±1.6纳克/毫升每小时（P<0.05），注射卡托普利后，子宫静脉PRA升至90±19纳克/毫升每小时（P<0.01），外周静脉PRA升至62±15纳克/毫升每小时（P<0.05）。注射沙拉新后，子宫静脉PRA从4.
