Uterine prostaglandin E secretion and uterine blood flow in the pregnant rabbit.
Uterine prostaglandin E secretion and uterine blood flow in the pregnant rabbit.
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怀孕兔子宫前列腺素E分泌和子宫血流量。
DOI：
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发表时间：
1975
影响因子：
15.9
通讯作者：
T. Ferris
中科院分区：
文献类型：
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作者：
R. Venuto;T. O'dorisio;J. H. Stein;T. Ferris
在妊娠家兔中进行研究，以评估前列腺素合成抑制对子宫血流的影响。使用放射性标记的微球测量心输出量和子宫胎盘血流量（UPBF）。用放射免疫法测定孕兔子宫静脉和外周动脉前列腺素E（PGE）浓度。无论是甲氰氨酯或吲哚美辛2 mg/kg，用于抑制前列腺素的合成。前列腺素抑制后，体循环动脉压从86 mm Hg增加到98 mm Hg（P <0.0001）。前列腺素合成抑制后，心输出量不变，为326 ml/min至7.8 ml/min。子宫静脉PGE浓度极高，为172.4 ng/ml，同时外周动脉PGE为2.1 NG/ml。静脉注射甲氨蝶呤或吲哚美辛使子宫静脉PGE降至23 ng/ml（P <0.01），动脉PGE降至1.0 ng/ml（P <0.05）。雄兔和未孕雌兔下动脉PGE均为0.37 ng/ml（P <0.05）。在非肾切除妊娠动物中的研究表明，子宫胎盘分泌的PGE大于肾脏分泌的五倍。这些研究表明，兔子宫胎盘单位是一个丰富的来源PGE，并表明，生产的血管活性脂质可能有一个关键作用，在怀孕期间调节UPBF。
Studies were performed in pregnant rabbits to assess the effect of inhibition of prostaglandin synthesis on uterine blood flow. Cardiac output and uteroplacental blood flow (UPBF) were measured using radiolabeled microspheres. Prostaglandin E (PGE) concentration was measured by radioimmunoassay in the uterine vein and peripheral artery of the pregnant nephrectomized rabbit. Either meclofenamate or indomethacin 2 mg/kg were utilized to inhibit prostaglandin synthesis. Systemic arterial pressure increased from 86 mm Hg to 98 mm Hg (P less than0.0001) after prostaglandin inhibition. Cardiac output was unchanged after the inhibition of prostaglandin synthesis, 326 ml/min to 7.8 ml/min. Uterine vein PGE concentration was extremely high, 172.4 ng/ml, with concomitant peripheral arterial PGE 2.1 NG/ML. Intravenous administration of either meclofenamate or indomethacin reduced uterine vein PGE to 23 ng/ml (P less than 0.01) and arterial PGE to 1.0 ng/ml (P less than 0.05). Male and nonpregnant female rabbits had lower arterial PGE, 0.37 ng/ml (P less 0.05). Studies in non-nephrectomized pregnant animals demonstrated that uteroplacental secretion of PGE was greater than five times renal secretion. These studies demonstrate that the rabbit uteroplacental unit is a rich source of PGE and suggest that production of the vasoactive lipid may have a key role in regulating UPBF during pregnancy.