Effect of prostaglandin I2 on ovine placental vasculature.
Effect of prostaglandin I2 on ovine placental vasculature.
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前列腺素 I2 对绵羊胎盘血管系统的影响。
DOI：
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发表时间：
1979
期刊：
影响因子：
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通讯作者：
A. Berssenbrugge
中科院分区：
文献类型：
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作者：
J. Rankin;T. Phernetton;D. Anderson;A. Berssenbrugge
在10只长期植入血管导管的近足月绵羊中观察了胎盘循环对前列腺素I2（母体剂量20 μ g/kg，胎儿剂量180 μ g/kg）的反应。用放射性微球测量前列腺素I2注射前和注射后90 s的血流量。给母体注射前列腺素I2使血压从109 ± 4降到69 ± 5 mmHg（P < 0.001），母体子叶的血管阻力从0.166 ± 0.018增加到0.209 ± 0.02 mmHg/（ml/min）（P < 0.001）。随着阻力从0.705 +/- 0.02下降到0.266 +/- 0.02 mmHg/（ml/min），无子叶子宫的血管床血管扩张。（P < 0.001）。前列腺素I2导致胎儿动静脉压从37.6 +/- 1.35降至26.0 +/- 1.6 mmHg。胎儿子叶的血管阻力无明显变化。我们观察到胎膜血管舒张，血管阻力从1.06 +/- 0.14降至0.75 +/- 0.10 mmHg/（ml/min）（P < 0.001）。前列腺素I2的输注显著抑制了胎盘和子宫对去甲肾上腺素的反应。我们尚未证明前列腺素I2在维持胎盘血管稳态中起直接作用，但它可能调节该器官对外源性血管活性剂的反应。
The response of the placental circulations to prostaglandin I2 (maternal dose 20 microgram/kg, fetal dose 180 microgram/kg) was observed in 10 near-term sheep with chronically implanted vascular catheters. The blood flows before and 90 s after the injection of prostaglandin I2 were measured using radioactive microspheres. The injection of prostaglandin I2 to the mother decreased th blood pressure from 109 +/- 4 to 69 +/- 5 mmHg (P < 0.001) and increased the vascular resistance of the maternal cotyledons from 0.166 +/- 0.018 to 0.209 +/- 0.02 mmHg/(ml/min) (P < 0.001). The vascular bed of the non-cotyledonary uterus vasodilated as the resistance fell from 0.705 +/- 0.02 to 0.266 +/- 0.02 mmHg/(ml/min). (P < 0.001). Prostaglandin I2 caused the fetal arteriovenous pressure to fall from 37.6 +/- 1.35 to 26.0 +/- 1.6 mmHg. There was no significant change in the vascular resistance of the fetal cotyledons. We observed vasodilation in the fetal membranes as vascular resistance fell from 1.06 +/- 0.14 to 0.75 +/- 0.10 mmHg/(ml/min) (P < 0.001). The infusion of prostaglandin I2 significantly depressed the response of the placenta and uterus to norepinephrine. We have not proved that prostaglandin I2 plays a direct role in maintaining placental vascular homeostasis but it may modulate the response of this organ to exogenous vasoactive agents.