PGA1输注治疗重度先兆子痫-一个重要的临床潜力。

M K Toppozada, S A Shaala, H A Moussa
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引用次数: 10

摘要

初步研究表明,静脉输注肾前列腺素A1 (PGA1)对重度先兆子痫患者有三种有益的临床反应;血压恢复正常,肾功能明显改善,成功引产。本研究旨在建立PGA1在严重毒血症中的治疗方案。21例重度先兆子痫患者(3组)静脉滴注PGA1,剂量范围为0.1 ~ 0.5 μ g /kgm/min,持续12 ~ 24 h,连续监测输注期间及输注后12 h的血压、子宫活动、FHR。0.1微克/公斤/分钟的剂量持续12小时是不够的,而0.5微克/公斤/分钟持续12小时可以引起良好的降压反应,并且在48小时内分娩的病例中观察到高血压在输注后反弹。从临床角度来看,24小时0.5微克/公斤/分钟的剂量似乎是最佳的,因为记录了对血压的满意效果,并且所有受试者在输注期间分娩了正常婴儿,输注后血压反弹很小或没有反弹。这种方法在治疗严重先兆子痫方面具有很大的潜力。
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Therapeutic use of PGA1 infusions in severe pre-eclampsia - a major clinical potential.

Pilot studies showed that, i.v. infusions of the renal prostaglandin A1 (PGA1) induced a triad of beneficial clinical responses in severe pre-eclampsia; the blood pressure became normotensive, renal function was markedly improved and labour was successfully induced. The present study was an attempt to develop a therapeutic schedule of PGA1 administration in severe toxemia. Twenty one cases of severe pre-eclampsia (in 3 equal groups) received i.v. infusions of PGA1 in a dose range of 0.1-0.5 microgram/kgm/min for 12 - 24 hours and the B.P., uterine activity and FHR were continuously monitored during and for 12 hours following the infusion period. The 0.1 microgram/Kgm/min dose for 12 hours was inadequate while 0.5 microgram/Kgm/min for 12 hours induced a good hypotensive response and the cases delivered within 48 hours but a post-infusion rebound in hypertension was observed. The dose of 0.5 microgram/Kgm/min for 24 hours appeared to be optimal in clinical terms since a satisfactory effect on B.P. was recorded and all the subjects delivered normal babies during the infusion period with minimal or no post-infusion rebound rise in B.P. This approach holds a major potential in the treatment of severe pre-eclampsia.

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Pre-eclampsia in a second pregnancy. A clinical follow-up study of 260 women with hypertension in pregnancy. Beta blocker therapy in 125 cases of hypertension during pregnancy. Disposition of the adrenergic blocker metoprolol in the late pregnant women, the amniotic fluid, the cord blood and the neonate. Maternal-fetal immunity: presence of specific cellular hyporesponsiveness and humoral suppressor activity in normal pregnancy and their absence in preeclampsia.
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