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  • Title: Fetal placental vascular responses to prostacyclin after angiotensin II-induced vasoconstriction.
    Author: Parisi VM, Walsh SW.
    Journal: Am J Physiol; 1989 Jul; 257(1 Pt 1):E102-7. PubMed ID: 2502024.
    Abstract:
    The vasodilator prostacyclin is produced by many fetal tissues and may serve to protect umbilical placental blood flow. We hypothesized that prostacyclin could reverse fetoplacental vasoconstriction produced by angiotensin II (ANG II). Studies were done in eight unanesthetized near-term ovine fetuses. After a control period, ANG II was infused into the fetal inferior vena cava at a rate of 0.5 microgram/min for 40 min. Twenty minutes after starting the ANG II infusion, an infusion of prostacyclin at a rate of 5 micrograms/min was added to the ANG II infusion. Blood flows were measured by the radioactive microsphere technique. Blood flow measurements were made during the control period, 20 min after starting the ANG II infusion, and 20 min after adding prostacyclin to the ANG II infusion. ANG II produced significant fetal hypertension and renal, intestinal, and placental vasoconstriction. Placental vascular resistance rose from 0.14 +/- 0.01 to 0.18 +/- 0.01 mmHg.min.kg fetal wt.ml-1 during the ANG II infusion period (P less than 0.05). The addition of prostacyclin to the ANG II infusion resulted in a return to control values for fetal blood pressure and renal and intestinal resistance. However, placental vasoconstriction was not reversed by addition of prostacyclin as placental vascular resistance remained significantly elevated over the control value (0.17 +/- 0.01 mmHg.min.kg fetal wt.ml-1). Although unchanged by ANG II infusion, fetal pH decreased significantly during the ANG II plus prostacyclin infusion period. We conclude that ANG II causes fetal hypertension and renal and intestinal vasoconstriction, which are reversed by prostacyclin.(ABSTRACT TRUNCATED AT 250 WORDS)
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