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Reproductive Sciences
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Article

Placental and Fetal Hemodynamics After Labetalol or Pindolol in a Sheep Model of Increased Placental Vascular Resistance and Maternal Hypertension

Tiina Erkinaro, MD, PhD*, Tomi Kavasmaa, MD, Laura Ylikauma, MB, Kaarin Makikallio, MD, PhD, Mervi Haapsamo, MD, Ganesh Acharya, MD, PhD, Pasi Ohtonen, MSc, Seppo Alahuhta, MD, PhD, and Juha Rasanen, MD, PhD

* To whom correspondence should be addressed. E-mail: tiina.erkinaro{at}pp.fimnet.fi.


  Abstract

We investigated the effects of labetalol and pindolol on uterine, placental, and fetal hemodynamics following norepinephrine-induced maternal hypertension in a sheep model of increased placental vascular resistance. Also, we examined fetal and placental hemodynamic responses to acute hypoxemia after antihypertensive medication. Norepinephrine increased maternal heart rate (HR), mean arterial pressure (MAP) and uterine vascular resistance (RUtA), and decreased uterine volume blood flow (QUtA). Both labetalol and pindolol decreased maternal HR, MAP, and RUtA, but did not restore QUtA. Fetal MAP was unaffected while fetal HR and placental volume blood flow (QUA) decreased and placental vascular resistance increased. During hypoxemia, which was induced by decreasing maternal inspiratory oxygen fraction, all these parameters remained unchanged in the labetalol group while fetal HR increased and QUA further decreased in the pindolol group. We conclude that labetalol and pindolol may compromise uterine and placental hemodynamics. Hypoxemic stress provokes divergent hemodynamic responses in fetuses exposed to these differently acting adrenoceptor antagonists.

First published on April 20, 2009, doi:10.1177/1933719109335068

Reproductive Sciences 2009;16:749.

A more recent version of this article appeared on August 1, 2009

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