Effects of nifedipine and sildenafil on placental hemodynamics and gas exchange during fetal hypoxemia in a chronic sheep model

Leena Alanne, Amarnath Bhide, Jonna Hoffren, Juulia Lantto, Heikki Huhta, Merja Kokki, Mervi Haapsamo, Ganesh Acharya, Juha Räsänen

Research output: Contribution to journalArticle

Abstract

Introduction: We hypothesized that nifedipine and sildenafil would have no detrimental effects on placental hemodynamics and gas exchange under fetal hypoxemia. Methods: In 33 chronically instrumented fetal sheep, placental volume blood flow (QPlac) and umbilical artery (UA) vascular impedance were measured by Doppler ultrasonography. Fetal carotid artery blood pressure and blood gas values were monitored. After baseline data collection, maternal and fetal hypoxemia were induced. Following hypoxemia phase data collection, 12 fetuses received sildenafil and 9 fetuses nifedipine infusion, and 12 fetuses served as controls receiving saline infusion. Data were collected 30 and 120 min after infusion was started. Then maternal oxygenation was normalized and normoxemia phase data were collected, while infusion was continued. Results: Hypoxemia significantly decreased fetal pO2 and blood pressure. In the sildenafil group at 30- and 120-min hypoxemia + infusion phases, fetal blood pressure and QPlac were significantly lower and pCO2 higher than at baseline without returning to baseline level at normoxemia + infusion phase. In hypoxemia, nifedipine did not affect fetal blood pressure or placental hemodynamics. Both in the sildenafil and nifedipine groups, fetal pO2 remained significantly lower at normoxemia + infusion phase than in the control group. Umbilical artery vascular impedance did not change during the experiment. Discussion: In fetal hypoxemia, sildenafil had detrimental effects on placental hemodynamics that disturbed placental gas exchange. Nifedipine did not alter placental hemodynamics in hypoxemia but disturbed placental gas exchange upon returning to normoxemia. Umbilical artery vascular impedance did not reflect alterations in placental hemodynamics.

Original languageEnglish (US)
Pages (from-to)103-108
Number of pages6
JournalPlacenta
Volume90
DOIs
StatePublished - Jan 15 2020

Fingerprint

Nifedipine
Sheep
Gases
Hemodynamics
Umbilical Arteries
Electric Impedance
Fetal Blood
Blood Pressure
Blood Vessels
Fetus
Mothers
Doppler Ultrasonography
Sildenafil Citrate
Hypoxia
Blood Volume
Carotid Arteries
Control Groups

Keywords

  • Blood flow
  • Fetus
  • Physiology
  • Pregnancy
  • Ultrasound

ASJC Scopus subject areas

  • Reproductive Medicine
  • Obstetrics and Gynecology
  • Developmental Biology

Cite this

Effects of nifedipine and sildenafil on placental hemodynamics and gas exchange during fetal hypoxemia in a chronic sheep model. / Alanne, Leena; Bhide, Amarnath; Hoffren, Jonna; Lantto, Juulia; Huhta, Heikki; Kokki, Merja; Haapsamo, Mervi; Acharya, Ganesh; Räsänen, Juha.

In: Placenta, Vol. 90, 15.01.2020, p. 103-108.

Research output: Contribution to journalArticle

Alanne, L, Bhide, A, Hoffren, J, Lantto, J, Huhta, H, Kokki, M, Haapsamo, M, Acharya, G & Räsänen, J 2020, 'Effects of nifedipine and sildenafil on placental hemodynamics and gas exchange during fetal hypoxemia in a chronic sheep model', Placenta, vol. 90, pp. 103-108. https://doi.org/10.1016/j.placenta.2019.12.014
Alanne, Leena ; Bhide, Amarnath ; Hoffren, Jonna ; Lantto, Juulia ; Huhta, Heikki ; Kokki, Merja ; Haapsamo, Mervi ; Acharya, Ganesh ; Räsänen, Juha. / Effects of nifedipine and sildenafil on placental hemodynamics and gas exchange during fetal hypoxemia in a chronic sheep model. In: Placenta. 2020 ; Vol. 90. pp. 103-108.
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T1 - Effects of nifedipine and sildenafil on placental hemodynamics and gas exchange during fetal hypoxemia in a chronic sheep model

AU - Alanne, Leena

AU - Bhide, Amarnath

AU - Hoffren, Jonna

AU - Lantto, Juulia

AU - Huhta, Heikki

AU - Kokki, Merja

AU - Haapsamo, Mervi

AU - Acharya, Ganesh

AU - Räsänen, Juha

PY - 2020/1/15

Y1 - 2020/1/15

N2 - Introduction: We hypothesized that nifedipine and sildenafil would have no detrimental effects on placental hemodynamics and gas exchange under fetal hypoxemia. Methods: In 33 chronically instrumented fetal sheep, placental volume blood flow (QPlac) and umbilical artery (UA) vascular impedance were measured by Doppler ultrasonography. Fetal carotid artery blood pressure and blood gas values were monitored. After baseline data collection, maternal and fetal hypoxemia were induced. Following hypoxemia phase data collection, 12 fetuses received sildenafil and 9 fetuses nifedipine infusion, and 12 fetuses served as controls receiving saline infusion. Data were collected 30 and 120 min after infusion was started. Then maternal oxygenation was normalized and normoxemia phase data were collected, while infusion was continued. Results: Hypoxemia significantly decreased fetal pO2 and blood pressure. In the sildenafil group at 30- and 120-min hypoxemia + infusion phases, fetal blood pressure and QPlac were significantly lower and pCO2 higher than at baseline without returning to baseline level at normoxemia + infusion phase. In hypoxemia, nifedipine did not affect fetal blood pressure or placental hemodynamics. Both in the sildenafil and nifedipine groups, fetal pO2 remained significantly lower at normoxemia + infusion phase than in the control group. Umbilical artery vascular impedance did not change during the experiment. Discussion: In fetal hypoxemia, sildenafil had detrimental effects on placental hemodynamics that disturbed placental gas exchange. Nifedipine did not alter placental hemodynamics in hypoxemia but disturbed placental gas exchange upon returning to normoxemia. Umbilical artery vascular impedance did not reflect alterations in placental hemodynamics.

AB - Introduction: We hypothesized that nifedipine and sildenafil would have no detrimental effects on placental hemodynamics and gas exchange under fetal hypoxemia. Methods: In 33 chronically instrumented fetal sheep, placental volume blood flow (QPlac) and umbilical artery (UA) vascular impedance were measured by Doppler ultrasonography. Fetal carotid artery blood pressure and blood gas values were monitored. After baseline data collection, maternal and fetal hypoxemia were induced. Following hypoxemia phase data collection, 12 fetuses received sildenafil and 9 fetuses nifedipine infusion, and 12 fetuses served as controls receiving saline infusion. Data were collected 30 and 120 min after infusion was started. Then maternal oxygenation was normalized and normoxemia phase data were collected, while infusion was continued. Results: Hypoxemia significantly decreased fetal pO2 and blood pressure. In the sildenafil group at 30- and 120-min hypoxemia + infusion phases, fetal blood pressure and QPlac were significantly lower and pCO2 higher than at baseline without returning to baseline level at normoxemia + infusion phase. In hypoxemia, nifedipine did not affect fetal blood pressure or placental hemodynamics. Both in the sildenafil and nifedipine groups, fetal pO2 remained significantly lower at normoxemia + infusion phase than in the control group. Umbilical artery vascular impedance did not change during the experiment. Discussion: In fetal hypoxemia, sildenafil had detrimental effects on placental hemodynamics that disturbed placental gas exchange. Nifedipine did not alter placental hemodynamics in hypoxemia but disturbed placental gas exchange upon returning to normoxemia. Umbilical artery vascular impedance did not reflect alterations in placental hemodynamics.

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KW - Fetus

KW - Physiology

KW - Pregnancy

KW - Ultrasound

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