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Statements

Subject Item
n2:RIV%2F00023001%3A_____%2F13%3A00058547%21RIV14-MZ0-00023001
rdf:type
skos:Concept n16:Vysledek
dcterms:description
A significant increase in cardiovascular medication use during pregnancy occurred in recent years. Only limited evidence on safety profiles is available, and little is known about the mechanisms of adverse effect on the fetus. We hypothesized that drug-induced bradycardia is the leading mechanism of developmental toxicity. Embryotoxicity was tested in ovo after administration of various doses of metoprolol, carvedilol, or ivabradine. Embryonic day (ED) 4 and 8 chick embryos were studied by video microscopy and ultrasound biomicroscopy ex ovo after intraamniotic injection of the drug for a period of 30 min. Stroke volume was calculated by the Simpson method and prolate ellipsoid formula. Significant dose-dependent mortality was achieved in embryos injected with carvedilol and ivabradine. In ED4 embryos, metoprolol, carvedilol, and ivabradine reduced the heart rate by 33%, 27%, and 55%, respectively, compared with controls (6%). In ED8 embryos this effect was more pronounced with a heart rate reduction by 71%, 54%, and 53%, respectively (controls, 36%). Cardiac output decreased in all tested groups but only proved significant in the metoprolol group in ED8 embryos. The number of beta-adrenergic receptors showed a downward tendency during embryonic development. A negative chronotropic effect of metoprolol, carvedilol, and ivabradine was increasingly pronounced with embryonic maturity despite a downward trend in the number of beta-adrenergic receptors. This effect was associated with reduced cardiac output in chick embryos, probably leading to premature death. Although standard doses of these drugs appear relatively safe, high doses have a potentially adverse effect on the fetus through reduced heart rate. A significant increase in cardiovascular medication use during pregnancy occurred in recent years. Only limited evidence on safety profiles is available, and little is known about the mechanisms of adverse effect on the fetus. We hypothesized that drug-induced bradycardia is the leading mechanism of developmental toxicity. Embryotoxicity was tested in ovo after administration of various doses of metoprolol, carvedilol, or ivabradine. Embryonic day (ED) 4 and 8 chick embryos were studied by video microscopy and ultrasound biomicroscopy ex ovo after intraamniotic injection of the drug for a period of 30 min. Stroke volume was calculated by the Simpson method and prolate ellipsoid formula. Significant dose-dependent mortality was achieved in embryos injected with carvedilol and ivabradine. In ED4 embryos, metoprolol, carvedilol, and ivabradine reduced the heart rate by 33%, 27%, and 55%, respectively, compared with controls (6%). In ED8 embryos this effect was more pronounced with a heart rate reduction by 71%, 54%, and 53%, respectively (controls, 36%). Cardiac output decreased in all tested groups but only proved significant in the metoprolol group in ED8 embryos. The number of beta-adrenergic receptors showed a downward tendency during embryonic development. A negative chronotropic effect of metoprolol, carvedilol, and ivabradine was increasingly pronounced with embryonic maturity despite a downward trend in the number of beta-adrenergic receptors. This effect was associated with reduced cardiac output in chick embryos, probably leading to premature death. Although standard doses of these drugs appear relatively safe, high doses have a potentially adverse effect on the fetus through reduced heart rate.
dcterms:title
Heart rate changes mediate the embryotoxic effect of antiarrhythmic drugs in the chick embryo Heart rate changes mediate the embryotoxic effect of antiarrhythmic drugs in the chick embryo
skos:prefLabel
Heart rate changes mediate the embryotoxic effect of antiarrhythmic drugs in the chick embryo Heart rate changes mediate the embryotoxic effect of antiarrhythmic drugs in the chick embryo
skos:notation
RIV/00023001:_____/13:00058547!RIV14-MZ0-00023001
n16:predkladatel
n17:ico%3A00023001
n3:aktivita
n7:P n7:V n7:Z n7:I
n3:aktivity
I, P(GA304/08/0615), P(GAP302/11/1308), V, Z(AV0Z50110509), Z(MSM0021620806), Z(MSM0021620858)
n3:cisloPeriodika
6
n3:dodaniDat
n20:2014
n3:domaciTvurceVysledku
n9:1867687
n3:druhVysledku
n10:J
n3:duvernostUdaju
n14:S
n3:entitaPredkladatele
n13:predkladatel
n3:idSjednocenehoVysledku
77140
n3:idVysledku
RIV/00023001:_____/13:00058547
n3:jazykVysledku
n19:eng
n3:klicovaSlova
bradycardia; pregnancy; embryotoxicity; embryonic heart; beta-blocking agents
n3:klicoveSlovo
n6:bradycardia n6:embryotoxicity n6:beta-blocking%20agents n6:pregnancy n6:embryonic%20heart
n3:kodStatuVydavatele
US - Spojené státy americké
n3:kontrolniKodProRIV
[6D98E012ECED]
n3:nazevZdroje
American journal of physiology: Heart and circulatory physiology
n3:obor
n18:FA
n3:pocetDomacichTvurcuVysledku
1
n3:pocetTvurcuVysledku
6
n3:projekt
n4:GA304%2F08%2F0615 n4:GAP302%2F11%2F1308
n3:rokUplatneniVysledku
n20:2013
n3:svazekPeriodika
304
n3:tvurceVysledku
Sedmera, David Ostadal, Bohuslav Kočková, Radka Hejnova, Lucie Novotný, Jiří Svatunkova, Jarmila
n3:wos
000316206400013
n3:zamer
n15:MSM0021620806 n15:MSM0021620858 n15:AV0Z50110509
s:issn
0363-6135
s:numberOfPages
8
n11:doi
10.1152/ajpheart.00679.2012