Cardiotoxicity of β-mimetic catecholamines during ontogenetic development - possible risks of antenatal therapy
Jazyk angličtina Země Kanada Médium print
Typ dokumentu časopisecké články, přehledy
PubMed
29633627
DOI
10.1139/cjpp-2017-0774
Knihovny.cz E-zdroje
- Klíčová slova
- beta-mimetic catecholamines, cardiotoxicity, cardiotoxicité, catécholamines bêta mimétiques, cœur immature, immature heart, preterm labor, tocolyse, tocolysis, travail avant terme,
- MeSH
- adenylátcyklasy metabolismus MeSH
- agonisté adrenergních beta-receptorů škodlivé účinky MeSH
- beta-adrenergní receptory metabolismus MeSH
- kardiotoxicita etiologie MeSH
- katecholaminy škodlivé účinky MeSH
- lidé MeSH
- signální transdukce účinky léků MeSH
- srdce účinky léků embryologie MeSH
- těhotenství MeSH
- tokolytika škodlivé účinky MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- těhotenství MeSH
- ženské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- přehledy MeSH
- Názvy látek
- adenylátcyklasy MeSH
- agonisté adrenergních beta-receptorů MeSH
- beta-adrenergní receptory MeSH
- katecholaminy MeSH
- tokolytika MeSH
Catecholamines are involved in the regulation of a wide variety of vital functions. The β-adrenergic receptor (β-AR) - adenylyl cyclase system has been identified early in embryogenesis before the heart has received adrenergic innervation. The structure of β-receptors in the immature myocardium is similar to that in adults; there are, however, significant quantitative developmental changes in the inotropic and chronotropic responsiveness. Information on the toxic effect of the β-AR agonists in the immature heart is surprisingly scarce, even though these agents are used in clinical practice both during pregnancy and in early postnatal development. Large doses of β-AR agonists induce malformations of the cardiovascular system; the type of change depends upon the time at which the β-AR agonist was administered during embryogenesis. During postnatal ontogeny, the cardiotoxicity of β-AR agonists increased from birth to adulthood. It seems likely that despite interspecies differences, developmental changes in the cardiac sensitivity to β-AR agonists may exist in all mammals, depending on the degree of maturation of the system involved in β-adrenergic signaling. All the existing data draw attention to the possible harmful consequences of the clinical use of β-AR agonists during early phases of cardiac development. Late effects of the early disturbances of the cardiac muscle cannot be excluded.
Citace poskytuje Crossref.org