Antenatal betamethasone alters vascular reactivity in adult female ovine cerebral arteries

Delrae M. Eckman, Brady A. Kerr, Mamta Fuloria, Steve A. Simandle, Suzanne E. Watt, James C. Rose, Jorge P. Figueroa

Research output: Contribution to journalArticle

4 Scopus citations

Abstract

Although the use of antenatal glucocorticoids has resulted in decreased neonatal morbidity/mortality, recent animal studies have raised concerns regarding adverse effects of these medications on postnatal cardiovascular function. We hypothesized that antenatal betamethasone (Beta) exposure alters cerebral vascular reactivity in adult female sheep. We observed that K-induced constriction was comparable in middle cerebral artery (MCA) from Beta-exposed animals and age-matched controls. Pressure-induced constriction was significantly attenuated in MCA from Beta-exposed compared with control sheep. Inhibition of NOS significantly augmented pressure-induced constriction in MCA from both Beta-exposed and control sheep, whereas cyclooxygenase (COX) inhibition augmented pressure-induced constriction only in MCA from Beta-exposed sheep. Furthermore, NOS and COX inhibition significantly attenuated bradykinin (BK)-induced dilation in MCA from both Beta-exposed and control sheep. However, there seemed to be a greater contribution of both NOS and COX to BK-induced dilation in Beta-exposed compared with control MCA. Our findings demonstrate that fetal exposure to a clinically relevant course of Beta alters cerebral vascular tone and reactivity in adult female sheep.

Original languageEnglish (US)
Pages (from-to)344-348
Number of pages5
JournalPediatric Research
Volume68
Issue number4
DOIs
StatePublished - Oct 1 2010

ASJC Scopus subject areas

  • Pediatrics, Perinatology, and Child Health

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    Eckman, D. M., Kerr, B. A., Fuloria, M., Simandle, S. A., Watt, S. E., Rose, J. C., & Figueroa, J. P. (2010). Antenatal betamethasone alters vascular reactivity in adult female ovine cerebral arteries. Pediatric Research, 68(4), 344-348. https://doi.org/10.1203/PDR.0b013e3181edb9fa