Research
Research summary
Chronic fetal hypoxia is a common complication of pregnancy and is associated with intrauterine growth restriction (IUGR). The IUGR fetus is likely delivered preterm and thereby treated with synthetic potent glucocorticoids, such as dexamethasone, to accelerate fetal lung maturation. Since both chronic fetal hypoxia and exposure to excess glucocorticoids are known to induce oxidative stress and oxidative stress is known to programme cardiovascular dysfunction, it is likely that the IUGR fetus treated with dexamethasone will be at an enhanced risk of developing cardiovascular disease. The aim our current programmes of research is to test whether maternal treatment with the mitochondrially-targeted antioxidant mito Q protects the IUGR fetus treated with synthetic steroids from developing cardiovascular disease.
Funding: British Heart Foundation
Publications
- Kane AD, Herrera EA, Camm EJ, Giussani DA, Vitamin C prevents intrauterine programming of in vivo cardiovascular dysfunction in the rat, Circ J. 2013;77(10):2604-11
- Giussani DA, Camm EJ, Niu Y, Richter HG, Blanco CE, Gottschalk R, Blake EZ, Horder KA, Thakor AS, Hansell JA, Kane AD, Wooding FB, Cross CM, Herrera EA, Developmental programming of cardiovascular dysfunction by prenatal hypoxia and oxidative stress, PLoS One. 2012;7(2):e31017. doi: 10.1371/journal.pone.0031017. Epub 2012 Feb 13
- Jellyman JK, Gardner DS, Edwards CM, Fowden AL, Giussani DA, Fetal cardiovascular, metabolic and endocrine responses to acute hypoxaemia during and following maternal treatment with dexamethasone in sheep, J Physiol. 2005 Sep 1;567(Pt 2):673-88
