The effects of chronic hypoxia in utero on cardiovascular regulation in the offspring

3040 20 17397 5 30807 document 17397 Rook11PhD.pdf application/pdf c1c2dc9c5469178dc4ccb39002d7d948 MD5 7942721 2011-12-02 14:06:37 http://etheses.bham.ac.uk//id/eprint/3040/1/Rook11PhD.pdf 3040 1 1 application/pdf application/pdf en public

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http://eprints.org/relation/isVersionOf http://etheses.bham.ac.uk/id/document/17397 http://eprints.org/relation/isVolatileVersionOf http://etheses.bham.ac.uk/id/document/17397 http://eprints.org/relation/isIndexCodesVersionOf http://etheses.bham.ac.uk/id/document/17397 archive 4031 disk0/00/00/30/40 2011-12-02 14:09:20 2019-01-18 12:42:57 2011-12-02 14:09:20 thesis show 0 Rook William Marshall Janice Coney Andrew ftp://ubira.bham.ac.uk/eTheses/3040_Rook/ University of Birmingham The effects of chronic hypoxia in utero on cardiovascular regulation in the offspring unpub QP 10col_mede A common consequence of the complications of pregnancy, such as preeclampsia, is reduced supply of nutrients, including oxygen, to the developing fetus. The consequences for the offspring are wide ranging, but include increased risk of cardiovascular disease. However, the mechanisms by which this occurs are poorly understood. Using a rodent model, this study has examined the regulation of blood vessels, particularly those supplying skeletal muscle, by local, endothelially-derived factors, and by the sympathetic nervous system, in adult rat offspring following chronic hypoxia in utero. The key findings include evidence that there are chronically high levels of oxidative stress in the skeletal muscle vasculature of the offspring. Further, the density of, and the activity in the sympathetic neurones supplying skeletal muscle blood vessels is markedly increased following chronic hypoxia in utero, but the vascular sensitivity to stimulation of these neurones is reduced. Following chronic hypoxia in utero, as the rats approached middle age, they became hypertensive relative to normal rats. Thus, the present study has offered some mechanistic insight, which adds to a growing body of literature, and which may help to explain why babies born of sub-optimal pregnancies are at higher risk of developing cardiovascular disease later in life. 2011-12 2011-08 graduation eng author unchecked This unpublished thesis/dissertation is copyright of the author and/or third parties. The intellectual property rights of the author or third parties in respect of this work are as defined by The Copyright Designs and Patents Act 1988 or as modified by any successor legislation. Any use made of information contained in this thesis/dissertation must be in accordance with that legislation and must be properly acknowledged. Further distribution or reproduction in any format is prohibited without the permission of the copyright holder. public University of Birmingham School of Clinical and Experimental Medicine d_ph british_heart_foundation 2011-12 graduation