Adopting an integrative approach, by combining studies of cardiovascular function with those at cellular and molecular levels, this study investigated whether maternal treatment with melatonin protects against programmed cardiovascular dysfunction in the offspring using an established rodent model of hypoxic pregnancy. Wistar rats were divided into normoxic (N) or hypoxic (H, 10% O ) pregnancy ± melatonin (M) treatment (5 μg·ml .day ) in the maternal drinking water.
View Article and Find Full Text PDFSignificance: Adopting a risk stratification system and appropriate listing of cases reduces the rates of intraoperative complications during phacoemulsification. Such listing would allow both safe surgery and enhance training, by ensuring an appropriately experienced surgeon is available to operate on a case or supervise and teach a junior surgeon.
Purpose: To assess if the application of a simple, robust, validated preoperative scoring system can reduce the rates of intraoperative complications if patients are assigned to the appropriately experienced surgeon's list and surgical time is modified accordingly.
The quality of the intrauterine environment interacts with our genetic makeup to shape the risk of developing disease in later life. Fetal chronic hypoxia is a common complication of pregnancy. This chapter reviews how fetal chronic hypoxia programmes cardiac and endothelial dysfunction in the offspring in adult life and discusses the mechanisms via which this may occur.
View Article and Find Full Text PDFHypoxia is a common challenge to the fetus, promoting a physiological defence to redistribute blood flow towards the brain and away from peripheral circulations. During acute hypoxia, reactive oxygen species (ROS) interact with nitric oxide (NO) to provide an oxidant tone. This contributes to the mechanisms redistributing the fetal cardiac output, although the source of ROS is unknown.
View Article and Find Full Text PDFFetal hypoxia is a common complication of pregnancy. It has been shown to programme cardiac and endothelial dysfunction in the offspring in adult life. However, the mechanisms via which this occurs remain elusive, precluding the identification of potential therapy.
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