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Statin treatment depresses the fetal defence to acute hypoxia via increasing nitric oxide bioavailability
Author(s) -
Kane Andrew D.,
Herrera Emilio A.,
Hansell Jeremy A.,
Giussani Dino A.
Publication year - 2012
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2011.217968
Subject(s) - pravastatin , fetus , hypoxia (environmental) , medicine , endocrinology , circulatory system , nitric oxide , fetal circulation , anesthesia , chemistry , pregnancy , cholesterol , biology , placenta , oxygen , organic chemistry , genetics
Non‐technical summary The fetal cardiovascular defence to episodes of reduced oxygenation, or acute hypoxia, includes redistribution of the cardiac output away from peripheral and towards essential circulations, such as those perfusing the brain – the so called brain‐sparing effect. The peripheral vasoconstriction is triggered by a chemoreflex and maintained by constrictor hormones. Nitric oxide (NO) synthesis during hypoxia opposes these mechanisms, but the balance of all effects favours constriction. Statins are drugs commonly used to lower cholesterol. Since women are delaying pregnancy until later in life, there is increasing clinical interest in treating pregnant women with statins. However, statins have other effects, including increasing NO levels, and their effects on the physiology of the fetus are completely unknown. Here, we show that fetal exposure to statins depresses the fetal peripheral constrictor response to acute hypoxia via increasing NO bioavailability. Use of statins in pregnancy should be viewed with caution.