title: Cardiovascular function in mice during normal pregnancy and in the absence of endothelial NO synthase.
abstract: In humans, the increased cardiovascular demands of pregnancy are met by increases in cardiac output (CO), stroke volume (SV), plasma volume (PV), and cardiac and aortic inner dimensions and a concurrent decrease in arterial pressure that indicates a fall in total peripheral vascular resistance. The mechanisms responsible for these changes are incompletely understood, but NO synthase (NOS) is believed to play a central role. We assessed whether C57Bl/6J (B6) mice show similar changes and whether these changes are altered in mice lacking the gene for endothelial NOS (eNOS). The CO of B6 mice increased 28% by day 9.5 of gestation because of a 25% increase in SV, and increased 48% by day 17.5 because of a 41% increase in SV. The increase in SV at day 17.5 was associated with a 27% increase in PV, a 15% decrease in arterial pressure, and 10% to 15% increases in aortic and left-ventricular inner dimensions. In the absence of eNOS, CO increased 22% by day 9.5 because of increases in SV (14%) and heart rate (9%), but increased no further by day 17.5. SV near term was lower than B6 mice despite similar 26% increases in PV and 14% decreases in arterial pressure in association with blunted left-ventricular chamber enlargement. All reported changes are P<0.05. We conclude that cardiovascular changes during pregnancy are similar in B6 mice and humans. eNOS plays a critical role in increasing stroke volume in late gestation by promoting cardiac remodeling.
authors.affiliation: Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Ontario, Canada.
authors.forename: Shathiyah
authors.initials: S
authors.lastname: Kulandavelu
authors.forename: Dawei
authors.initials: D
authors.lastname: Qu
authors.forename: S Lee
authors.initials: SL
authors.lastname: Adamson
mesh_terms: D000818:Animals; D001794:Blood Pressure; D001810:Blood Volume; D002302:Cardiac Output / Q000502:physiology; D002320:Cardiovascular Physiological Phenomena; D004452:Echocardiography; D005260:Female; D006339:Heart Rate; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D052250:Nitric Oxide Synthase Type III / Q000172:deficiency* / Q000502:physiology; D011247:Pregnancy / Q000502:physiology*; D013318:Stroke Volume; D013997:Time Factors; D020257:Ventricular Remodeling
chemical_list: D052250:Nitric Oxide Synthase Type III