| First Author | Kulandavelu S | Year | 2006 |
| Journal | Hypertension | Volume | 47 |
| Issue | 6 | Pages | 1175-82 |
| PubMed ID | 16636199 | Mgi Jnum | J:135750 |
| Mgi Id | MGI:3794398 | Doi | 10.1161/01.HYP.0000218440.71846.db |
| Citation | Kulandavelu S, et al. (2006) Cardiovascular function in mice during normal pregnancy and in the absence of endothelial NO synthase. Hypertension 47(6):1175-82 |
| abstractText | 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. |
