title: Cigarette exposure induces changes in maternal vascular function in a pregnant mouse model.
abstract: Smoking is associated with multiple adverse pregnancy outcomes, including fetal growth restriction. The objective of this study was to determine whether cigarette smoke exposure during pregnancy in a mouse model affects the functional properties of maternal uterine, mesenteric, and renal arteries as a possible mechanism for growth restriction. C57Bl/CJ mice were exposed to whole body sidestream smoke for 4 h/day. Smoke particle exposure was increased from day 4 of gestation until late pregnancy (day 16-19), with mean total suspended particle levels of 63 mg/m(3), representative of moderate-to-heavy smoking in humans. Uterine, mesenteric, and renal arteries from late-pregnant and virgin mice were isolated and studied in a pressure-arteriograph system (n = 23). Plasma cotinine was measured by ELISA. Fetal weights were significantly reduced in smoke-exposed compared with control fetuses (0.88 +/- 0.1 vs. 1.0 +/- 0.08 g, P < 0.02), while litter sizes were not different. Endothelium-mediated relaxation responses to methacholine were significantly impaired in both the uterine and mesenteric vasculature of pregnant mice exposed to cigarette smoke during gestation. This difference was not apparent in isolated renal arteries from pregnant mice exposed to cigarette smoke; however, relaxation was significantly reduced in renal arteries from smoke-exposed virgin mice. In conclusion, we found that passive cigarette smoke exposure is associated with impaired vascular relaxation of uterine and mesenteric arteries in pregnant mice. Functional maternal vascular perturbations during pregnancy, specifically impaired peripheral and uterine vasodilation, may contribute to a mechanism by which smoking results in fetal growth restriction.
authors.affiliation: Magee-Womens Research Institute, 204 Craft Ave., Pittsburgh, PA 15213, USA. rgandley@mwri.magee.edu
authors.forename: Robin E
authors.initials: RE
authors.lastname: Gandley
authors.forename: Arun
authors.initials: A
authors.lastname: Jeyabalan
authors.forename: Ketaki
authors.initials: K
authors.lastname: Desai
authors.forename: Stacy
authors.initials: S
authors.lastname: McGonigal
authors.forename: Jennifer
authors.initials: J
authors.lastname: Rohland
authors.forename: Julie A
authors.initials: JA
authors.lastname: DeLoia
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D001835:Body Weight / Q000502:physiology; D003367:Cotinine / Q000097:blood; D004195:Disease Models, Animal; D005260:Female; D005317:Fetal Growth Retardation / Q000209:etiology* / Q000503:physiopathology; D008638:Mesenteric Arteries / Q000502:physiology; D051379:Mice; D008810:Mice, Inbred C57BL; D009929:Organ Size / Q000502:physiology; D011247:Pregnancy; D011249:Pregnancy Complications, Cardiovascular / Q000209:etiology* / Q000503:physiopathology; D012077:Renal Artery / Q000502:physiology; D012907:Smoking / Q000009:adverse effects*; D014028:Tobacco Smoke Pollution / Q000009:adverse effects*; D055988:Uterine Artery / Q000502:physiology; D014664:Vasodilation / Q000502:physiology
chemical_list: D014028:Tobacco Smoke Pollution; D003367:Cotinine