title: Chronic hypoxia augments uterine artery distensibility and alters the circumferential wall stress-strain relationship during pregnancy.
abstract: Pregnancy-associated increases in uterine artery (UA) blood flow are due, in part, to vasoactive and growth-related changes that enlarge UA diameter. Although active and passive mechanical factors can contribute to this enlargement, their role is less well understood. We hypothesized that pregnancy increased UA distensibility and/or decreased myogenic tone. Given the fetal growth restriction and lower UA flow seen under chronic hypoxia, we further hypothesized that chronic hypoxia opposed these normal active and passive mechanical changes. UA were isolated from 12 nonpregnant and 12 pregnant (0.7 gestation) guinea pigs housed under normoxia or chronic hypoxia (3,960 m) and studied by pressure myography. Pregnancy increased UA diameter similarly under normoxia and hypoxia. Although chronic hypoxia raised resting tone in UA from nonpregnant guinea pigs to approximately 20% and tone was greater in preconstricted pregnant chronically hypoxic vs. normoxic UA (both P<0.01), there was an absence of myogenic response (i.e., an increase in tone with rising pressure) in all groups. Pregnancy increased UA distensibility 1.5-fold but did not change stiffness or the stress-strain relationship. Compared with vessels from normoxic pregnant animals, hypoxic pregnancy raised UA distensibility fourfold, decreased stiffness (rate constant b=3.80+/-1.06 vs. 8.92+/-1.25, respectively, P<0.01), lowered elastin by 50%, and shifted the stress-strain relationship upward such that four times as much strain was present at a given stress. We concluded that increased distensibility and low myogenic tone contribute to enlarging UA diameter and raising UA blood flow during pregnancy. Chronic hypoxia exaggerates the rise in distensibility and alters the stress-strain relationship in ways that may provoke vascular injury.
authors.affiliation: Center for Women's Health Research and Cardiovascular Pulmonary Research Laboratory, Department of Prventive Medicine and Biometrics, University of Colorado at Denver, USA. stephanie.mateev@ucdmc.ucdavis.edu
authors.forename: Stephanie N
authors.initials: SN
authors.lastname: Mateev
authors.forename: Rhonda
authors.initials: R
authors.lastname: Mouser
authors.forename: David A
authors.initials: DA
authors.lastname: Young
authors.forename: Robert P
authors.initials: RP
authors.lastname: Mecham
authors.forename: Lorna G
authors.initials: LG
authors.lastname: Moore
mesh_terms: D000818:Animals; D001158:Arteries / Q000033:anatomy & histology / Q000502:physiology*; D001696:Biomechanical Phenomena; D001783:Blood Flow Velocity / Q000502:physiology; D001835:Body Weight / Q000502:physiology; D002908:Chronic Disease; D004730:Endothelium, Vascular / Q000033:anatomy & histology / Q000502:physiology*; D005260:Female; D006168:Guinea Pigs; D000860:Hypoxia / Q000503:physiopathology*; D011225:Pre-Eclampsia / Q000503:physiopathology; D011247:Pregnancy; D011270:Pregnancy, Animal / Q000502:physiology*; D012039:Regional Blood Flow / Q000502:physiology; D014599:Uterus / Q000098:blood supply* / Q000502:physiology; D014664:Vasodilation / Q000502:physiology*