title: Inflammation-induced fetal growth restriction in rats is associated with altered placental morphometrics.
abstract: BACKGROUND
  Evidence links alterations in placental shape and size to fetal growth restriction (FGR). Here we determined whether alterations in placental morphometrics are linked to FGR induced by abnormal maternal inflammation.
  
  
  METHODS
  We used an inflammation-induced model of FGR in which pregnant rats receive lipopolysaccharide (LPS) on gestational days (GD) 13.5-16.5. Fetal weights were matched to various parameters of placental morphometrics including weight, area, minor and major axes lengths and thickness.
  
  
  RESULTS
  Compared with saline administration, LPS administration was associated with altered placental morphometrics, including reduced placental weight, decreased placental area and a trend towards reduced placental thickness. When data were dichotomized as FGR or normal-sized fetuses within treatment groups, a significant increase in the placental-weight-to-fetal-weight ratio and placental thickness was observed only in the saline-associated FGR subgroup. Multivariable linear regression revealed that the lengths of the major and minor placental axes were predictors of fetal weight, regardless of treatment modality. Subgroup regression analysis by treatment revealed that the lengths of the major and minor placental axes were predictors of fetal weight in the saline-treatment group while only the minor placental axis was a predictor of fetal weight in the LPS cohort. Finally, placental area and the length of the minor placental axis were correlated with implantation site location only in the saline-treatment group.
  
  
  CONCLUSIONS
  These findings indicate that inflammation-induced FGR is associated with alterations in placental morphometrics. Our data reveal that the mechanisms leading to inflammation-induced FGR may be different from the mechanisms leading to idiopathic FGR.
authors.affiliation: Department of Biomedical and Molecular Sciences, Queen's University, Kingston, Ontario K7L 3N6, Canada. Electronic address: 4tc16@queensu.ca.
authors.forename: T
authors.initials: T
authors.lastname: Cotechini
authors.affiliation: Clinical Research Centre, Kingston General Hospital, Kingston, Ontario, Canada; Department of Public Health Sciences, Queen's University, Kingston, Ontario, Canada.
authors.forename: W J
authors.initials: WJ
authors.lastname: Hopman
authors.affiliation: Department of Biomedical and Molecular Sciences, Queen's University, Kingston, Ontario K7L 3N6, Canada. Electronic address: grahamc@queensu.ca.
authors.forename: C H
authors.initials: CH
authors.lastname: Graham
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D010064:Embryo Implantation; D005260:Female; D047109:Fetal Development; D005317:Fetal Growth Retardation / Q000276:immunology* / Q000473:pathology; D020567:Fetal Weight; D016014:Linear Models; D008070:Lipopolysaccharides; D010920:Placenta / Q000473:pathology; D010929:Placentation; D011247:Pregnancy; D017208:Rats, Wistar; D012965:Sodium Chloride
chemical_list: D008070:Lipopolysaccharides; D012965:Sodium Chloride
keywords: Fetal growth restriction; Inflammation; Minor axis; Placenta; Placental morphometry; Pre-eclampsia