title: In-utero and neonatal exposure to secondhand smoke causes vascular dysfunction in newborn rats.
abstract: OBJECTIVE
  We sought to determine the effects of secondhand smoke (SHS) exposure on vascular reactivity in newborn and infant rats.
  
  
  BACKGROUND
  Secondhand smoke exposure increases cardiovascular risk. Secondhand smoke-induced endothelial dysfunction has been demonstrated in older teenagers and young adults. We have previously shown in adult rabbits that SHS induces atherogenesis and endothelial dysfunction. The effects of SHS on vascular function in the offspring of SHS-exposed mothers and in infants are unknown.
  
  
  METHODS
  In this study the effects of in-utero (21 days) and neonatal (28 days) exposure to SHS were examined in 80 rats, 4 weeks of age, in a 2-by-2 design study. Rats were exposed to sidestream smoke in smoking chambers. Aortic rings were excised and isometric force responses to phenylephrine, acetylcholine, A23187 and nitroglycerin were studied in organ baths.
  
  
  RESULTS
  Neonatal SHS exposure reduced animal weight (p=0.009). In-utero exposure increased the sensitivity (decreased the EC50) of aortic rings to phenylephrine (p < 0.0005), as did neonatal exposure (p=0.01). Maximal contraction to phenylephrine was reduced by in-utero exposure (p=0.04). In-utero SHS exposure reduced maximal endothelium-dependent relaxation to acetylcholine (p=0.04) and increased the EC50 (p=0.05), suggesting impaired sensitivity to acetylcholine. In-utero exposure decreased the sensitivity (increased the EC50) to the endothelium-independent vasodilator nitroglycerin (p=0.003).
  
  
  CONCLUSIONS
  Secondhand smoke has detrimental effects on vascular smooth muscle function in the newborn.
authors.affiliation: Division of Cardiology, University of California, San Francisco, Moffitt Hospital, USA. stuart.hutchison@utoronto.ca
authors.forename: S J
authors.initials: SJ
authors.lastname: Hutchison
authors.forename: S A
authors.initials: SA
authors.lastname: Glantz
authors.forename: B Q
authors.initials: BQ
authors.lastname: Zhu
authors.forename: Y P
authors.initials: YP
authors.lastname: Sun
authors.forename: T M
authors.initials: TM
authors.lastname: Chou
authors.forename: K
authors.initials: K
authors.lastname: Chatterjee
authors.forename: P C
authors.initials: PC
authors.lastname: Deedwania
authors.forename: W W
authors.initials: WW
authors.lastname: Parmley
authors.forename: K
authors.initials: K
authors.lastname: Sudhir
mesh_terms: D000109:Acetylcholine / Q000008:administration & dosage; D000818:Animals; D000831:Animals, Newborn; D001013:Aorta, Thoracic / Q000187:drug effects / Q000503:physiopathology; D000001:Calcimycin / Q000008:administration & dosage; D003367:Cotinine / Q000097:blood; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D005260:Female; D005500:Follow-Up Studies; D007476:Ionophores / Q000008:administration & dosage; D018811:Maternal Exposure / Q000009:adverse effects*; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000503:physiopathology; D009538:Nicotine / Q000097:blood; D005996:Nitroglycerin / Q000008:administration & dosage; D010656:Phenylephrine; D011247:Pregnancy; D051381:Rats; D014028:Tobacco Smoke Pollution / Q000009:adverse effects*; D014652:Vascular Diseases / Q000097:blood / Q000139:chemically induced* / Q000503:physiopathology; D014661:Vasoconstriction / Q000187:drug effects; D014662:Vasoconstrictor Agents / Q000008:administration & dosage; D014665:Vasodilator Agents / Q000008:administration & dosage
chemical_list: D007476:Ionophores; D014028:Tobacco Smoke Pollution; D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; D010656:Phenylephrine; D000001:Calcimycin; D009538:Nicotine; D005996:Nitroglycerin; D003367:Cotinine; D000109:Acetylcholine