title: Effects of second-hand smoke and gender on infarct size of young rats exposed in utero and in the neonatal to adolescent period.
abstract: OBJECTIVE
  We sought to assess the effects of second-hand smoke (SHS) and gender on infarct size in young rats exposed in utero or in the neonatal to adolescent period, or both.
  
  
  BACKGROUND
  We previously demonstrated that exposure to SHS increases infarct size in a rat model of ischemia and reperfusion, with a dose-response relation. These results are consistent with epidemiologic studies demonstrating that SHS increases risk of death from heart disease.
  
  
  METHODS
  Thirty-one pregnant female rats were randomly divided into two groups: those exposed to SHS and a control group (non-SHS). After 3 weeks, each rat had given birth to 10 to 12 rats. One hundred one neonatal rats were divided into four groups according to exposure to SHS in utero (SHSu) and randomized to SHS exposure in the neonatal to adolescent period (SHSna). After 12 weeks, all rats were subjected to 17 min of left coronary artery occlusion and 2 h of reperfusion.
  
  
  RESULTS
  Birth mortality was higher in the SHSu group than in the non-SHSu group (11.9% vs. 2.8%, p < 0.001). Body weight of neonatal rats at 3 and 4 weeks in the two SHSu groups was lower than that of rats in the two non-SHSu groups (p < 0.001). Exposure to SHSna increased endothelin-1 levels in plasma (p = 0.001). In all 70 young rats who survived the neonatal period, infarct size (Infarct mass/Risk area x 100%) was greater in the SHSna groups than in the non-SHSna groups (p = 0.005) and in the male groups than in the female groups (p < 0.001).
  
  
  CONCLUSIONS
  Exposure to SHS in the neonatal to adolescent period and male gender increased myocardial infarct size in a young rat model of ischemia and reperfusion. These results are consistent with epidemiologic studies demonstrating that SHS increases the health risk to neonates and adolescents.
authors.affiliation: Department of Medicine and Cardiovascular Research Institute, University of California San Francisco, 94143-0124, USA.
authors.forename: B Q
authors.initials: BQ
authors.lastname: Zhu
authors.forename: Y P
authors.initials: YP
authors.lastname: Sun
authors.forename: K
authors.initials: K
authors.lastname: Sudhir
authors.forename: R E
authors.initials: RE
authors.lastname: Sievers
authors.forename: A E
authors.initials: AE
authors.lastname: Browne
authors.forename: L
authors.initials: L
authors.lastname: Gao
authors.forename: S J
authors.initials: SJ
authors.lastname: Hutchison
authors.forename: T M
authors.initials: TM
authors.lastname: Chou
authors.forename: P C
authors.initials: PC
authors.lastname: Deedwania
authors.forename: K
authors.initials: K
authors.lastname: Chatterjee
authors.forename: S A
authors.initials: SA
authors.lastname: Glantz
authors.forename: W W
authors.initials: WW
authors.lastname: Parmley
mesh_terms: D000804:Angiotensin II / Q000097:blood; D000818:Animals; D000831:Animals, Newborn; D001835:Body Weight; D019332:Endothelin-1 / Q000097:blood; D005260:Female; D008297:Male; D009203:Myocardial Infarction / Q000209:etiology / Q000473:pathology*; D015428:Myocardial Reperfusion Injury / Q000209:etiology / Q000473:pathology*; D009206:Myocardium / Q000473:pathology; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D012307:Risk Factors; D012737:Sex Factors; D014028:Tobacco Smoke Pollution / Q000009:adverse effects*
chemical_list: D019332:Endothelin-1; D014028:Tobacco Smoke Pollution; D000804:Angiotensin II