title: Endotoxemia severely affects circulation during normoxia and asphyxia in immature fetal sheep.
abstract: OBJECTIVE
  The purpose of the present study was to determine whether endotoxins (lipopolysaccharides, LPS) affect the fetal cardiovascular system in a way likely to cause brain damage.
  
  
  METHODS
  Thirteen fetal sheep were chronically instrumented at a mean gestational age of 107 +/- 1 days. After control measurements of organ blood flow (microsphere method), blood gases, and acid base balance were obtained, seven of 13 fetuses received LPS (53 +/- 3 microg/kg fetal weight) intravenously. Sixty minutes later, asphyxia was induced by occlusion of the maternal aorta for 2 minutes. Measurements of organ blood flows were made at -60, -1, +2, +4, +30, and +60 minutes.
  
  
  RESULTS
  Unlike in the control group, after LPS infusion there was a significant decrease in arterial oxygen saturation (-46%; P <.001) and pH (P <.001). In LPS-treated fetuses the portion of combined ventricular output directed to the placenta decreased significantly (-76%; P <.001), whereas output to the fetal body (+60%; P <.001), heart (+167%; P <.05), and adrenals (+229%; P <.01) increased. Furthermore, during asphyxia circulatory centralization was impaired considerably in LPS-treated fetuses, and there was clear evidence of circulatory decentralization. This decentralization caused a severe decrease in cerebral oxygen delivery by 70%. Within 30 minutes after induction of asphyxia five of seven LPS-treated fetuses died, whereas all control fetuses recovered completely.
  
  
  CONCLUSIONS
  Endotoxemia severely impaired fetal cardiovascular control during normoxia and asphyxia, resulting in a considerable decrease in cerebral oxygen delivery. These effects might have important effects in the development of fetal brain damage associated with intrauterine infection.
authors.affiliation: Department of Obstetrics and Gynecology, University of Bochum, Bochum, Germany.
authors.forename: Y
authors.initials: Y
authors.lastname: Garnier
authors.forename: A
authors.initials: A
authors.lastname: Coumans
authors.forename: R
authors.initials: R
authors.lastname: Berger
authors.forename: A
authors.initials: A
authors.lastname: Jensen
authors.forename: T H
authors.initials: TH
authors.lastname: Hasaart
mesh_terms: D000818:Animals; D001237:Asphyxia / Q000503:physiopathology*; D001794:Blood Pressure; D002245:Carbon Dioxide / Q000097:blood; D002302:Cardiac Output; D019446:Endotoxemia / Q000150:complications*; D005260:Female; D005315:Fetal Diseases / Q000503:physiopathology*; D005865:Gestational Age; D006340:Heart Rate, Fetal; D006439:Hemodynamics; D006863:Hydrogen-Ion Concentration; D008070:Lipopolysaccharides / Q000494:pharmacology; D010100:Oxygen / Q000097:blood; D011247:Pregnancy; D012756:Sheep
chemical_list: D008070:Lipopolysaccharides; D002245:Carbon Dioxide; D010100:Oxygen