title: Effects of propofol on hemodynamic and inflammatory responses to endotoxemia in rats.
abstract: OBJECTIVE
  To document the effects of propofol on the hemodynamic and inflammatory responses to endotoxemia in an animal model.
  
  
  METHODS
  Randomized, prospective laboratory study.
  
  
  METHODS
  University experimental laboratory.
  
  
  METHODS
  Thirty-two male rats.
  
  
  METHODS
  The animals were randomly assigned to one of four groups: a) endotoxemia group (n = 8), which received intravenous Escherichia coli endotoxin (15 mg/kg over 2 mins); b) control group (n = 8), which was treated identically to the endotoxemia group except for the substitution of 0.9% saline for endotoxin; c) propofol group (n = 8), which was treated identically to the control group but also received propofol (10 mg/kg bolus, followed by infusion at 10 mg/kg/hr) immediately after the injection of 0.9% saline; and d) propofol-endotoxemia group (n = 8), which was treated identically to the endotoxemia group with the additional administration of propofol (10 mg/kg bolus, followed by infusion at 10 mg/kg/hr) immediately after endotoxin injection.
  
  
  RESULTS
  Hemodynamics, arterial blood gases, and acid-base status were recorded and the blood propofol concentrations and plasma cytokine concentrations were measured during the 5-hr observation. Microscopic findings of lung tissue for each group were obtained at necropsy. The systolic arterial pressure and heart rate of the propofol-endotoxemia group were similar to those of the endotoxemia group. The increases in the plasma cytokine (tumor necrosis factor, interleukin-6, and interleukin-10) concentrations, in the base deficit, and in the infiltration of neutrophils in the air space or vessel walls of the lungs were attenuated in the propofol-endotoxemia group compared with the endotoxemia group.
  
  
  CONCLUSIONS
  Propofol attenuated cytokine responses, base deficit, and activation of neutrophils to endotoxemia. These findings suggest that propofol may inhibit inflammatory response and prevent the development of metabolic acidosis during endotoxemia.
authors.affiliation: Department of Anesthesiology and Intensive Care Medicine, School of Medicine, Kanazawa University, Japan. taniyan@med.kanazawa-u.ac.jp
authors.forename: T
authors.initials: T
authors.lastname: Taniguchi
authors.forename: K
authors.initials: K
authors.lastname: Yamamoto
authors.forename: N
authors.initials: N
authors.lastname: Ohmoto
authors.forename: K
authors.initials: K
authors.lastname: Ohta
authors.forename: T
authors.initials: T
authors.lastname: Kobayashi
mesh_terms: D000818:Animals; D004353:Drug Evaluation, Preclinical; D019446:Endotoxemia / Q000097:blood / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology; D004927:Escherichia coli Infections / Q000097:blood / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology; D006439:Hemodynamics / Q000187:drug effects; D006993:Hypnotics and Sedatives / Q000097:blood / Q000494:pharmacology / Q000627:therapeutic use*; D008168:Lung / Q000187:drug effects / Q000473:pathology; D008297:Male; D015742:Propofol / Q000097:blood / Q000494:pharmacology / Q000627:therapeutic use*; D011446:Prospective Studies; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D018746:Systemic Inflammatory Response Syndrome / Q000097:blood / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology
chemical_list: D006993:Hypnotics and Sedatives; D015742:Propofol