title: Effects of perfluorohexane vapor in the treatment of experimental lung injury.
abstract: BACKGROUND
  We investigated the effects of vaporized perfluorohexane (PFH) on pulmonary vascular tone, pulmonary vascular resistance and peak inspiratory pressure as well as lipid mediator formation in the treatment of calcium ionophore induced lung injury in a model of the isolated perfused and ventilated rabbit lungs.
  
  
  METHODS
  Lung injury was induced in isolated perfused and ventilated rabbit lungs by calcium ionophore A23187. Lungs were treated with either 4.5 vol.% (4.5 vol.% PFH; n = 6) or 18 vol.% (18 vol.% PFH; n = 6) PFH. Six lungs remained untreated (Control). In addition 5 lungs (PFH-sham) remained uninjured receiving 18 vol.% PFH only. Mean pulmonary artery pressure (mPAP), peak inspiratory pressure (P(max)), and lung weight (weight) were monitored for 120 min. Experiments were terminated before when the increase in lung weight exceeded 40 g. Perfusate samples were taken at regular intervals for analysis of TXB(2), 6-keto-PGF(1) and LTB(4).
  
  
  RESULTS
  Controls reached the study end point significantly earlier than both PFH groups. Significant differences were found for a weight gain of 10 g and 20 g between the control and the 4.5 vol.% PFH and the 18 vol.% PFH. Differences in mPAP were more pronounced in the 4.5 vol.% PFH. However increases in P(max) were more marked in 4.5 vol.% PFH. TXA(2)-, PGI(2)-, and LTB(4)-levels were significantly lower in PFH groups. Uninjured lungs remained unaffected by the presence of 18 vol.% PFH.
  
  
  CONCLUSIONS
  Inflammatory lung injury was attenuated by the treatment with 4.5 vol.% PFH and 18 vol.% PFH vapor in the isolated perfused rabbit lung. Therapeutic effects were more pronounced with a concentration of 4.5 vol.% PFH.
authors.affiliation: Department of Anesthesiology and Intensive Care Medicine, University Hospital Carl Gustav Carus, Dresden, Germany. bleyl@rcs.urz.tu-dresden.de
authors.forename: Jörg U
authors.initials: JU
authors.lastname: Bleyl
authors.forename: Axel R
authors.initials: AR
authors.lastname: Heller
authors.forename: Manuel
authors.initials: M
authors.lastname: Heintz
authors.forename: Matthias
authors.initials: M
authors.lastname: Schlemmer
authors.forename: Roland
authors.initials: R
authors.lastname: Koch
authors.forename: Marcelo Gama
authors.initials: MG
authors.lastname: de Abreu
authors.forename: Matthias
authors.initials: M
authors.lastname: Hübler
authors.forename: Peter M
authors.initials: PM
authors.lastname: Spieth
authors.forename: Thea
authors.initials: T
authors.lastname: Koch
mesh_terms: D000818:Animals; D000001:Calcimycin; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D011464:Epoprostenol / Q000378:metabolism; D005260:Female; D005466:Fluorocarbons / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use*; D066298:In Vitro Techniques; D007476:Ionophores; D007975:Leukotriene B4 / Q000378:metabolism; D008168:Lung / Q000098:blood supply / Q000187:drug effects / Q000473:pathology; D055370:Lung Injury / Q000139:chemically induced / Q000188:drug therapy* / Q000378:metabolism; D009929:Organ Size / Q000187:drug effects; D011175:Positive-Pressure Respiration; D011651:Pulmonary Artery / Q000187:drug effects / Q000503:physiopathology; D011652:Pulmonary Circulation / Q000187:drug effects; D011654:Pulmonary Edema / Q000517:prevention & control; D011817:Rabbits; D013928:Thromboxane A2 / Q000378:metabolism; D014655:Vascular Resistance / Q000187:drug effects; D014835:Volatilization
chemical_list: D005466:Fluorocarbons; D007476:Ionophores; D007975:Leukotriene B4; D000001:Calcimycin; D013928:Thromboxane A2; D011464:Epoprostenol; C078626:perflexane