title: Prevention of ischemia reperfusion injury by positive pulmonary venous pressure in isolated rat lung.
abstract: Pulmonary ischemia-reperfusion (I/R) without tissue hypoxia induces inflammatory cytokine mRNA expression in the lung under the condition of 0 mm Hg pulmonary venous pressure (0PVP), which might be a cause of I/R injury. Our aim is to determine whether the pulmonary vascular endothelium expresses cytokine mRNAs and their corresponding proteins or develops I/R injury when positive PVP is maintained during ischemia to provide a positive stretch to the endothelium throughout the ischemic period. In isolated, perfused, and ventilated rat lungs, the right and left pulmonary arteries were isolated, and the left lung was selectively occluded for 60 min and then reperfused for 30 min. During ischemia, the left atrial pressure was maintained at 5 mm Hg (5PVP) or 0PVP. TNF-alpha, IL-1beta, IL-6, and IL-10 mRNA expression in the lungs was evaluated by RT-PCR and in situ hybridization, and the production and localization of corresponding proteins were determined by staining with fluorescence-labeled antibodies against the cytokines and an antibody against CD34. Pulmonary vascular/epithelial permeability was evaluated by measuring albumin content in bronchoalveolar lavage (BAL) fluid and wet/dry ratio. At 5PVP, there were no increases in the left lung perfusion pressure, albumin content in BAL fluid, wet/dry ratio, or expression of cytokine mRNAs and their corresponding proteins on the vascular endothelium by I/R. In contrast, at 0PVP, the increased expression of cytokine mRNAs and their corresponding proteins on the vascular endothelium by I/R was verified. The finding that the application of 5PVP during ischemia abolished the expression of cytokine mRNAs and their corresponding proteins as well as the I/R injury gives us new insights in the study of lung preservation for transplantation.
authors.affiliation: Department of Critical Care Medicine, Tokyo Medical and Dental University, Tokyo 113-8519, Japan.
authors.forename: Gabriela S
authors.initials: GS
authors.lastname: Georgieva
authors.forename: Shunichi
authors.initials: S
authors.lastname: Kurata
authors.forename: Satoshi
authors.initials: S
authors.lastname: Ikeda
authors.forename: Shu
authors.initials: S
authors.lastname: Teng
authors.forename: Iyoko
authors.initials: I
authors.lastname: Katoh
authors.forename: Yoshinobu
authors.initials: Y
authors.lastname: Eishi
authors.forename: Chieko
authors.initials: C
authors.lastname: Mitaka
authors.forename: Takasuke
authors.initials: T
authors.lastname: Imai
mesh_terms: D000818:Animals; D002199:Capillary Permeability / Q000276:immunology; D016207:Cytokines / Q000276:immunology; D005786:Gene Expression Regulation / Q000276:immunology; D007150:Immunohistochemistry; D008168:Lung / Q000098:blood supply* / Q000276:immunology / Q000473:pathology; D055370:Lung Injury; D008297:Male; D009924:Organ Culture Techniques; D011651:Pulmonary Artery / Q000276:immunology / Q000473:pathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000276:immunology / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D014690:Venous Pressure / Q000276:immunology
chemical_list: D016207:Cytokines