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Cytokine mRNA expression in unilateral ischemic-reperfused rat lung with salt solution supplemented with low-endotoxin or standard bovine serum albumin

¹Department of Critical Care Medicine and ²Department of Biochemical Genetics, Medical Research Institute, Graduate School, Tokyo Medical and Dental University, Bunkyo-ku, Tokyo 113-8519; and ³RIKEN, The Institute of Physical and Chemical Research, Wako, Saitama 351-0198, Japan

Submitted 29 July 2003 ; accepted in final form 8 September 2003

Our aim was to determine whether cytokine mRNA expression is induced by experimental manipulation including artificial perfusate or ischemia-reperfusion (I/R) in an isolated, perfused rat lung model. Constant pulmonary flow [Krebs-Henseleit solution supplemented with lowendotoxin (LE) or standard (ST) bovine serum albumin 4%, 0.04 ml/g body wt] and ventilation were maintained throughout. Right and left pulmonary arteries were isolated, and the left pulmonary artery was occluded for 60 min and then reperfused for 30 min. Analysis of tumor necrosis factor-, IL-1, IL-6, IL-10, and IFN- mRNA expression by RT-PCR and evaluation of vascular permeability by bronchoalveolar lavage (BAL) fluid albumin content were conducted separately in right and left lung. Both LE and ST groups (each 12 rats) showed increases in vascular permeability by I/R (BAL fluid albumin content: 5.53 ± 1.55 vs. 15.63 ± 8.87 and 4.76 ± 2.71 vs. 16.72 ± 4.85 mg·ml BAL fluid^-1·g lung dry wt^-1, mean ± SD; right vs. left lung in LE and ST groups, P < 0.05 between right and left). Cytokine mRNA expression was significantly higher in the I/R lung than in the control lung in the LE group, whereas it was higher in the control lung in the ST group (P < 0.05). mRNAs of not only proinflammatory but also anti-inflammatory cytokines were expressed in I/R lung, which are expected to aggravate I/R injury. The reversed pattern of cytokine mRNA expression in the ST group was possibly due to the longer perfusion of control lung with perfusate containing endotoxin, which caused no lung damage without I/R.

ischemia-reperfusion injury; reverse transcriptase-polymerase chain reaction; endotoxin

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