Elucidation of pathophysiology of ischemia reperfusion injury jn isolated perfused rat lungs

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Isolated rat lung model perfused with Krebs-Henseleit solution added with 4% albumin was developed, in which right and left pulmonary arteries were isolated to enable preferential perfusion to each one of lungs with the same ventilation to the both lung maitained. Our hypothesis is that the genes of inflammatory cytokines would be induced in ischemic lung to cause the ischemia-reperfusion injury. After the left lung were exposed to ischemia for 60-100 min followed by reperfusion for 0-20 min, a few strips weighing about 100 mg were obtained separately in the perfused and ischemic lungs. Total RNA was extracted from these lung specimens by the method described by Chomczynski and Sacchi and DNAs of TNF-α, IL-1β, IL-10 and Interferon-γ were obtained by RT-PCR using MPCR primer, optimal temperatures and cycles. The obtained DNAs were electrophoresed in the agarose gel added with ethidium bromide. The genes of TNF-α, IL-1β and IL-6 in the control right lung lobe were detected more than in the left ischemic lung. Contrarily, the gene of IL-10 in the ischemic lung was detected more than in the control right lobe. Interfeorn-γ did not show significent difference between the both lobes. The reason why the inflammatory cyotokines appeared greater in the control right lung lobe than in the ischemic left lobe was supposed to the amount of endotoxin contained in the standard bovine serum albumin which were preferentially perfused through right lung during ischemia of left lung. Although the inflammatory cytokines were induced in the right and left lungs, left lung only showed ischemia reperfusion injury which suggested that interactions of any mediators induced by inflammatory cytokines and oxygen radicals would attack the cell membrane and cause the pulmonary edema.