Prevention and treatment for reperfusion injuny in thoracic surgery

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Importance of reactive oxygen species released through interaction of leukocyte-endothelial cell in ischemia-reperfusion injury of the lung is not yet fully understood. A novel selectin blocker OJ-R9188, which inhibits the interaction may alleviate oxidative stress and pulmonary dysfunction after warm ischemia reperfusion. Rat lungs were reperfused at 37℃ for 60 min with an ex vivo model, and were divided into three groups (n=10). In Fresh group, lungs were reperfused immediately after harvest. In OJ-R (-) and OJ-R (+) groups, lungs were reperfused after warm ischemia at 37℃ for 90 min. In OJ-R (+) group, rats received 100 μg/body of OJ-R9188 intravenously 10 min before the harvest. Electron spin resonance method was used to assess the direct scavenging activity of OJ-R9188. Both shunt fractions and wet/dry weight ratios of the lung tissue after reperfusion in OJ-R (+) group were significantly lower than those in OJ-R (-) group. Oxidative DNA damage in the alveolar wall of OJ-R (+) group, assessed by immunohistochemical quantitation of 8-hydroxy-2'deoxyguanosine, was significantly lower than that of OJ-R (-) group. Immunostaining of 3-nitro-L-tyrosine, which represents nitric oxide-mediated oxidative damage, was also more intense in OJ-R (-) group than in OJ-R (+) group. Direct scavenging activity of OJ-R9188 was not observed, and the number of leukocytes infiltrated to the lung tissue as seen by myeloperoxidase activity was not different between OJ-R (-) and OJ-R (+) groups. A novel selectin blocker OJ-R9188 improves pulmonary function after warm ischemia-reperfusion and alleviates reperfusion-induced oxidative alveolar damage.