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Experimental Study Of Cytokine And Lung Ischemia-reperfusion Injury Induced By Unilateral Blocking Pulmonary Artery And Veins

Posted on:2010-12-03Degree:MasterType:Thesis
Country:ChinaCandidate:M YangFull Text:PDF
GTID:2194330302955739Subject:Oncology
Abstract/Summary:PDF Full Text Request
Following with the surgical technique's rapid development, more and more patients who suffered from local advanced non-small-cell lung cancer received operation, which gave satisfactory short-term and long-term effect. Blocking single-side pulmonary artery and veins was one of the techniques usually used in pulmonary surgery, which could reduce bleeding and make the operation easier. This technique would provide more opportunity to those who could not tolerate total pneumonectomy because of their cardiopulmonary function. However, there was few study on pathophysiological characteristic of lung ischemia-reperfusion injury induced by unilateral blocking pulmonary artery and veins. The present study was performed to investigate following problems in lung ischemia-reperfusion injury induced by unilateral blocking pulmonary artery and veins.StudyⅠEstablishment of rabbit lung ischemia-reperfusion injury model induced by unilateral blocking pulmonary artery and veinsObjective: To introduce rabbit lung ischemia-reperfusion injury model applied to the technique of unilateral blocking pulmonary artery and veins.Methods: 72 New Zealand rabbits were randomly divided into 2 groups: groupⅠ, control group; groupⅡ, unilateral blocking pulmonary artery and veins. GroupⅠjust underwent thoracic and denudated pulmonary artery and veins. GroupⅡblocked left pulmonary artery and veins for 1 hour, then removed artery clamp from pulmonary veins and artery in turn. Partial pressure of oxygen, the content of MDA and the wet/dry ratio of the lung tissue were recorded at the time of opening chest, 1 hour after pulmonary artery and veins blocking and 1, 2, 4, 6 hours following reperfusion. Pathological changes of the lung were also observed at each time point.Results: All rabbits were survived after surgery. The arterial partial pressure of oxygen in groupⅠwas significantly lower than that in groupⅡ(P<0.05). And there were significant different in MDA and wet/dry ratio between groupⅠand groupⅡ(P<0.05). Pathological study revealed that obvious injury happened at the time of 4 hours reperfusion in groupⅡ, while the pathologic changes began to recover at the time of 6 hours reperfusion.Conclusions: The model is based on the technique of unilateral blocking pulmonary artery and veins in pulmonary surgery, which is feasible and reliable, and this thus can be used for following study.StudyⅡChange of cytokines in lung and plasma during lung ischemia-reperfusion injury induced by unilateral blocking pulmonary artery and veinsObjective: To investigate the characterization of cytokines in lung ischemia- reperfusion injury induced by blocking pulmonary artery and veins.Methods: 72 New Zealand rabbits were randomly divided into 2 groups: groupⅠ, control group; groupⅡ, unilateral blocking pulmonary artery and veins. The model was established as described in studyⅠ. The contents of TNF-αand IL-8, IL-10 of lung tissue and plasma were recorded at the time of opening chest, 1 hour after pulmonary artery and veins blocking, and 1, 2, 4, 6 hours following reperfusion. Results: The level of TNF-αin lung tissue was significantly higher at the time of 2 hours reperfusion in groupⅡthan that in groupⅠ, which peaked 4 hours following reperfusion in groupⅡ. And the content of IL-8 of lung tissue increased significantly after 4 hours reperfusion (P<0.05), while IL-10 increased after 6 hours (P<0.05). However, TNF-αsecretion in plasma was significantly detected after 6 hours reperfusion. A trend to increased induction of IL-8 and IL-10 of plasma was noted which was not significantly different between groupⅠand groupⅡ.Conclusions: The content of TNF-αand IL-8, IL-10 increases significantly in lung tissue after ischemia-reperfusion, while the trend in plasma is delayed.StudyⅢThe effect of exogenous interleukin-10 on relieving lung ischemia-reperfusion injury induced by unilateral blocking pulmonary artery and veinsObjective: To investigate the effect of exogenous interleukin-10 on lung ischemia-reperfusion injury induced by blocking pulmonary artery and veins.Methods: 24 New Zealand rabbits were randomly divided into 4 groups: groupⅠ, control group; groupⅡ, blocking left pulmonary artery and veins; groupⅢ, normal sodium+blocking left pulmonary artery and veins, groupⅣ, IL-10+blocking left pulmonary artery and veins. The model was established as described in studyⅠ. Lung ischemia reperfusion injury (IRI) was induced by blocking Left pulmonary artery and veins for 1 hour then opening for 4 hours. Normal sodium solution was injected into the trachea before blocking among groupⅢ, while IL-10 (20μg/kg) was injected into the trachea among groupⅣ. Lung function was evaluated by partial pressure of oxygen (PaO2) four hours after reperfusion from pulmonary vein. Then the rabbits were killed with their left lung taken out to undergo pathological examination. The contents of MDA,MPO,TNF-α,IL-8 and wet/dry ratio of lung tissue were also detected.Results: Compare with groupⅠ, The PaO2 level of groupⅡwas significantly lower(P<0.01). And The W/D ratio, levels of MDA, MPO, TNF-αand IL-8 of groupⅡsignificantly increased (P<0.01). The PaO2 level of groupⅣwas significantly higher than those of groupⅡ(P<0.05). The W/D ratio, levels of MDA and MPO of groupⅣwere significantly lower than those of groupⅡ(P<0.05). The level of TNF-αof groupⅣwas significantly lower than that of groupⅡ(P<0.01). However, there was no significantly difference between groupⅢand groupⅡon the index mentioned before. Fewer tissue edema and interstitial inflammation were found in lungs of groupⅣ.Conclusions: Exogenous IL-10 can ameliorate lung ischemia-reperfusion injury induced by unilateral blocking Left pulmonary artery and veins.
Keywords/Search Tags:unilateral blocking pulmonary artery and veins, ischemia-reperfusion, lung injury, cytokines, interleukin-10
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