Influence of inflammatory cells on early-stage reperfusion injury of canine lung allograft
Journal Title: Di-er Junyi Daxue Xuebao - Year 2008, Vol 29, Issue 6
Abstract
Objective:To investigate the roles of donor alveolar macrophages and the recipient circulating neutrophils in early-stage reperfusion injury of lung allograft,and to study the interaction between the 2 kinds of cells.Methods: Twenty pairs of size- and weight-matched adult mongrel dogs were randomly assigned to 4 groups: C (control),D (leukocyte-depleted blood reperfusion),M (macrophage inhibition) and DM (leukocyte-depleted plus macrophage inhibition).The 20 cases of left lung transplantations were performed by the same surgeon.All procedures were identical,except that the donors in Group M and DM received the macrophage inhibitor gadolinium chloride (14 mg/kg) intravenously 24 h before operation,and that the recipients in Group D and DM underwent initial 10 min reperfusion with leukocyte-depleted blood collected from donors' inferior vena cava.All lung allografts were reperfused for 2 h.Results: Compared with Group D and C,macrophage inhibition ameliorated PO2/FiO2 and mean pulmonary arterial pressure (mPAP) consistently after 30 min reperfusion in Group M and DM; the parameters of lung reperfusion injury (malonaldehyde activity,wet/dry ratio) at 120 min after reperfusion were also significantly improved (P<0.05).Initial leukocyte-depleted reperfusion had no remarkable influence on allograft reperfusion injury,although it reduced pulmonary leukostasis (myeloperoxidase activity) significantly at 120 min after reperfusion.There were no significant interactions between leukocyte-depletion and macrophage inhibition in oxygenation,mPAP,wet/dry ratio,malonaldehyde and myeloperoxidase activity.Conclusion: It is the donor alveolar macrophages,not the recipient circulating neutrophils that can aggravate the inflammatory cascade in lung allografts during 2 h after reperfusion and no interaction is detected between them.
Authors and Affiliations
Xing-an WANG
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