MAJOR HISTOCOMPATIBILITY COMPLEX EXPRESSION AND LUNG ISCHEMIA-REPERFUSION IN RATS

Background. Clinical studies in kidney and liver transplantation have suggested that poor early function is associated with increased graft loss due to rejection. Ischemia-reperfusion injury may contribute to r ejection by enhancing graft immunogenicity. Methods. A rat model of un ilateral in situ pulmonary ischemia-reperfusion was used to examine cl ass II major histocompatibility complex (MHC) antigen expression. The effects of deflation during ischemia (which augments subsequent injury ) as well as concurrent allostimulation were also examined, Major hist ocompatibility complex expression was examined 9 days after ischemia u sing the binding of radiolabeled anti-class II antibody and immunohist ochemistry. Results. Four hours of ischemia in full inflation or 2 hou rs of atelectatic ischemia both led to severe lung injury. Ischemia-re perfusion injury led to greater MHC expression in the ischemic lung co mpared with the nonischemic side. Allostimulation with mononuclear cel ls did not increase MHC expression in the nonischemic lung but did enh ance the increase found in the ischemic lung. This was not due to a gr aft-versus-host response because allostimulation with F-1 cells also l ed to a significant increase. Conclusions. Severe ischemic lung injury leads to significant increases in MHC expression, detectable after 9 days of reperfusion. Deflation during ischemia, which augments lung in jury, also augments increased MHC expression. Concurrent allostimulati on with foreign mononuclear cells appears to potentiate increased MHC expression after ischemia. Increases in graft MHC expression may enhan ce immunogenicity and increase the rejection response.