Ischemia-reperfusion injury (IRI) is inevitable in solid organ transplantation, due to the transplanted organ being ischemic for prolonged periods prior to transplantation followed by reperfusion. The complement molecule C3 is present in the circulation and is also synthesized by tissue parenchyma in early response to IRI and the final stable fragment of activated C3, C3d, can be detected on injured tissue for several days post-IRI. Complement activation post-IRI was monitored noninvasively by single photon emission computed tomography (SPECT) and CT using 99m Tc-recombinant complement receptor 2 (99m Tc-rCR2) in murine models of cardiac transplantation following the induction of IRI and compared to 99m Tc-rCR2 in C3-/- mice or with the irrelevant protein 99m Tc-prostate-specific membrane antigen antibody fragment (PSMA).

 

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