Ischemia-Induced Interleukin-8 Release After Human Heart Transplantation

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Abstract
Background Interleukin-8 (IL-8) secreted from endothelial cells is a powerful neutrophil chemoattractant and activator. We hypothesized that human endothelial cells deprived of oxygen would secrete IL-8, which might translate into elevated IL-8 production after cardiac ischemia. Furthermore, we hypothesized that coronary sinus (CS) IL-8 levels would be particularly high after cardiac preservation for transplantation, due to extended ischemic times. Methods and Results Human saphenous vein endothelial cells exposed to a hypoxic environment (P o 2 P <.05). Further analysis of the CS samples revealed that a biochemical marker of myocyte injury (myoglobin) was similarly elevated in the CTX patients compared with the non-CTX patients (3340±625 versus 1151±525 ng/mL, respectively, P <.05). Conclusions These differences may reflect the longer ischemic times of CTX compared with non-CTX hearts (161±10 versus 80±6 minutes, P <.0001) and suggest that the neutrophil chemoattractant/activator IL-8 may contribute to myocyte injury after prolonged hypothermic cardiac ischemia, as occurs during human cardiac transplantation.