Role of spleen in hepatic ischemia reperfusion injury: Splenic congestion during ischemia accelerates leukocyte infiltration within the liver after reperfusion

Aim: The precise mechanism by which prophylactic splenectomy reduces hepatic ischemia-reperfusion injury (IRI) are still unclear. In this study, we focused on the histological changes of spleen during hepatic IRI, and tested how splenectomy provided cytoprotective effects against hepatic IRI.

Methods: Rats underwent 70% warm hepatic IRI with or without splenectomy prior to IRI. To determine whether splenic congestion by itself induces liver damage in the absence of hepatic IRI, we also undertook a splenic vein clamp model.

Results: Liver injury and macrophage and neutrophil infiltration into the liver after reperfusion were significantly depressed in the animals with prophylactic splenectomy, compared to those without splenectomy. Histology of the spleens showed noted congestion during hepatic ischemia (hepatic hilar clamp), which promptly disappeared after declamping. At 6 and 24 h after reperfusion, the spleens showed remarkable recongestion and parenchymal damage, and the splenic venous level of interleukin-2, which is secreted by T cells and enhances macrophage recruitment, and its mRNA levels within the spleen were significantly elevated. In the splenic vein clamp model, the splenic vein clamp by itself produced a certain liver injury and macrophage infiltration within liver even without hepatic IRI.

Conclusion: Spleen plays an important role as an accelerator in hepatic IRI, because splenic congestion and parenchymal damage during ischemia-reperfusion promote splenic IL-2 excretion and macrophage infiltration within the liver, which in turn exacerbate hepatic injury.