In the present study, we investigated the role of the spleen in experimental hepatic ischemia/reperfusion in the rat. After a 90‐min period of ischemia in the left and middle hepatic lobes, the ischemia was released and the liver was reperfused for up to 24 h. Plasma alanine aminotransferase reached a peak 3 h after the onset of reperfusion, and gradually decreased thereafter. A histological examination revealed evidence of hepatocellular necrosis and degeneration, especially 24 h after the onset of reperfusion. In addition, there was a noticeable accumulation of polymorphonuclear cells in the liver following ischemia/reperfusion. A splenectomy performed just prior to ischemia/reperfusion reduced both biochemical and histological hepatocellular injury. The number of polymorphonuclear cells in the liver following ischemia/reperfusion was significantly reduced in rats subjected to splenectomy, suggesting that the increase in polymorphonuclear cells may contribute to liver injury. The number of mononuclear cells also increased in the marginal zones of the spleen following ischemia/reperfusion, and appeared to be derived from the splenic monocyte/macrophage population, based on immunohistochemical studies. The spleen plays an important role in the pathogenesis of hepatic ischemia/reperfusion injury and the splenic monocyte/macrophage population contributes to liver damage.

No abstract

No abstract

Imaging and clinical features in 6 cirrhotic patients complicated with small hepatocellular carcinoma with a large spontaneous splenorenal shunt were studied in comparison with control patients without such a collateral. The diameter of portal vein (PV) was smaller than that of splenic vein (SV) measuring on an angiogram and the diametric ratio (PV/SV) was significantly smaller than that in control group. This fact, the diameter of PV was smaller than that of SV, brings a clue to find out a splenorenal shunt on the first examination using ultrasonography. The endoscopic findings suggested that a large splenorenal shunt may prevent development of advanced esophageal varices. The increased risk of recurrence hepatic encephalopathy in the patients with a large splenorenal shunt was indicated by clinical findings, and the therapeutic procedure as transcatheter arterial embolization therapy may induce encephalopathy as well.

No abstract