Partial splenic embolization in children with hypersplenism.

Partial splenic embolization (PSE) was successfully accomplished in 10 of 11 children, aged 2-9, who had portal hypertension or variceal bleeding. Nine of the 11 children had undergone portoenterostomy (Kasai operation) for biliary atresia, and two had portal vein thrombosis. After embolization these children had a longer period of fever (mean = 23.7 days) and elevated white blood cell (WBC) count (above 10,000, mean = 13.6 days) than adults who have undergone the same procedure. The leukopenia and thrombocytopenia of hypersplenism were corrected by PSE in seven of eight children, and the condition of the eighth child improved. Among ten patients who had experienced episodes of variceal hemorrhage, the frequency of bleeding episodes was reduced from an average of 2.87 per year before PSE to 0.67 per year after PSE. There were no splenic abscesses and no other significant complications of the treatment. Ultrasound (US) evaluation after embolization demonstrated hypoechogenicity of the infarcted areas and tiny, linear echoes scattered throughout the spleen typical of postinfarction intravascular gas. All nine children who underwent follow-up Tc-99m sulfur colloid scanning showed evidence of splenic regeneration, though none has had recurrence of clinical symptoms. Splenic regeneration following PSE may occur more frequently in children than in adults.

Bile secretion and liver cell heterogeneity in the rat.

The contribution of hepatocytes of different acinar zones to bile salt transport and to the secretion of the BSNDF was studied in the rat. Changes in the removal of 14C-taurocholate from blood, in the biliary secretion of taurocholate, and in canalicular flow were determined after damage of the periportal (acinar zone 1) or centrilobular (acinar zone 3) areas by allyl alcohol or bromobenzene, respectively. The extent of cell necrosis was quantitated by light microscopy, and the quality of the intracellular damage was assessed by electron microscopy. After either periportal or centrilobular damage, surviving cells responded to an intravenous infusion of taurocholate by secreting bile salts into bile at a rate similar to controls. However, following the administration of 14C-taurocholate at high concentrations and as a single bolus, the rate of removal of this isotope from blood was slower than in controls. Both experiments suggested that periportal and centrilobular hepatocytes had the capability for bile salt transport. Consequently, since the concentration of bile salts in sinusoidal blood at each zone determines the relative contribution of hepatocytes to bile salt transport, periportal cells probably transport the largest amount of bile salts reaching the acinus. Canalicular bile flow, on the other hand, decreased following centrilobular cell damage, and this was associated with a high concentration of bile salts in bile. This suggested that at bile salt loads near physiological concentrations, the predominant contribution of centrilobular hepatocytes is to the secretion of the BSNDF.