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Levels of the lysosomal enzymes beta-glucuronidase and beta-hexosaminidase were determined in tissues from rats at 1-7 weeks after permanent bile duct occlusion (28 animals) and sham operation (16 animals). With increasing duration of bile duct occlusion, increasing levels were found in the liver and spleen, whereas levels were unaffected in the pancreas, kidneys, brain, muscle, and skin. Histochemical investigation showed that the lysosomal enzymes accumulated in the hepatocytes and in the increasing numbers of reticuloendothelial cells of the liver and spleen during cholestasis. No significant accumulation of lysosomal enzymes was seen in the pancreas. In preparations of isolated hepatocytes and non-parenchymal cells increased specific activity of lysosomal enzymes in cholestasis appeared in both cellular fractions. It is assumed that the serum increase of lysosomal enzymes in late cholestasis is partly due to a release from activated macrophages in the liver and spleen.

A case of liver metastases from colon carcinoma showing a low density ring sign is presented. Cadaver studies suggest that this sign can be produced by compressed liver cells and sinusoids.

Studies of the activity uptake of radiolabelled 99mTc2S7 colloid in different tissues showed a moderately increased uptake in the lung 1 week and a greatly increased uptake 3 weeks after permanent bile duct occlusion. Three weeks after bile duct occlusion the activity uptake was also slightly increased in the spleen and moderately reduced in the liver. In pulmonary tissue of cholestatic rats, the levels of alkaline and acid phosphatase, beta-glucuronidase, and beta-hexosaminidase were determined after 6 weeks. The pulmonary contents of beta-glucuronidase was increased tenfold, and that of beta-hexosaminidase was increased fourfold in cholestasis. Histochemical investigation showed that the lysosomal enzymes were located in the macrophages, which in cholestasis were abundant in alveolar walls and inside alveoli. Macrophages were also frequently seen to engorge pulmonary veins.

Two female patients (75 and 68 yr old) developed jaundice 4 and 7 weeks respectively after treatment with flucloxacillin. Liver biopsies showed intrahepatic cholestasis. After cessation of the drug, the liver tests became normal.

The hepatic artery and the portal vein of 12 human cadaver livers with metastases of various sizes and origins were injected with Microfil. The microvascular appearances of the metastases were studied in order to receive an explanation to findings at angiography and contrast enhanced computed tomography. Histologic examinations were also performed of Microfil-injected specimens.

Ten dogs were repeatedly subjected to barbiturate anaesthesia at different intervals. Blood samples and liver biopsy specimens were obtained during each anaesthesia. Alkaline phosphatase activity, dem