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2 6 ~ Medical Research Society Solutes which penetrate cell membranes poorly, such as mannitol, if administered intravascularly as hypertonic solutions, will osmotically shrink the swollen cells, terminate the ‘no-reflow’ and allow prompt return of blood flow. This reduces the ischaemic injury to the tissue and protects the organ from functional failure. COMMUNICATIONS 1. THE MEASUREMENT OF BILIARY COPPER SECRETION I N HUMANS D. J. FROMMER Department of Medicine, Royal Free Hospital Wilson’s disease is characterized by the accumulation of copper in the body, the toxic action of which is believed to be responsible for the hepatic, cerebral and other manifestations. Copper is absorbed by the upper small intestine, concentrated in the liver and incorporated into caeruloplasmin or excreted from the body via the biliary system and the gastrointestinal tract. The cause of the accumulation of copper, especially in the liver, in Wilson’s disease is uncertain. Using 64Cu or 67Cu various workers have found evidence for increased absorption or decreased excretion in the intestine. The biliary secretion of copper into the duodenum was measured in eight patients with Wilson’s disease (three were untreated, with hepatic dysfunction) and ten control subjects (three with hepatic dysfunction). The method of Go et al. (1970, Gastroenterology, 58, 321) was used with the modification of omitting a gastric marker. A multi-lumen tube was passed into the duodenum so that juice was aspirated at the duodeno-jejunal junction while the duodenum was perfused at 5 ml/min with an amino-acid solution containing a non-absorbed marker W r C1,. Gastric juice was also aspirated. Collecting periods of 20 min were used and the perfusions were continued for 2-3 h. Copper concentrations of the aspirate were measured by wet ashing of the samples and extracting with zinc dibenzyldithiocarbamate. The secretion of copper was calculated from the following equation: The mean concentration of copper in the duodenal aspirate in Wilson’s disease, 7.6k0.6 pg/100 ml (SEM, n = 48), was significantly lower than that in the control group, 16-8k1.4 pg/100 ml (n = 73, P < 0.001). The mean biliary copper secretion rate in the Wilson’s disease patients, 8.6+0.8 pg/20 min (n = 47), was also significantly(P<O.001) below that of the control patients, 16-4kO.8pg/20 rnin (n = 74). The presence of liver dysfunction made no significant difference to the secretion rates in either group of patients. These results suggest that in Wilson’s disease the liver is unable to secrete copper in adequate amounts into bile leading to an accumulation of copper within the body. 2. THE EFFECT O F RETICULOENDOTHELIAL BLOCKADE ON HEPATIC PHAGOCYTOSIS AND THE IMMUNE RESPONSE R. L. SOUHAMI Department of Experimental Pathology, St Mary’s Hospital Medical School, and Department of Clinical Haematology, University College Hospital Medical School (Introduced by E. R. HUEHNS) In normal mice SO-SO% of 51Cr-labelled sheep red blood cells (sheep RBC), injected intravenously, are localized in the liver and 2-5% in the spleen. In the experiments to be described, blockade of the reticuloendothelial system was induced by a single intravenous injection of colloidal carbon. The effect of blockade was to depress the hepatic uptake of sheep RBC to only 10% of the injected dose. The suppression of hepatic uptake began within 5 rnin after the blockading injection, and had reached a maximum by 6 h. The suppression of hepatic uptake of sheep RBC was accompanied by a marked increase of splenic uptake (to 40% of the injected dose). regardless of the dose of sheep RBC. This redistribution of sheep RBC from liver to spleen was accompanied by an increased production of humoral antibody in blockaded mice, and an increase in numbers of antibody forming cells in the spleen. The ‘stimulation’ of the immune response could be accounted for entirely by CuoxS1Crlx V , the redistribution of antigen. cu, = Recovery from blockade took place over 4 days CrD and this recovery process was prevented by irradiation where Cu, = copper secreted in pg/20 min period with X-rays. Labelling with 3H-thymidine during CuD = copper content in pg of 1 ml of duo- recovery from blockade demonstrated large numbers denal aspirate of labelled Kupffer cells in the liver. Animals which CrD = SICr C13 content of 1 ml duodenal were irradiated, but whose bone marrow was shielded, aspirate recovered normally from blockade. Crl = 51CrC13 content of 1 ml perfusing fluid These results suggest that an increased immune V 1 = volume of fluid perfusing duodenum response occurs when the hepatic sequestration of a over 20 min particulate antigen is prevented. This mechanism may The recovery of marker in the duodenal aspirate in play a part in producing hypergammaglobulinaemia the two groups of patients did not differ significantly. in cirrhosis of the liver and other liver diseases. The