Chronic liver failure induced by portocaval anastomosis (PCA) in Wistar rats resulted in a dramatic increase in histamine concentration in hypothalamus and a smaller, but clearly pronounced, elevation in the rest of brain. Between 10 and 120 days following surgery, shunted rats exhibited a histamine level 2.4- to 13-fold higher in hypothalamus and 1.5- to 2.5-fold higher in the rest of brain as compared to their control, sham-operated pairs. There were no significant changes in histamine concentration in the other examined tissues. The increase in brain histamine could not be attributed to the inhibition of its degradation, because activity of histamine N-methyltransferase remained unchanged for at least 40 days. Although the activity of histidine decarboxylase also remained unchanged when measured at a saturating concentration of L-histidine, the increase in histamine content in brain seems to be due to its enhanced synthesis brought about by increased availability of L-histidine in the tissue, as indicated by two to four times higher concentrations of this amino acid in PCA rats.

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The effect of different concentrations of zinc ions on the in vitro release of histamine from isolated rat peritoneal mast cells induced by compound 48/80 and Triton X-100, as well as the influence of the in vivo administration of zinc ions on the subsequent in vitro release of histamine from isolated peritoneal mast cells and lung tissue, have been investigated. The results show that intraperitoneal administration of zinc for 20 days significantly inhibited the spontaneous ~elease of histamine from lung tissue as well as that induced by a low dose of compound 48/80. The in vitro addition of zinc ions to isolated mast cells significantly inhibited the release of histamine induced by low doses of compound 48/80 but not by high doses or by Triton X-100. Inhibition of histamine release increased up to 100 % with increase in the zinc ions concentration up to 10 -3 M. An inhibition of the histamine release from mast cells and lung tissue from animals which had received in vivo injection of zinc was also observed.The results indicate that the inhibitory action of zinc ions on the release of histamine is connected with an action on the biomembrane rather than on the histamine binding within the mast cells.

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The prior treatment of guinea pigs with nicotinamide diminished the symptoms of experimental bronchial asthma and the intensity of anaphylactic shock. Nicotinamide was also found to inhibit anaphylactic mast cell degranulation in mice and histamine release from rat-isolated peritoneal mast cells by compound 48/80. The role of nicotinamide in bronchial asthma is discussed.