Abstract
The anaphylactic histamine release from guinea-pig and rat lung tissues was completely or largely depressed by oxygen lack, respiratory inhibitors and uncouplers of oxidative phosphorylation when the incubation medium was devoid of glucose (1-7). Similar inhibition has been found of compound 48/80-induced histamine release from rat lung tissue and of degranulation of rat mesentery mast cells (6, 8, 9). Since these inhibitions were largely overcome by the presence of glucose (4-9), and phlorizin (10) and 2-deoxyglucose (7) inhibited these glucose-dependent release of histamine, glycolysis should be considered to take part in supplying the energy required for these processes. Chymotrypsin is also known to cause histamine release (11) and degranulation of mast cells (11, 12), and the latter action is also blocked by anoxia and glucose has a preventive effect on this block.
There are a number of works demonstrating the histamine-releasing or degranulating effect of compound 48/80 and some other agents including anti-serum (13) on isolated mast cells or mixed cell suspension taken from rat peritoneal fluid. However, the observations relevant to glucose dependency are all based on the experiments with excised tissues but not with isolated cells, because an anaerobic experiment with isolated mast cells seems to have not yet been successful. Thus, Keller and Beeger (14) reported that the introduction of nitrogen gas into the cell suspension resulted in a complete destruction of mast cells; Moran et al. (15) were unable to demonstrate an inhibition of 48/80induced amine release from mixed peritoneal cells by incubating in their supposedly oxygen-free atmosphere in the absence of glucose.
In the present experiments, with isolated mast cells, the glucose-dependent degranulation by compound 48/80, α-chymotrypsin and anti-serum is demonstrated under nitrogen anaerobiosis with success, and the effects of some inhibitors including phlorizin and 2-deoxyglucose are studied. Observations in aerobiosis are also described.
