Exercise is known to induce an immediate leucocytosis, the magnitude of which is related, in most instances, to the intensity and duration of the work. On finishing exercise, however, the leucocyte count may change in any one of several different ways. The pattern of postexercise changes in the leucocyte count is determined mainly by the time which has elapsed since beginning exercise, rather than the work intensity or the total work done, if, for example, exercise has been intermittent. Consideration of, firstly, the circumstances under which the plasma concentrations of catecholamines and cortisol have been found separately to correlate with the leucocyte count at the finish of exercise, and, secondly, the effects on the leucocyte count of exogenous administration of these substances has led us to develop a model which can satisfactorily account for all of the principal changes in the leucocyte count that have been noted during and after exercise. It is proposed that catecholamines produced during exercise act to increase the ratio of circulating to non-circulating leucocytes, while cortisol acts, by a mechanism which involves a time lag, to increase the total number of leucocytes in the vascular compartment. Examination of previously published reports shows that many contain results which support this model. Using the model as a basis, some predictions are made that can be tested experimentally, and some experiments are suggested which should help elucidate the mode of action of catecholamines and cortisol.

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A novel. Bis-indolylmaleimide. Ro 31-8425, bearing a conformationally restricted side chain, inhibits protein kinasc C isolated from rat brain and human neutrophils with a high degree of selectivity over CAMP-dependent kinase and Ca'-/calmodulin-dependent kinase. It also inhibits phorbol ester-induced intracellular events known to be mediated by protein kinase C (p47 phosphorylaticn in intact platelets. CD3 and CD4 down-regulation in T-cells). Ro 31-8425 inhibited supcroxide generation in human neutrophils activated by both receptor stimuli (formyl-methionyl-leucylphcnylalanine. opsonized zymosan. IgG and heat aggrcgatcd IgG) and post-receptor stimuli (I .2-dioctanoylglycerol and fluoride). The compound also blocked antigen driven, but not IL-2 induced, T-cell proliferation. These results support a central role for protein kinase C in the activation of the respiratory burst and antigen-driven T-cell proliferation.

Summary1. The mast-cell distribution in the various layers of the ileum has been described.2. Histamine-content, anaphylactic histamine-release and the anaphylactic dose-response curve of the full-thickness ileum and of the longitudinal muscle strip have been measured and compared. 3. Tetrodotoxin 10-7 g/ml had no obvious effect on the anaphylactic doseresponse curve of either preparation. This suggests that the plexus is not of any great importance in the Schultz-Dale reaction. 4. Exposure of the longitudinal muscle strip to octylamine 10-3 g/ml for 1 min reduced the mast cell content by 95-100%. After this treatment the dose-response curve to antigen was eliminated, although the muscle still responded to small doses of histamine and to anaphylactic mediators. Pretreatment of antibody with octylamine did not impair passive sensitization and subsequent response to antigenic challenge. This suggests that the classical Schultz-Dale reaction in the strip is mediated mainly by mast cells, and possibly other cells, and is probably not due to a direct effect of the antigen-antibody reaction on the smooth muscle. 5. The typical three-phase anaphylactic response (quick contraction, quick relaxation, slow contraction) of full-thickness ileum is discussed and com-