Plasma histamine in asthmatic and control subjects following exercise: influence of circulating basophils and different assay techniques.

Abstract

Arterial plasma histamine concentrations were measured after exercise in 10 subjects with extrinsic atopic asthma, 10 who were non-atopic and non-asthmatic and seven who were atopic but non-asthmatic, by a single isotope radioenzymatic assay. Significantly higher plasma histamine concentrations were found in the asthmatic subjects before exercise than in the nonatopic controls (p < 0-05). The mean histamine concentration rose after exercise in all groups but the increased levels were not significantly different from pre-exercise values. Similarly, mean circulating basophil counts increased in all groups after exercise, and a highly significant correlation was found between basophil counts and whole blood histamine concentrations (p < 0.001). In vitro studies showed that there was a significant correlation between the number of basophils added to plasma samples and the concentrations of histamine subsequently detected. Although the mean concentrations of plasma histamine and whole blood histamine and number of basophils in the atopic control group were intermediate between those found in the atopic asthmatic and non-atopic controls, none of the differences was significant. Venous plasma histamine concentrations after exercise were measured in a further five subjects with extrinsic atopic asthma and five non-atopic, non-asthmatic subjects before and after exercise with the more sensitive and specific double isotope radioenzymatic assay. Concentrations of plasma histamine measured by this assay were about one tenth of those measured by the single isotope radioenzymatic assay. Although a small rise in mean plasma histamine concentration occurred in both groups after exercise there was no significant difference in these levels either between or within the groups. We find no evidence from these studies on measurement of peripheral blood histamine to support the hypothesis that mast cell mediator release is implicated in the pathogenesis of exercise induced asthma.Exercise induced asthma is a phenomenon which can be demonstrated in varying proportions of patients with both extrinsic atopic asthma and cryptogenic non-atopic asthma.' Several observations suggest that mast cells and their mediators may play a part in the pathogenesis. A short refractory period occurs after an episode of exercise induced asthma, during which exercise can no longer lead to airflow obstruction, suggesting the possibility of depletion of mediator stores from mast cells.2 Sodium cromoglycate, a drug thought to act by stabilising

Evidence for mast cell activation during exercise-induced bronchoconstriction

“…This confusion is probably due to the technical difficulties with measuring small changes in circulating concentrations of histamine following exercise. Since the basophil is another potential source of histamine, it has been suggested that the increases in plasma or whole-blood histamine can be attributed to the basophilia which ensues exercise [20,39]. However, NAGAKURA et al [40] demonstrated a rise in histamine that was restricted to those who had experienced EIB, despite the fact that both EIB-positive and EIB-negative asthmatics had similar postexercise basophilia.…”

H1 receptor‐mediated vasodilatation contributes to postexercise hypotension

“…It has been suggested that exercise causes histamine release; however, this is difficult to assess in humans as red blood cells actively take up histamine (Campos et al 1999). Histamine levels have been measured in arterial and venous whole blood as well as venous plasma during and after high‐intensity exercise (Duner & Pernow, 1958; Harries et al 1979; Hartley et al 1981; Morgan et al 1983; Campos et al 1999). However, these studies do not agree on an adequate method for collecting and analysing the concentration of histamine.…”

The therapeutic index of antihistamines

“…The potential involvement of histamine is evidenced from two sets of data. First is the observation of elevated plasma histamine levels in stable asthma (37)(38)(39); consistent with this is the long recognized weak bronchodilator actions of both the older and newer antihistamines (40)(41)(42)(43)(44)(45). Second are the observations under experimental conditions that elevated plasma histamine levels accompany bronchoconstriction following provocation with allergen (46,47), exercise (48)(49) and adenosine (50) but not isocapnic hyperventilation (51).…”