Pulmonary platelet kinetics in asthma.

Abstract

Platelets produce a range of bronchoconstrictor mediators. Measurements of plasma factors have implicated platelet activation in allergic asthma, and sensitised guineapigs challenged with ovalbumin show pulmonary platelet aggregation accompanying bronchoconstriction. To investigate this further we injected autologous platelets labelled with indium 111 and red cells labelled with technetium 99m into three young volunteers with atopic asthma and three nonasthmatic volunteers and, after equilibration of platelets between blood and splenic pool, monitored lung 99mTc and "I'In activities continuously. Comparison with the corresponding activities in blood samples allowed calculation of pulmonary platelet to red cell transit time ratio (tp/tr). This ratio was 0.9, 1.02, and 0.98 in the non-asthmatic subjects compared with 1.04, 0.97, and 1.17 in the asthmatic subjects. This argues against the existence of an intrapulmonary platelet pool in normal subjects; transpulmonary transit time was slightly prolonged in one asthmatic subject. Bronchial challenge with Dermatophagoides pteronyssinus was performed in the asthmatic subjects and monitoring continued for a further 30 minutes. Antigen induced falls in FEV, of 20-50% were accompanied by small decreases in the "I' In but not in the 99mTc lung signal. In line with this k/er fell to 0.89, 0.89, and 1.05. Antigen induced bronchoconstriction was therefore not accompanied by intrapulmonary platelet accumulation. Platelet survival was normal at 10.2 days in both groups of subjects.Platelets produce many potent bronchoconstrictor mediators, including thromboxanes,' cyclic endoperoxides,2 slow reacting substance,3 5-hydroxytryptamine,4 and histamine.5 Platelet activating factor is released by IgE mediated activation of basophils and alveolar macrophages.6 Platelet activating factor contracts smooth muscle by a direct action and produces platelet dependent bronchoconstriction in guineapigs7 and baboons.8 In man platelet activation has been implicated in asthma by the demonstration of increased blood levels of platelet factor 4 (PF4)9 and 13 thromboglobulin"' 10 minutes after antigen induced bronchoconstriction. Platelet accumulation has been demonstrated in the lungs of sensitised guineapigs challenged with antigen.'2 To evaluate the relevance of this observation to human asthma we have monitored lung radioactivity continuously in asthmatic subjects, previously injected with autologous

The role of platelets in the pathophysiology of asthma

“…This supports data indicating platelet sequestration in the bronchial circulation of challenged atopic asthmatics [63]. These findings are, nevertheless, inconclusive, as other reports show no reduction in platelet survival time and no evident platelet sequestration in the pulmonary microvasculature [64,65]. One finding that is widely acknowledged, is the prolonged bleeding time observed in atopic subjects [66,67].…”

Cardiopulmonary responses of asthmatic children to exercise: Analysis of systolic and diastolic cardiac function

“…Impaired gas exchange due to pressure differences, insufficient surface area increased transit time of red blood cells and platelets and insufficient alveolar ventilation-perfusion results in rapid development of dyspnea during exercise, and thus limits physical capacity. [30][31][32][33] This occurs even in mild asthma. 9 In patients with asthma, increased end-expiratory lung volume, lower physical activity and a more sedentary lifestyle than healthy people of the same age are other reasons for lower exercise tolerance.…”

Platelet aggregation, secretion, and coagulation changes in children with asthma

“…In our study, we demonstrated lowest platelet counts in peripheral blood of patients with mild persistent asthma. This is also inconclusive that other studies demonstrated platelet survival time within normal limits [28,30]. This is also inconclusive that other studies demonstrated platelet survival time within normal limits [28,30].…”