THE LINK BETWEEN EXERCISE, RESPIRATORY HEAT EXCHANGE, AND THE MAST CELL IN BRONCHIAL ASTHMA

The Lancet ◽  
1983 ◽  
Vol 321 (8323) ◽  
pp. 520-522 ◽  
Author(s):  
T.H Lee ◽  
B.K Assoufi ◽  
A.B Kay
2008 ◽  
pp. 69-74
Author(s):  
A. G. Prikhodko ◽  
A. V. Kolosov

Prevalence and clinical and physiological features of coldinduced bronchial hyperreactivity in patients with respiratory diseases were shown. In patients with chronic bronchitis, coldinduced bronchial hyperreactivity was associated with worsening of lung ability to condition the inspired air. Disorders of respiratory heat exchange in patients with bronchial asthma were not the leading cause of coldinduced bronchoconstriction, which was associated with high sensitivity of airway receptors and IgEdependent mechanisms. A set of diagnostic criteria allowing detection of the dominant mechanism of airway cold hyperreactivity was proposed.


2008 ◽  
pp. 59-62
Author(s):  
E. V. Zakharova

The aim of the study was to investigate airway conditioning function and cold hyperresponsiveness in patients with bronchial asthma (BA) and nasal polyps. One hundred and eleven asthma patients with or without chronic polypous rhinosinusitis (CPR) were examined. Respiratory heat exchange and cold airway hyperresponsiveness were assessed using thermometry of expired air during quiet breathing and isocapnic hyperventilation with cold air in comparison with a group of healthy persons. The conditioning nasal function was worsened in BA patients with CPRS. Disorders of nasal heat exchange led to decreased temperature of the exhaled air during quiet breathing and cold hyperventilation. These disorders were closely related to increased frequency and severity of cold airway hyperresponsiveness.


1979 ◽  
Vol 46 (3) ◽  
pp. 467-475 ◽  
Author(s):  
E. C. Deal ◽  
E. R. McFadden ◽  
R. H. Ingram ◽  
R. H. Strauss ◽  
J. J. Jaeger

We have hypothesized that it is the total heat flux in the tracheobronchial tree during exercise that determines the degree of postexertional obstruction in asthma, and have developed quanititative expressions that relate these two events. We tested this hypothesis by comparing the observed responses to exercise, while our subjects inhaled dry air at various temperatures ranging from subzero to 80 degrees C in a random fashion, to those that we predicted would occur based upon calculations of respiratory heat exchange. We further determined if heat could be transferred from the inspired air to the mucosa so as to offset evaporative losses from the airways. The observed responses fell as air temperature was increased from -11 to +37 degrees C and exactly matched theoretical predictions. Above 37 degrees C, the observed response exceeded predictions, indicating that it was not possible to provide sufficient heat per se in the air to offset the vaporization of water. However, when small amounts of water vapor were added to the inspirate at high temperatures, bronchospasm was virtually abolished and the response again closely matched theoretical expectations. We conclude that the magnitude of exercise-induced asthma is directly proportional to the thermal load placed on the airways and that this reaction is quantifiable in terms of respiratory heat exchange.


CHEST Journal ◽  
1984 ◽  
Vol 85 (4) ◽  
pp. 465-470 ◽  
Author(s):  
W.C. Hodgson ◽  
D.J. Cotton ◽  
G.D. Werner ◽  
D.W. Cockcroft ◽  
J. A Dosman

1984 ◽  
Vol 57 (2) ◽  
pp. 608-609 ◽  
Author(s):  
E. C. Deal ◽  
E. R. McFadden ◽  
R. H. Ingram ◽  
J. J. Jaeger

1996 ◽  
Vol 33 (2) ◽  
pp. 89-95 ◽  
Author(s):  
Takeshi Koshino ◽  
Yasuo Arai ◽  
Yasufumi Miyamoto ◽  
Yasushi Sano ◽  
Makiko Itami ◽  
...  

Allergy ◽  
2007 ◽  
Vol 63 (1) ◽  
pp. 140-141 ◽  
Author(s):  
G. Bochenek ◽  
E. Niżankowska ◽  
A. Gielicz ◽  
A. Szczeklik

Author(s):  
R D Farley ◽  
K R Patel

Exercise-induced asthma is prevalent in many asthmatics and during the winter months can be exacerbated by cold air inhalation. A laboratory facility was required to permit early diagnosis of cold air sensitivity in these patients. This paper describes the development of a modular air conditioning system to produce a range of inhalative thermal burdens and the microcomputer interfacing to measure the rate of airway heat loss imposed. A single-stage refrigerator was built capable of cooling 150 1/min air to —25°C. This was also used to generate dry ambient temperature air by rewarming the chilled air supply. An air humidifier was developed based upon natural convection and evaporation. It was capable of raising 150 1/min ambient air to 37°C, 100 per cent relative humidity. In two pilot studies of 18 asthmatics it was found that the rate of respiratory heat exchange could be correlated with the magnitude of post exertional bronchoconstriction (lung dysfunction) and that exercise-induced asthma could be minimized by attenuating the rate of airway heat loss.


2019 ◽  
Vol 2019 ◽  
pp. 1-9
Author(s):  
Yuan Gao ◽  
Qiaoling Fei ◽  
Ruijuan Qi ◽  
Rui Hou ◽  
Yixin Han ◽  
...  

Shuang-Huang-Lian (SHL), an herbal formula of traditional Chinese medicine, is clinically used for bronchial asthma treatment. Our previous study found that SHL prevented basophil activation to suppress Th2 immunity and stabilized mast cells through activating its mitochondrial calcium uniporter. Sporadic clinical reports that SHL was used for the treatment of bronchial asthma can be found. Thus, in this study, we systematically investigated the effects of SHL on asthmatic responses using a shrimp protein (SP)- induced mouse model. SHL significantly inhibited airway inspiratory and expiratory resistance, and histological studies suggested it reduced thickness of airway smooth muscle and infiltration of inflammation cells. It also could alleviate eosinophilic airway inflammation (EAI), including reducing the number of eosinophils and decreasing eotaxin and eosinophil peroxidase levels in the bronchoalveolar lavage fluid (BALF). Further studies indicated that SHL suppressed SP-elevated mouse mast cell protease-1 and IgE levels, prevented Th2 differentiation in mediastinal lymph nodes, and lowered Th2 cytokine (e.g., IL-4, IL-5, and IL-13) production in BALF. In conclusion, SHL attenuates airway hyperresponsiveness and EAI mainly via the inhibition of mast cell activation and Th2 immunity, which may help to elucidate the underlying mechanism of SHL on asthma treatment and support its clinical use.


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