4.3 Review

Is loaded breathing an inflammatory stimulus?

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CURRENT OPINION IN CRITICAL CARE
卷 11, 期 1, 页码 1-9

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LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/00075198-200502000-00002

关键词

respiratory muscles; cytokines; oxidative stress; control of breathing

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Purpose of review To summarize recent data including that loaded breathing generates an inflammatory response. Recent findings Loaded breathing initiates as inflammatory response consisting of elevation of plasma cytokines and recruitment and activation of lymphocyte subpopulations. These cytokines do not originate from monocytes but are instead produced within a diphragm secondary to hte increased muscle activation. Oxidative stress is a major stimulus for the cytokine induction induction secondary secondary to loaded breathing. The productionof cytokines within the diaphragm may mediate the diaphragm muscle fibre injury that occurs with strenuous contractions, or contribute to the expected repair process. These cytokines may also compromise diaphragmatic contractility or contribute to the development of muslce cachexia. They may also have systemic effects, mobilizing glucose from the liver and free fatty acids from the adipose tissue to the strenuously working respiratory muscles. At the same time, they stimulate the the hypothalamic pituitary adrenal axis, leading to the production of adrenocorticotropic hormone and beta-endorphins. The adrenocorticotropic hormone response may be represent an attempt of the organism to reduce the injury occuring in the respiratory muscles through the production of glucocorticoids and the induction of the acute-phase response proteins. The beta-endorphin response would decrease the activation of the respiratory muscles and change the pattern of breathing which becomes more rapid and shallow, possibly in an attempt to reduce and/or prevent further injury to the respiratory muscles Summary Loaded breathing is an immune challenge for the body, initiating and inflammatory response. Further studies are needed to elucidate the role of this response in the development of ventilatory failure.

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