Acute alveolar hypoxia often causes pulmonary edema which is associated with pulmonary inflammation and later on, with transition into fibrosis. Strong sympathetic activation and elevated plasma levels of catecholamines (CAs) induce similar changes in the lung. Adrenergic mechanisms are involved in circulatory changes, in formation and resolution of pulmonary edema, in the activation of proinflammatory cytokines as well as in the regulation of the extracellular matrix. As hypoxia is associated with sympathetic activation, the question arises for the role of CAs in the pathogenesis of hypoxia-induced pulmonary injury. In this review, the pathogenesis of pulmonary injury in conditions with elevated CA levels is compared with the development of hypoxia-induced lung injury. In both conditions, elevated pulmonary capillary pressure is considered to play a pivotal role in the formation of pulmonary edema. This edema is accompanied by activation of proinflammatory cytokines and inflammation, and is followed by development of fibrosis. Pathogenic mechanisms of CA- and hypoxia-induced pulmonary injuries are characterized. Similar time courses and pathogenic features of the two models of lung injury might be explained by hypoxia-induced sympathetic activation and norepinephrine release as well as by stimulation and upregulation of pulmonary α1-adrenoceptors.
Keywords: Catecholamines, hypoxia, pulmonary edema, pulmonary capillary pressure, inflammation, extracellular matrix, matrix metalloproteinases, pulmonary fibrosis
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