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Edema, Inflammation and Fibrosis - Comparison Between Catecholamine- and Hypoxia-Induced Pulmonary Injuries

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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; extracellular matrix; hypoxia; inflammation; matrix metalloproteinases; pulmonary capillary pressure; pulmonary edema; pulmonary fibrosis

Document Type: Research Article


Publication date: 2008-11-01

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  • Vascular Disease Prevention publishes reviews as well as original papers to update all those concerned with this topic at the clinical or scientific level. In addition to clinically relevant topics, we consider reviews and original papers dealing with the more scientific aspects of vascular disease prevention. This includes the evaluation of emerging vascular risk factors, research dealing with the pathogenesis of atherosclerosis and the investigation of new treatment options both at the clinical and scientific level (e.g. epidemiology, patient-based studies, experimental models, in vitro experiments or molecular research). Therefore, another function of Vascular Disease Prevention is to bridge the gap between clinical practice and ongoing laboratory-based research.

    In particular, we welcome critical reviews and comments on recent trials. This is a topic that requires regular updates because of the large number of trials published every year.

    Debates are encouraged in the correspondence section of this journal.
    The editorial structure of Vascular Disease Prevention is set up with the aim of dealing with the submitted material as rapidly as possible. Specialist editors will provide a more expert and rapid assessment unlike a more centralized editorial structure.
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