Abstract
Pulmonary oedema (PO) can emerge from mechanical disorders in pulmonary circulation leading to elevated fluid filtration in the lung, or from increased vascular permeability due to inflammatory or toxic injury of the alveolarcapillary barrier. A number of these disorders causing PO is associated with increased catecholamine (CA) levels in plasma and lung tissue and/or increased sympathetic activation such as neurogenic PO, high-altitude PO or PO in patients with phaeochromocytoma. Experimental CA stimulation in animals induced PO after less than one hour of infusion. Both α- and β-adrenergic mechanisms are involved in the pathogenesis but also in the resolution of PO. CAs increase pulmonary capillary pressure and thus, enhance fluid filtration into the pulmonary interstitium. Additionally, by activation of proinflammatory cytokines, they induce pulmonary inflammation that may lead to capillary leak. Finally, they play an important role in the regulation of alveolar fluid clearance. The present paper considers the pathways by which CAs contribute to the development of PO of various origin.
Keywords: nitric oxide (NO), high altitude pulmonary oedema (HAPE), capillary permeability, Acute respiratory distress syndrome (ARDS), right ventricular systolic pressure (RVSP), Inflammation, Cytokines
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