Contribution of α- and β-Adrenergic Mechanisms to the Development of Pulmonary Edema. (7th August 2012)

• Record Type: Journal Article
• Authors: Rassler, Beate
• Other Names: Borger Peter Academic Editor.; Rippe B. Academic Editor.
• Is Part Of: Scientifica. Volume 2012(2012)
• Publication Date: 2012-08-07
• Subjects: Life sciences -- Periodicals; Biology -- Periodicals; Medicine -- Periodicals; Biological Science Disciplines; Medicine; Biology; Life sciences; Medicine; Periodicals; Electronic journals; Periodicals; 500
• DOI: 10.6064/2012/829504
• Languages: English
• ISSNs: 2090-908X

Abstract

Abstract : Endogenous or exogenous catecholamines can induce pulmonary edema (PE). This may occur in human pathologic conditions such as in pheochromocytoma or in neurogenic pulmonary edema (NPE) but can also be provoked after experimental administration of adrenergic agonists. PE can result from stimulation with different types of adrenergic stimulation. Withα -adrenergic treatment, it develops more rapidly, is more severe with abundant protein-rich fluid in the alveolar space, and is accompanied by strong generalized inflammation in the lung. Similar detrimental effects ofα -adrenergic stimulation have repeatedly been described and are considered to play a pivotal role in NPE or in PE in patients with pheochromocytoma. Althoughβ -adrenergic agonists have often been reported to prevent or attenuate PE by enhancing alveolar fluid clearance, PE may also be induced byβ -adrenergic treatment as can be observed in tocolysis. In experimental models, infusion ofβ -adrenergic agonists induces less severe PE thanα -adrenergic stimulation. The present paper addresses the current understanding of the possible contribution ofα - andβ -adrenergic pathways to the development of PE.