Contribution of alpha- and beta-Adrenergic Mechanisms to the Development of Pulmonary Edema

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 a. er experimental administration of adrenergic agonists. PE can result from stimulation with different types of adrenergic stimulation. With alpha-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 of alpha-adrenergic stimulation have repeatedly been described and are considered to play a pivotal role in NPE or in PE in patients with pheochromocytoma. Although beta-adrenergic agonists have often been reported to prevent or attenuate PE by enhancing alveolar fluid clearance, PE may also be induced by beta-adrenergic treatment as can be observed in tocolysis. In experimental models, infusion of beta-adrenergic agonists induces less severe PE than alpha-adrenergic stimulation. The present paper addresses the current understanding of the possible contribution of alpha-and beta-adrenergic pathways to the development of PE.