Contribution ofα- andβ-Adrenergic Mechanisms to the Development of Pulmonary Edema

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

Role of posterior hypothalamus in hypobaric hypoxia induced pulmonary edema

“…It is also possible that it could be due to excessive sympathetic drive . There are studies which report that while administration of large doses of alpha-adrenergic agonists such as phenylepinephrine result in pulmonary edema (Rassler, 2012), administration of alpha-receptor antagonists such as phentolamine reduce it markedly (Davison et al, 2012;Rassler, 2012). In a study which compared the effects of various vasodilators on the hemodynamic parameters of HAPE, it was observed that phentolamine alone and in combination with oxygen provided the maximum benefit emphasizing the significance of the sympathetic nervous system in HAPE.…”

Intraoperative hemodynamics monitoring in a patient with pheochromocytoma multisystem crisis: a case report

“…Before surgery, the patient developed non-cardiogenic pulmonary edema, which is rarely seen in those with pheochromocytoma [6]. Given that there was an abnormal increase in IL-6 levels, the pulmonary edema could have been attributed to the inflammatory mechanism, by which the overproduction of IL-6 caused from elevated catecholamine levels disrupts the endothelial junction, leading to capillary leakage [6].…”

“…Given that there was an abnormal increase in IL-6 levels, the pulmonary edema could have been attributed to the inflammatory mechanism, by which the overproduction of IL-6 caused from elevated catecholamine levels disrupts the endothelial junction, leading to capillary leakage [6]. Another pathophysiological The FloTrac™-derived value of APCO, which is calculated based on analysis of the peripheral arterial pressure waveform without external calibration, has theoretically a more rapid response than PACO.…”

“…Surgical resection of the tumor is the definitive treatment, but inadequate preoperative optimization of alpha-and/or beta-blockade can increase perioperative mortality and morbidity in patients with pheochromocytoma [1,2]. The mortality can reach as high as 85% in the presence of a hyperadrenergic crisis [3][4][5], a life-threatening endocrine emergency leading to multiple organ failure, which is characterized by hypertensive crises, subsequent cardiogenic shock, pulmonary edema, acute liver and renal insufficiency, encephalopathy, and hyperthermia [2,6]. Because of its severity, patients developing a hyperadrenergic crisis require preoperative prophylactic stabilization of circulatory hemodynamics [1,2,4,5].…”

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“…Adzick reporta en una serie de pacientes operadas en Vanderbilt una ocurrencia de edema pulmonar en el postoperatorio inmediato de aproximadamente 8% 44 . Esta alta incidencia se relaciona con uso de tocolíticos durante el intraoperatorio 45 , tratamiento que necesariamente se extiende a las siguientes 48 h del postoperatorio. Reportes de congestión pulmonar han sido descritos especialmente con nitroglicerina 46,47 y agonistas Beta miméticos 48 , aunque en nuestra experiencia el único caso de congestión pulmonar fue en una paciente que recibió nitroglicerina como tocolisis durante el intraoperatorio y se mantuvo con Atósiban posteriormente.…”