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Pathogenetic Mechanisms of Neurogenic Pulmonary Edema
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SYSNO ASEP 0446969 Document Type J - Journal Article R&D Document Type Journal Article Subsidiary J Článek ve WOS Title Pathogenetic Mechanisms of Neurogenic Pulmonary Edema Author(s) Šedý, Jiří (FGU-C)
Kuneš, Jaroslav (FGU-C) RID, ORCID
Zicha, Josef (FGU-C) RID, ORCID, SAISource Title Journal of Neurotrauma - ISSN 0897-7151
Roč. 32, č. 15 (2015), s. 1135-1145Number of pages 11 s. Language eng - English Country US - United States Keywords baroreflex-induced bradycardia ; blood pressure rise ; blood volume redistribution ; neurogenic pulmonary edema ; spinal cord injury ; sympathetic nervous system Subject RIV ED - Physiology R&D Projects GAP304/12/0259 GA ČR - Czech Science Foundation (CSF) Institutional support FGU-C - RVO:67985823 UT WOS 000363936800001 EID SCOPUS 84936992953 DOI 10.1089/neu.2014.3609 Annotation Neurogenic pulmonary edema (NPE) is a life-threatening complication of central nervous system (CNS) injuries. NPE may develop as a result of activation of specific CNS trigger zones located in the brainstem, leading to a rapid sympathetic discharge, rise in systemic blood pressure, baroreflex-induced bradycardia, and enhanced venous return resulting in pulmonary vascular congestion characterized by interstitial edema, intra-alveolar accumulation of transudate, and intra-alveolar hemorrhages. Degree of anesthesia is a crucial determinant for the extent of NPE development in experimental models because of its influence on sympathetic nervous system activity. Attenuation of sympathetic nerve activity or abolition of reflex bradycardia completely prevent NPE development in our experimental model Workplace Institute of Physiology Contact Lucie Trajhanová, lucie.trajhanova@fgu.cas.cz, Tel.: 241 062 400 Year of Publishing 2016
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