Please use this identifier to cite or link to this item: http://dx.doi.org/10.25673/34880
Title: Vasoplegia in patients with sepsis and septic shock: pathways and mechanisms
Author(s): Burgdorff, Anna-Maria
Bucher, Michael
Schumann, Julia
Granting Institution: Martin-Luther-Universität Halle-Wittenberg
Issue Date: 2017-11-01
Type: Article
Language: English
Publisher: Universitäts- und Landesbibliothek Sachsen-Anhalt
Subjects: vasoplegia
sepsis
cytokines
vasoactive receptors
hypotension
endotoxemia
Abstract: At intensive care units sepsis is still one of the most frequent reasons for death. In the past years lots of therapeutic strategies have been checked out without desired success. One of the key factors for death is hypotension due to vasodilatation with vascular hyposensitivity. The underlying pathways, however, are not sufficiently explained. Endotoxemia induces inflammatory mediators, which is followed by vasoplegia and decreased cardiac contractility. Inhibition of these mediators is described to diminish mortality rates in animal models but without confirmation in humans. Further on a downregulation of vasoconstrictive receptors like angiotensin-, adrenergic- and vasopressin-receptors is seen in sepsis, which is associated with a hyporesponsiveness to vasoconstrictive mediators. Animal studies verify that receptor-downregulation is linked to the inflammatory mediators mentioned above. Anti-inflammatory therapy with glucocorticoids is described to improve responsiveness to catecholamins with higher survival in rats though there is no clinical significance in humans. Hence there is the urgent need for in-depth studies investigating the underlying mechanisms of vasoplegia in order to develop effective therapeutic strategies for the treatment of septic patients.
URI: https://opendata.uni-halle.de//handle/1981185920/35080
http://dx.doi.org/10.25673/34880
Open Access: Open access publication
License: (CC BY-NC-ND 4.0) Creative Commons Attribution NonCommercial NoDerivatives 4.0
Original Publication: 10.1177/0300060517743836
Appears in Collections:Medizinische Fakultät MLU

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