Schäper, Jörn

[["dc.bibliographiccitation.artnumber","23"],["dc.bibliographiccitation.journal","BMC Anesthesiology"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Enigk, Fabian"],["dc.contributor.author","Wagner, Antje"],["dc.contributor.author","Samapati, Rudi"],["dc.contributor.author","Rittner, Heike"],["dc.contributor.author","Brack, Alexander"],["dc.contributor.author","Mousa, Shaaban A."],["dc.contributor.author","Schaefer, Michael"],["dc.contributor.author","Habazettl, Helmut"],["dc.contributor.author","Schaeper, Joern"],["dc.date.accessioned","2018-11-07T09:41:21Z"],["dc.date.available","2018-11-07T09:41:21Z"],["dc.date.issued","2014"],["dc.description.abstract","Background: The sympathetic nervous system is considered to modulate the endotoxin-induced activation of immune cells. Here we investigate whether thoracic epidural anesthesia with its regional symapathetic blocking effect alters endotoxin-induced leukocyte-endothelium activation and interaction with subsequent endothelial injury. Methods: Sprague Dawley rats were anesthetized, cannulated and hemodynamically monitored. E. coli lipopolysaccharide (Serotype 0127: B8, 1.5 mg x kg(-1) x h(-1)) or isotonic saline (controls) was infused for 300 minutes. An epidural catheter was inserted for continuous application of lidocaine or normal saline in endotoxemic animals and saline in controls. After 300 minutes we measured catecholamine and cytokine plasma concentrations, adhesion molecule expression, leukocyte adhesion, and intestinal tissue edema. Results: In endotoxemic animals with epidural saline, LPS significantly increased the interleukin-1 beta plasma concentration (48%), the expression of endothelial adhesion molecules E-selectin (34%) and ICAM-1 (42%), and the number of adherent leukocytes (40%) with an increase in intestinal myeloperoxidase activity (26%) and tissue edema (75%) when compared to healthy controls. In endotoxemic animals with epidural infusion of lidocaine the values were similar to those in control animals, while epinephrine plasma concentration was 32% lower compared to endotoxemic animals with epidural saline. Conclusions: Thoracic epidural anesthesia attenuated the endotoxin-induced increase of IL-1 beta concentration, adhesion molecule expression and leukocyte-adhesion with subsequent endothelial injury. A potential mechanism is the reduction in the plasma concentration of epinephrine."],["dc.identifier.doi","10.1186/1471-2253-14-23"],["dc.identifier.isi","000335075800001"],["dc.identifier.pmid","24708631"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10104"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/33708"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1471-2253"],["dc.rights","CC BY 2.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.0"],["dc.title","Thoracic epidural anesthesia decreases endotoxin-induced endothelial injury"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","134"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Anesthesiology"],["dc.bibliographiccitation.lastpage","142"],["dc.bibliographiccitation.volume","118"],["dc.contributor.author","Schaeper, Joern"],["dc.contributor.author","Wagner, Antje"],["dc.contributor.author","Enigk, Fabian"],["dc.contributor.author","Brell, Bernhard"],["dc.contributor.author","Mousa, Shaaban A."],["dc.contributor.author","Habazettl, Helmut"],["dc.contributor.author","Schaefer, Michael"],["dc.date.accessioned","2018-11-07T09:30:51Z"],["dc.date.available","2018-11-07T09:30:51Z"],["dc.date.issued","2013"],["dc.description.abstract","Background: Endotoxin-induced activation of monocytes may lead to extravasation of cells, excessive production of nitric oxide, and subsequent epithelial injury in the gut. Regional sympathetic blockade by means of thoracic epidural anesthesia has been implicated to protect the epithelial barrier. This study tested the hypothesis that thoracic epidural anesthesia decreases epithelial permeability by attenuating monocytic production of nitric oxide and nitrosative stress. Methods: Rats were anesthetized, hemodynamically monitored, and mechanically ventilated. Endotoxemia was induced by an intravenous bolus injection of Escherichia coli lipopolysaccharide. Either lidocaine 2% or normal saline was injected as a bolus, followed by a continuous infusion via an epidural catheter. Three hundred minutes after injection of lipopolysaccharide or normal saline, gut epithelial permeability to fluorescein isothiocyanate-dextran (4 kDa), intestinal expression of inducible nitric oxide synthase by macrophages, and lipid peroxidation represented by 8-isoprostane tissue concentration were quantified. Results: Thoracic epidural anesthesia significantly attenuated the endotoxin-induced increases in gut epithelial permeability (437 [293, 492] vs. 628 [532, 1,042] ng/ml, median [quartiles], P = 0.03), expression of nitric oxide synthase (2 [1,2] vs. 7 [5,8] cells per 384 mu m(2), P = 0.003), macrophage infiltration, and lipid peroxidation (22,460 +/- 11,476 vs. 37,840 +/- 17,551 pg/ml, mean +/- SD, P = 0.05). Conclusions: Thoracic epidural anesthesia attenuates endotoxin-induced gut epithelial injury. This is likely due to a decrease in monocytic extravasation and intestinal nitrosative stress. As possible mechanisms, direct nerve-immune interplay, a reduction in plasma catecholamines, or a systemic lidocaine effect has to be considered."],["dc.identifier.doi","10.1097/ALN.0b013e3182784c93"],["dc.identifier.isi","000312536800019"],["dc.identifier.pmid","23221864"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/31410"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","0003-3022"],["dc.title","Regional Sympathetic Blockade Attenuates Activation of Intestinal Macrophages and Reduces Gut Barrier Failure"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]