Schäper, Jörn

[["dc.bibliographiccitation.firstpage","1203"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Journal of Clinical Medicine"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Moerer, Onnen"],["dc.contributor.author","Huber-Petersen, Jan Felix"],["dc.contributor.author","Schaeper, Joern"],["dc.contributor.author","Binder, Claudia"],["dc.contributor.author","Wand, Saskia"],["dc.date.accessioned","2021-06-01T09:42:37Z"],["dc.date.available","2021-06-01T09:42:37Z"],["dc.date.issued","2021"],["dc.description.abstract","Direct complications in patients receiving extracorporeal (veno-venous) membrane oxygenation (vvECMO) are mainly either due to bleeding or thromboembolism. We aimed to evaluate the course of routine coagulation parameters and the activity of different coagulation factors—with special focus on factor XIII (F XIII)—before, during and after vvECMO in acute respiratory distress syndrome (ARDS) patients. The activity of coagulation factors and rotational thrombelastometry were analyzed in 20 ECMO patients before (T-1) and 6 h (T0), one (T1), three (T3) and seven days (T7) after the implantation, as well as one and three days after the termination of ECMO. F XIII activity was already severely decreased to 37% (30/49) before ECMO. F XIII activity was the only coagulation factor continuously declining during vvECMO, being significantly decreased at T3 (31% (26/45) vs. 24% (18/42), p = 0.0079) and T7 (31% (26/45) vs. 23% (17/37), p = 0.0037) compared to T0. Three days after termination of vvECMO, platelet count and fibrinogen nearly doubled and factors II, V, XI and XIII showed spontaneous significant increases. Severe ARDS patients showed a considerably diminished factor XIII activity before vvECMO initiation and its activity continuously declined later on. Thus, incorporation of F XIII monitoring into the regular hemostaseologic routine during vvECMO therapy seems advisable. Due to the potential development of a hypercoagulatory state after the termination of vvECMO, tight hemostasiologic monitoring should persist in the initial phase after ECMO termination."],["dc.description.sponsorship","Fonds de dotation CSL Behring pour la recherche"],["dc.identifier.doi","10.3390/jcm10061203"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85301"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.publisher","MDPI"],["dc.relation.eissn","2077-0383"],["dc.rights","https://creativecommons.org/licenses/by/4.0/"],["dc.title","Factor XIII Activity Might Already Be Impaired before Veno-Venous ECMO in ARDS Patients: A Prospective, Observational Single-Center Cohort Study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["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.artnumber","1056"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Journal of Clinical Medicine"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Wand, Saskia"],["dc.contributor.author","Huber-Petersen, Jan Felix"],["dc.contributor.author","Schäper, Jörn"],["dc.contributor.author","Binder, Claudia"],["dc.contributor.author","Moerer, Onnen"],["dc.date.accessioned","2019-07-25T09:26:11Z"],["dc.date.available","2019-07-25T09:26:11Z"],["dc.date.issued","2019"],["dc.description.abstract","Extracorporeal (veno-venous) membrane oxygenation (vvECMO) has been shown to have negative effects on platelet number and function. This study aimed to gain more information about the impact of vvECMO on platelet function assessed by multiple electrode aggregometry (MEA). Twenty patients with the indication for vvECMO were included. Platelet function was analyzed using MEA (Multiplate®) before (T-1), 6 h (T0), one (T1), two (T2), three (T3), and seven (T4) days after the beginning of vvECMO. Median aggregational measurements were already below the normal reference range before vvECMO initiation. Platelet aggregation was significantly reduced 6 h after vvECMO initiation compared to T-1 and spontaneously recovered with a significant increase at T2. Platelet count dropped significantly between T-1 and T0 and continuously decreased between T0 and T4. At T4, ADP-induced platelet aggregation showed an inverse correlation with the paO2 in the oxygenator. Platelet function should be assessed by MEA before the initiation of extracorporeal circulation. Although ECMO therapy led to a further decrease in platelet aggregation after 6 h, all measurements had recovered to baseline on day two. This implies that MEA as a whole blood method might not adequately reflect the changes in platelet function in the later stages of extracorporeal circulation."],["dc.identifier.doi","10.3390/jcm8071056"],["dc.identifier.pmid","31330966"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16300"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/62040"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.publisher","MDPI"],["dc.relation.eissn","2077-0383"],["dc.relation.issn","2077-0383"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Platelet Function Disturbance During Veno-Venous ECMO in ARDS Patients Assessed by Multiple Electrode Aggregometry-A Prospective, Observational Cohort Study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","236"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Neurocritical Care"],["dc.bibliographiccitation.lastpage","247"],["dc.bibliographiccitation.volume","34"],["dc.contributor.author","Hernández-Durán, Silvia"],["dc.contributor.author","Salfelder, Clara"],["dc.contributor.author","Schaeper, Joern"],["dc.contributor.author","Moerer, Onnen"],["dc.contributor.author","Rohde, Veit"],["dc.contributor.author","Mielke, Dorothee"],["dc.contributor.author","von der Brelie, Christian"],["dc.date.accessioned","2021-04-14T08:26:05Z"],["dc.date.available","2021-04-14T08:26:05Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1007/s12028-020-01029-8"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/81829"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","1556-0961"],["dc.relation.issn","1541-6933"],["dc.title","Mechanical Ventilation, Sedation and Neuromonitoring of Patients with Aneurysmal Subarachnoid Hemorrhage in Germany: Results of a Nationwide Survey"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e56397"],["dc.bibliographiccitation.issue","131"],["dc.bibliographiccitation.journal","Journal of Visualized Experiments"],["dc.contributor.author","Schregel, Katharina"],["dc.contributor.author","Behme, Daniel"],["dc.contributor.author","Tsogkas, Ioannis"],["dc.contributor.author","Knauth, Michael"],["dc.contributor.author","Maier, Ilko"],["dc.contributor.author","Karch, André"],["dc.contributor.author","Mikolajczyk, Rafael"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Schäper, Jörn"],["dc.contributor.author","Hinz, José"],["dc.contributor.author","Liman, Jan"],["dc.contributor.author","Psychogios, Marios-Nikos"],["dc.date.accessioned","2018-04-23T11:47:45Z"],["dc.date.available","2018-04-23T11:47:45Z"],["dc.date.issued","2018"],["dc.description.abstract","This manuscript describes a streamlined protocol for the management of patients with acute ischemic stroke, which aims at the minimization of time from hospital admission to reperfusion. Rapid restoration of cerebral blood flow is essential for the outcomes of patients with acute ischemic stroke. Endovascular treatment (EVT) has become the standard of care to accomplish this in patients with acute stroke due to large vessel occlusion (LVO). To achieve reperfusion of ischemic brain regions as fast as possible, all in-hospital time delays have to be carefully avoided. Therefore, management of patients with acute ischemic stroke was optimized with an interdisciplinary standard operating procedure (SOP). Stroke neurologists, diagnostic as well as interventional neuroradiologists, and anesthesiologists streamlined all necessary processes from patient admission and diagnosis to EVT of eligible patients. Target times for every step were established. Actually achieved times were prospectively recorded along with clinical data and imaging scores for all endovascularly treated stroke patients. These data were regularly analyzed and discussed in interdisciplinary team meetings. Potential issues were evaluated and all staff involved was trained to adhere to the SOP. This streamlined patient management approach and enhanced interdisciplinary collaboration reduced time from patient admission to reperfusion significantly and was accompanied by a beneficial effect on clinical outcomes."],["dc.identifier.doi","10.3791/56397"],["dc.identifier.gro","3142064"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/13388"],["dc.language.iso","en"],["dc.notes.intern","lifescience updates Crossref Import"],["dc.notes.status","final"],["dc.relation.issn","1940-087X"],["dc.title","Optimized Management of Endovascular Treatment for Acute Ischemic Stroke"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Critical Care"],["dc.bibliographiccitation.volume","24"],["dc.contributor.author","Reintam Blaser, Annika"],["dc.contributor.author","Preiser, Jean-Charles"],["dc.contributor.author","Fruhwald, Sonja"],["dc.contributor.author","Wilmer, Alexander"],["dc.contributor.author","Wernerman, Jan"],["dc.contributor.author","Benstoem, Carina"],["dc.contributor.author","Casaer, Michael P."],["dc.contributor.author","Starkopf, Joel"],["dc.contributor.author","van Zanten, Arthur"],["dc.contributor.author","Rooyackers, Olav"],["dc.contributor.author","Jakob, Stephan M."],["dc.contributor.author","Loudet, Cecilia I."],["dc.contributor.author","Bear, Danielle E."],["dc.contributor.author","Elke, Gunnar"],["dc.contributor.author","Kott, Matthias"],["dc.contributor.author","Lautenschläger, Ingmar"],["dc.contributor.author","Schäper, Jörn"],["dc.contributor.author","Gunst, Jan"],["dc.contributor.author","Stoppe, Christian"],["dc.contributor.author","Nobile, Leda"],["dc.contributor.author","Fuhrmann, Valentin"],["dc.contributor.author","Berger, Mette M."],["dc.contributor.author","Oudemans-van Straaten, Heleen M."],["dc.contributor.author","Arabi, Yaseen M."],["dc.contributor.author","Deane, Adam M."],["dc.date.accessioned","2021-04-14T08:26:31Z"],["dc.date.available","2021-04-14T08:26:31Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1186/s13054-020-02889-4"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17318"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/81974"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.notes.intern","Merged from goescholar"],["dc.relation.eissn","1364-8535"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Gastrointestinal dysfunction in the critically ill: a systematic scoping review and research agenda proposed by the Section of Metabolism, Endocrinology and Nutrition of the European Society of Intensive Care Medicine"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["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"]]