Jacobshagen, Claudius

[["dc.bibliographiccitation.firstpage","267"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Clinical Research in Cardiology"],["dc.bibliographiccitation.lastpage","276"],["dc.bibliographiccitation.volume","99"],["dc.contributor.author","Jacobshagen, Claudius"],["dc.contributor.author","Pelster, Theresa"],["dc.contributor.author","Pax, Anja"],["dc.contributor.author","Horn, Wiebke"],["dc.contributor.author","Schmidt-Schweda, Stephan"],["dc.contributor.author","Unsoeld, Bernhard W."],["dc.contributor.author","Seidler, Tim"],["dc.contributor.author","Wagner, Stephan"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Maier, Lars S."],["dc.date.accessioned","2017-09-07T11:46:04Z"],["dc.date.available","2017-09-07T11:46:04Z"],["dc.date.issued","2010"],["dc.description.abstract","Post-cardiac arrest myocardial dysfunction is a common phenomenon after return of spontaneous circulation (ROSC) and contributes to hemodynamic instability and low survival rates after cardiac arrest. Mild hypothermia for 24 h after ROSC has been shown to significantly improve neurologic recovery and survival rates. In the present study we investigate the influence of therapeutic hypothermia on hemodynamic parameters in resuscitated patients and on contractility in failing human myocardium. We analyzed hemodynamic data from 200 cardiac arrest survivors during the hypothermia period. The initial LVEF was 32.6 +/- A 1.2% indicating a significantly impaired LV function. During hypothermia induction, the infusion rate of epinephrine could be significantly reduced from 9.1 +/- A 1.3 mu g/min [arrival intensive care unit (ICU) 35.4A degrees C] to 4.6 +/- A 1.0 mu g/min (34A degrees C) and 2.8 +/- A 0.5 mu g/min (33A degrees C). The dobutamine and norepinephrine application rates were not changed significantly. The mean arterial blood pressure remained stable. The mean heart rate significantly decreased from 91.8 +/- A 1.7 bpm (arrival ICU) to 77.3 +/- A 1.5 bpm (34A degrees C) and 70.3 +/- A 1.4 bpm (33A degrees C). In vitro we investigated the effect of hypothermia on isolated ventricular muscle strips from explanted failing human hearts. With decreasing temperature, the contractility increased to a maximum of 168 +/- A 23% at 27A degrees C (n = 16, P < 0.05). Positive inotropic response to hypothermia was accompanied by moderately increased rapid cooling contractures as a measure of sarcoplasmic reticulum (SR) Ca(2+) content, but can be elicited even when the SR Ca(2+) release is blocked in the presence of ryanodine. Contraction and relaxation kinetics are prolonged with hypothermia, indicating increased Ca(2+) sensitivity as the main mechanism responsible for inotropy. In conclusion, mild hypothermia stabilizes hemodynamics in cardiac arrest survivors which might contribute to improved survival rates in these patients. Mechanistically, we demonstrate that hypothermia improves contractility in failing human myocardium most likely by increasing Ca(2+)-sensitivity."],["dc.identifier.doi","10.1007/s00392-010-0113-2"],["dc.identifier.gro","3142931"],["dc.identifier.isi","000277014600001"],["dc.identifier.pmid","20130890"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/4240"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/389"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Springer"],["dc.publisher.place","Heidelberg"],["dc.relation.issn","1861-0684"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Effects of mild hypothermia on hemodynamics in cardiac arrest survivors and isolated failing human myocardium"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","290"],["dc.bibliographiccitation.issue","16"],["dc.bibliographiccitation.journal","Circulation"],["dc.bibliographiccitation.lastpage","291"],["dc.bibliographiccitation.volume","116"],["dc.contributor.author","Jacobshagen, Claudius"],["dc.contributor.author","Kortlepel, Swantje"],["dc.contributor.author","Unsoeld, Bernhard W."],["dc.contributor.author","Kogler, Harald"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Maier, Lars. S."],["dc.date.accessioned","2018-11-07T10:57:43Z"],["dc.date.available","2018-11-07T10:57:43Z"],["dc.date.issued","2007"],["dc.identifier.isi","000250394301341"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50318"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.publisher.place","Philadelphia"],["dc.relation.conference","80th Annual Scientific Session of the American-Heart-Association"],["dc.relation.eventlocation","Orlando, FL"],["dc.relation.issn","0009-7322"],["dc.title","Inhibition of phosphatidylinositol 3-kinase (PI3K) improves contractility in alpha-adrenergic stimulated myocardium"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","18"],["dc.bibliographiccitation.journal","Circulation"],["dc.bibliographiccitation.volume","118"],["dc.contributor.author","Unsoeld, Bernhard W."],["dc.contributor.author","Schuster, Manfred"],["dc.contributor.author","Loibner, Hans"],["dc.contributor.author","Becker, Alexander"],["dc.contributor.author","Seidler, Tim"],["dc.contributor.author","Jacobshagen, Claudius"],["dc.contributor.author","Kuba, Keiji"],["dc.contributor.author","Imai, Yumiko"],["dc.contributor.author","Penninger, Josef"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.date.accessioned","2018-11-07T11:09:55Z"],["dc.date.available","2018-11-07T11:09:55Z"],["dc.date.issued","2008"],["dc.format.extent","S947"],["dc.identifier.isi","000262104503504"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53105"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.publisher.place","Philadelphia"],["dc.relation.conference","81st Annual Scientific Session of the American-Heart-Association"],["dc.relation.eventlocation","New Orleans, LA"],["dc.relation.issn","0009-7322"],["dc.title","Angiotensin-Converting-Enzyme 2 (rhACE2) Potently Attenuates the Negative Hemodynamic Effects of Angiotensin II (ATII) and Improves Post-Myocardial Infarction (MI) Remodeling"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","European Heart Journal"],["dc.bibliographiccitation.volume","29"],["dc.contributor.author","Jacobshagen, Claudius"],["dc.contributor.author","Unsoeld, Bernhard W."],["dc.contributor.author","Seidler, Tim"],["dc.contributor.author","Schott, Peter"],["dc.contributor.author","Maier, Lars. S."],["dc.contributor.author","Hasenfuß, Gerd"],["dc.date.accessioned","2018-11-07T11:11:18Z"],["dc.date.available","2018-11-07T11:11:18Z"],["dc.date.issued","2008"],["dc.format.extent","265"],["dc.identifier.isi","000208702501245"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53401"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.publisher.place","Oxford"],["dc.relation.issn","0195-668X"],["dc.title","Large volume, ice-cold intravenous fluid for therapeutic hypothermia does not compromise the respiratory situation in patients after cardiac arrest"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","20"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Cardiovascular Therapeutics"],["dc.bibliographiccitation.lastpage","26"],["dc.bibliographiccitation.volume","33"],["dc.contributor.author","Unsoeld, Bernhard W."],["dc.contributor.author","Teucher, Nils"],["dc.contributor.author","Didie, Michael"],["dc.contributor.author","Sossalla, Samuel"],["dc.contributor.author","Jacobshagen, Claudius"],["dc.contributor.author","Seidler, Tim"],["dc.contributor.author","Schillinger, Wolfgang"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.date.accessioned","2017-09-07T11:44:39Z"],["dc.date.available","2017-09-07T11:44:39Z"],["dc.date.issued","2015"],["dc.description.abstract","BackgroundPantoprazole has been shown to exert a negative inotropic effect in isolated myocardium. The purpose of this study was to evaluate the hemodynamic effects of pantoprazole in vivo in healthy myocardium and in the setting of heart failure. Methods and ResultsHealthy mice and mice with heart failure 4weeks after myocardial infarction induced by permanent LAD ligation were instrumented with a Millar Mikrotip conductance catheter to record pressure-volume loops. Pantoprazole was infused at rates of 3 and 10mg/kg/min intravenously, and hemodynamic parameters were recorded. Infusion of pantoprazole at increasing rates lead to a significant decline of end systolic LV pressure by decreasing heart rate, myocardial contractility and arterial elastance. These effects were quick, beginning immediately with the infusion and usually reaching a plateau after 2 or 3min of infusion. The effects on blood pressure and heart rate were of comparable size in healthy mice and mice with MI. However, in sham-operated mice, there was a compensatory increase in stroke volume that sufficed to maintain cardiac output at a constant level, which was missing in mice with MI. In 4 of 13 mice with MI infusion of 10mg/kg/min pantoprazole lead to pump failure, which was lethal in 2 of these animals. ConclusionAt higher infusion rates, pantoprazole is able to induce negative hemodynamic responses. In particular, in the setting of heart failure, these effects can lead to significant impairment of cardiac function. Therefore, high infusion rates of pantoprazole should be avoided especially in heart failure patients."],["dc.identifier.doi","10.1111/1755-5922.12102"],["dc.identifier.gro","3141966"],["dc.identifier.isi","000348660500004"],["dc.identifier.pmid","25529757"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/3057"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Wiley-blackwell"],["dc.relation.eissn","1755-5922"],["dc.relation.issn","1755-5914"],["dc.title","Negative Hemodynamic Effects of Pantoprazole at High Infusion Rates in Mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","21"],["dc.bibliographiccitation.journal","Circulation"],["dc.bibliographiccitation.volume","124"],["dc.contributor.author","Jacobshagen, Claudius"],["dc.contributor.author","Schmidt-Schweda, Stephan"],["dc.contributor.author","Pelster, Theresa"],["dc.contributor.author","Pax, Anja"],["dc.contributor.author","Unsoeld, Bernhard W."],["dc.contributor.author","Seidler, Tim"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Maier, Lars. S."],["dc.date.accessioned","2018-11-07T08:49:42Z"],["dc.date.available","2018-11-07T08:49:42Z"],["dc.date.issued","2011"],["dc.identifier.isi","000299738700061"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21528"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.publisher.place","Philadelphia"],["dc.relation.issn","0009-7322"],["dc.title","Trends in Postresuscitation Care: A 7-Year Experience After Implementation of Therapeutic Hypothermia"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","European Heart Journal"],["dc.bibliographiccitation.volume","28"],["dc.contributor.author","Jacobshagen, Claudius"],["dc.contributor.author","Grueber, M."],["dc.contributor.author","Teucher, N."],["dc.contributor.author","Schmidt, A."],["dc.contributor.author","Unsoeld, Bernhard W."],["dc.contributor.author","Toischer, Karl"],["dc.contributor.author","Van, P. Nguyen"],["dc.contributor.author","Kogler, Harald"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.date.accessioned","2018-11-07T10:58:55Z"],["dc.date.available","2018-11-07T10:58:55Z"],["dc.date.issued","2007"],["dc.format.extent","424"],["dc.identifier.isi","000208702202250"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50575"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.publisher.place","Oxford"],["dc.relation.issn","0195-668X"],["dc.title","Inhibited phosphorylation of PTEN attenuates the transition from cardiac hypertrophy to heart failure and reduces mortality in aortic-banded mice"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","6841"],["dc.bibliographiccitation.journal","Frontiers in Bioscience"],["dc.bibliographiccitation.lastpage","6849"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Jacobshagen, Claudius"],["dc.contributor.author","Kortlepel, Swantje"],["dc.contributor.author","Unsoeld, Bernhard W."],["dc.contributor.author","Sowa, Thomas"],["dc.contributor.author","Koegler, Harald"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Maier, Lars S."],["dc.date.accessioned","2017-09-07T11:48:45Z"],["dc.date.available","2017-09-07T11:48:45Z"],["dc.date.issued","2008"],["dc.description.abstract","Recent studies have demonstrated that phosphoinositide 3-kinases (PI3Ks) play a fundamental role in regulating myocardial contractility. However, even though alpha(1)-adrenergic receptor stimulation is known to activate PI3Ks, the impact of this pathway on the inotropic effects of alpha(1)-stimulation is unclear. Isolated rabbit ventricular myocytes were preincubated with the PI3K inhibitor wortmannin (WM, 0.1 mu mol/L)). The alpha(1) agonist phenylephrine (PE, 10 mu mol/L) induced a significantly stronger increase in contractility in WM-treated versus control myocytes (Fractional shortening in % of resting cell length: 6.14+/-0.33%; n=26 versus 4.85+/0.33%; n=26, P<0.05). Furthermore, pretreatment with WM significantly increased the positive inotropic effect of PE in intact muscle strips from rabbit hearts. Mechanistically, we demonstrate that in WM-treated myocytes PE increased phospholamban (PLN) phosphorylation and intracellular Ca2+ transients to a significantly greater extent than in control myocytes. In summary, this is the first study to demonstrate that inhibition of PI3K by increasing PLN phosphorylation and Ca2+ transients significantly improves contractility in alpha(1)-adrenergically stimulated myocardium. This may have clinical implications for the treatment of decreased cardiac function in acute heart failure."],["dc.identifier.doi","10.2741/3192"],["dc.identifier.gro","3143306"],["dc.identifier.isi","000255885000272"],["dc.identifier.pmid","18508698"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/806"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Frontiers In Bioscience Inc"],["dc.relation.issn","1093-9946"],["dc.title","Inhibition of PI3K improves contractility in alpha(1)-adrenergically stimulated myocardium"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","European Heart Journal"],["dc.bibliographiccitation.volume","26"],["dc.contributor.author","Jacobshagen, Claudius"],["dc.contributor.author","Grueber, M."],["dc.contributor.author","Unsoeld, Bernhard W."],["dc.contributor.author","Nguyen van, P."],["dc.contributor.author","Koegler, Harald"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.date.accessioned","2018-11-07T10:56:04Z"],["dc.date.available","2018-11-07T10:56:04Z"],["dc.date.issued","2005"],["dc.format.extent","100"],["dc.identifier.isi","000233987100396"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/49928"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.publisher.place","Oxford"],["dc.relation.conference","27th Congress of the European-Society-of-Cardiology"],["dc.relation.eventlocation","Stockholm, SWEDEN"],["dc.relation.issn","1522-9645"],["dc.relation.issn","0195-668X"],["dc.title","Celecoxib, a cycloxygenase-2 inhibitor, prevents hypertrophic response in cardiomyocytes through inhibition of Akt/GSK-3beta signaling"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1223"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Resuscitation"],["dc.bibliographiccitation.lastpage","1228"],["dc.bibliographiccitation.volume","80"],["dc.contributor.author","Jacobshagen, Claudius"],["dc.contributor.author","Pax, Anja"],["dc.contributor.author","Unsoeld, Bernhard W."],["dc.contributor.author","Seidler, Tim"],["dc.contributor.author","Schmidt-Schweda, Stephan"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Maier, Lars S."],["dc.date.accessioned","2017-09-07T11:46:46Z"],["dc.date.available","2017-09-07T11:46:46Z"],["dc.date.issued","2009"],["dc.description.abstract","International guidelines for cardiopulmonary resuscitation recommend mild hypothermia (32-34 degrees C) for 12-24 h in comatose survivors of cardiac arrest. To induce therapeutic hypothermia a variety of external and intravascular cooling devices are available. A cheap and effective method for inducing hypothermia is the infusion of large volume, ice-cold intravenous fluid. There are concerns regarding the effects of rapid infusion of large volumes of fluid on respiratory function in cardiac arrest survivors. We have retrospectively studied the effects of high volume cold fluid infusion on respiratory function in 52 resuscitated cardiac arrest patients. The target temperature of 32-34 degrees C was achieved after 4.1 +/- 0.5 h (cooling rate 0.48 degrees C/h). During this period 3427 +/- 210 mL ice-cold fluid was infused. Despite significantly reduced LV-function (EF 35.8 +/- 2.2%) the respiratory status of these patients did not deteriorate significantly. On intensive care unit admission the mean PaO(2). was 231.4 +/- 20.6 mmHg at a F(i)O(2) of 0.82 +/- 0.03 (PaO(2)/F(i)O(2) = 290.0 +/- 24.1) and a PEEP level of 7.14 +/- 0.31 mbar. Until reaching the target temperature of <= 34 degrees C the F(i)O(2) could be significantly reduced to 0.63 +/- 0.03 with unchanged PEEP level (7.23 +/- 0.36 mbar). Under these conditions the PaO(2)/F(i)O(2) ratio slightly decreased to 247.5 +/- 18.5 (P = 0.0893). Continuing the saline infusion to achieve a body temperature of 33 degrees C, the F(i)O(2) Could be further reduced with unchanged PEEP. The infusion of large volume, ice-cold fluid is an effective and inexpensive method for inducing therapeutic hypothermia. Resuscitation from cardiac arrest is associated with a deterioration in respiratory function. The infusion of large Volumes of cold fluid does not cause a statistically significant further deterioration in respiratory function. A larger, randomized and prospective study is required to assess the efficacy and safety of ice-cold fluid infusion for the induction of therapeutic hypothermia. (C) 2009 Elsevier Ireland Ltd. All rights reserved."],["dc.identifier.doi","10.1016/j.resuscitation.2009.06.032"],["dc.identifier.gro","3143033"],["dc.identifier.isi","000272009600003"],["dc.identifier.pmid","19674825"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/503"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Elsevier Ireland Ltd"],["dc.relation.issn","0300-9572"],["dc.title","Effects of large volume, ice-cold intravenous fluid infusion on respiratory function in cardiac arrest survivors"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]