Teucher, Nils

[["dc.bibliographiccitation.firstpage","553"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Clinical Research in Cardiology"],["dc.bibliographiccitation.lastpage","563"],["dc.bibliographiccitation.volume","101"],["dc.contributor.author","Puls, Miriam"],["dc.contributor.author","Viel, Tanja"],["dc.contributor.author","Danner, Bernhard C."],["dc.contributor.author","Jacobshagen, Claudius"],["dc.contributor.author","Teucher, Nils"],["dc.contributor.author","Hanekop, Gunnar"],["dc.contributor.author","Schoendube, Friedrich"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Seipelt, Ralf G."],["dc.contributor.author","Schillinger, Wolfgang"],["dc.date.accessioned","2017-09-07T11:48:50Z"],["dc.date.available","2017-09-07T11:48:50Z"],["dc.date.issued","2012"],["dc.description.abstract","Transcatheter aortic valve implantation (TAVI) has recently developed into an acceptable alternative to conventional surgery in high-risk patients. However, information on the identification of patients gaining most benefit from this procedure is still limited. The aim of this study was to evaluate safety and efficacy of TAVI in different patient cohorts. Between August 2008 and December 2010, 180 high-risk patients underwent TAVI at our institution (97 transapical and 83 transfemoral approaches). Periprocedural complications as well as mortality and incidence of MACCE during follow-up were recorded. Mean age was 82 +/- A 5 years, and mean logistic EuroScore 27 +/- A 14%. In the total cohort, 30-day mortality was 8.9% and 12-month survival (according to Kaplan-Meier-analysis) 72%, with no significant differences between the two approaches. However, a significant difference in survival was obvious after stratification of patients according to logistic EuroScore mortality estimates. Survival proportions at 1 year were 62% in patients with logistic EuroScore > 40%, 71% in patients with EuroScore 20-40% and 80% in octogenarians with EuroScore < 20% (P = 0.009). Furthermore, the observed median event-free survival as an indicator for morbidity ranged between 315 days in the first, 442 days in the second and 710 days in the third group (P = 0.1). TAVI proved to be feasible with reproducible results. However, mortality and rehospitalization rates were considerably high in specific patient cohorts, suggesting that the risk-to-benefit ratio of TAVI should be validated individually. In the present study, octogenarians with logistic EuroScore < 20% could be identified as candidates apparently gaining high benefit from the procedure."],["dc.identifier.doi","10.1007/s00392-012-0426-4"],["dc.identifier.gro","3142507"],["dc.identifier.isi","000305397200006"],["dc.identifier.pmid","22350751"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8091"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8866"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: Edwards Lifesciences"],["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","The risk-to-benefit ratio of transcatheter aortic valve implantation in specific patient cohorts: a single-centre experience"],["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","673"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","European Journal of Heart Failure"],["dc.bibliographiccitation.lastpage","680"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Schillinger, Wolfgang"],["dc.contributor.author","Teucher, Nils"],["dc.contributor.author","Christians, Claus"],["dc.contributor.author","Kohlhaas, Michael"],["dc.contributor.author","Sossalla, Samuel"],["dc.contributor.author","Van Nguyen, Phuc"],["dc.contributor.author","Schmidt, Albrecht G."],["dc.contributor.author","Schunck, Ortwin"],["dc.contributor.author","Nebendahl, Klaus"],["dc.contributor.author","Maier, Lars S."],["dc.contributor.author","Zeitz, Oliver"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.date.accessioned","2017-09-07T11:52:27Z"],["dc.date.available","2017-09-07T11:52:27Z"],["dc.date.issued","2006"],["dc.description.abstract","We investigated the hypothesis that increased intracellular [Na+](i) in heart failure contributes to preservation of SR Ca2+ load which may become particularly evident at slow heart rates. [Na+]i in SBFI-loaded myocytes from rabbits with pacing-induced heart failure (PHF) was significantly higher at each frequency as compared to Sham-operated animals. Furthermore, PHF rabbits demonstrated reduced SR Ca2+-ATPase protein levels (-37%, p < 0.04) but unchanged Na+/Ca2+ exchanger protein levels. At 0.25 Hz, isometric force was similar in cardiac trabeculae from PHF rabbits as compared to control (PHF, 3.6 +/- 1.3; Sham, 4.4 +/- 0.6 mN/mm(2)). Rapid cooling contractures (RCCs) were unchanged indicating preserved SR Ca2+ load at this frequency. In Sham, isometric twitch force increased with rising frequencies to 29.0 +/- 2.8 mN/mm(2) at 3.0 Hz (p < 0.05) as compared to 0.25 Hz. RCCs showed a parallel increase by 186 +/- 47% (p < 0.01). In PHF, frequency-dependent increase in force (15.8 +/- 4.7 mN/mm(2) at 3.0 Hz) and RCCs (increase by 70 +/- 40%) were significantly blunted. Thus, in PHF in rabbits SR Ca2+ load is preserved at low frequencies despite decreased SR Ca2+-ATPase expression. This may result from [Na+](i)-dependent changes in Na+/Ca2+ exchanger activity. (c) 2006 European Society of Cardiology. Published by Elsevier B.V All rights reserved."],["dc.identifier.doi","10.1016/j.ejheart.2006.01.013"],["dc.identifier.gro","3143598"],["dc.identifier.isi","000242383300002"],["dc.identifier.pmid","16540370"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1130"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","1388-9842"],["dc.title","High intracellular Na+ preserves myocardial function at low heart rates in isolated myocardium from failing hearts"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","996"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Cardiovascular Research"],["dc.bibliographiccitation.lastpage","1003"],["dc.bibliographiccitation.volume","57"],["dc.contributor.author","Schillinger, Wolfgang"],["dc.contributor.author","Ohler, A."],["dc.contributor.author","Embry, S. L."],["dc.contributor.author","Muller, F"],["dc.contributor.author","Christians, Claus"],["dc.contributor.author","Janssen, P. M. L."],["dc.contributor.author","Kogler, H."],["dc.contributor.author","Teucher, Niels"],["dc.contributor.author","Pieske, Burkert"],["dc.contributor.author","Seidler, Tim"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.date.accessioned","2021-06-01T10:50:03Z"],["dc.date.available","2021-06-01T10:50:03Z"],["dc.date.issued","2003"],["dc.description.abstract","Objectives: The functional consequences of Na+/Ca2+ exchanger (NCX) overexpression in heart failure have been controversially discussed. NCX function strongly depends on intracellular sodium which has been shown to be increased in heart failure. Methods and results: We investigated the Na+/K+-ATPase (NKA) inhibitor ouabain (0.5-16 mumol/l) in electrically stimulated, isotonically contracting adult rabbit cardiocytes overexpressing NCX after adenoviral gene transfer (Ad-NCX-GFP, 48 h culture time). Myocytes transfected with adenovirus encoding for green fluorescent protein (Ad-GFP) served as a control. Contractions were analyzed by video-edge detection. In the Ad-NCX-GFP group, the maximum inotropic response was significantly reduced by 50.7% (P < 0.05). This was a result of an enhanced susceptibility to contracture after exposure to the drug (median concentration (25-75%): 4 (4-8) vs. 8 (6-16) mumol/l, P < 0.05). When analyzing relaxation before contracture, the maximum relaxation velocity was reduced (0.15 +/- 0.04 vs. 0.27 +/- 0.04 mum/s, P < 0.05) and the time from peak shortening to 90% of relaxation was increased (298 +/- 39 vs. 185 +/- 15 ms, P < 0.05). No differences in systolic and diastolic parameters were observed with the Na+ channel modulator BDF9198 (1 mumol/l). Conclusions: Inhibition of NKA by ouabain induces a combined diastolic and systolic dysfunction in NCX overexpressing rabbit myocytes. This may be the consequence of cytoplasmic Ca2+ overload due to inhibition of forward mode or induction of reverse mode Na+/Ca2+ exchange. In end-stage failing human myocardium and during digitalis treatment this mechanism may be of major importance. (C) 2003 European Society of Cardiology. Published by Elsevier Science B.V. All rights reserved."],["dc.identifier.doi","10.1016/S0008-6363(02)00829-5"],["dc.identifier.gro","3144121"],["dc.identifier.isi","000181975100014"],["dc.identifier.pmid","12650877"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/86511"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","0008-6363"],["dc.title","The functional effect of adenoviral Na+/Ca2+ exchanger overexpression in rabbit myocytes depends on the activity of the Na+/K+-ATPase"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["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.journal","European Heart Journal"],["dc.bibliographiccitation.volume","25"],["dc.contributor.author","Schillinger, Wolfgang"],["dc.contributor.author","Teucher, N."],["dc.contributor.author","Zeitz, O."],["dc.contributor.author","Christians, C."],["dc.contributor.author","Kohlhaas, M."],["dc.contributor.author","van Nguyen, P."],["dc.contributor.author","Maier, Lars. S."],["dc.contributor.author","Hasenfuß, Gerd"],["dc.date.accessioned","2018-11-07T10:46:39Z"],["dc.date.available","2018-11-07T10:46:39Z"],["dc.date.issued","2004"],["dc.format.extent","557"],["dc.identifier.isi","000224056502234"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/47795"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","W B Saunders Co Ltd"],["dc.publisher.place","London"],["dc.relation.conference","ESC Congress 2004"],["dc.relation.eventlocation","Munich, GERMANY"],["dc.relation.issn","0195-668X"],["dc.title","Contractility and intracellular sodium in pacing-induced heart failure"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","17"],["dc.bibliographiccitation.journal","Circulation"],["dc.bibliographiccitation.volume","110"],["dc.contributor.author","Teucher, N."],["dc.contributor.author","Sossalla, Samuel T."],["dc.contributor.author","Sag, Can Martin"],["dc.contributor.author","Kockskaemper, Jens"],["dc.contributor.author","Unsoeld, Bernhard W."],["dc.contributor.author","Schondube, F. A."],["dc.contributor.author","Schworer, H."],["dc.contributor.author","Maier, Lars. S."],["dc.contributor.author","Schillinger, Wolfgang"],["dc.date.accessioned","2018-11-07T10:44:36Z"],["dc.date.available","2018-11-07T10:44:36Z"],["dc.date.issued","2004"],["dc.format.extent","31"],["dc.identifier.isi","000224783500140"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/47308"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.publisher.place","Philadelphia"],["dc.relation.conference","77th Scientific Meeting of the American-Heart-Association"],["dc.relation.eventlocation","New Orleans, LA"],["dc.relation.issn","0009-7322"],["dc.title","Pantoprazole induces a dose-dependent and reversible depression of contractile function in human myocardium"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","391"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Clinical Research in Cardiology"],["dc.bibliographiccitation.lastpage","399"],["dc.bibliographiccitation.volume","98"],["dc.contributor.author","Schillinger, Wolfgang"],["dc.contributor.author","Hoernes, Nina"],["dc.contributor.author","Teucher, Nils"],["dc.contributor.author","Sossalla, Samuel"],["dc.contributor.author","Sehrt, Daniel"],["dc.contributor.author","Jung, Klaus"],["dc.contributor.author","Huenlich, Mark"],["dc.contributor.author","Unsoeld, Bernhard W."],["dc.contributor.author","Geiling, Bianca"],["dc.contributor.author","Ramadori, Giuliano"],["dc.contributor.author","Hilgers, Reinhard"],["dc.contributor.author","Schwoerer, Harald"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.date.accessioned","2017-09-07T11:47:26Z"],["dc.date.available","2017-09-07T11:47:26Z"],["dc.date.issued","2009"],["dc.description.abstract","Reports on cardiac problems with oral proton pump inhibitors have caused extensive safety reviews by the US Food and Drug Administration. We provide additional data on acute cardiac effects of an intravenous application. Echocardiography was performed in 18 healthy volunteers after administration of a common high-dose regimen of pantoprazole (80 mg i.v. bolus followed by 8 mg/h for 1 h) or placebo. The design included a randomized, double-blind, placebo-controlled cross-over trial. Ejection fraction (%, mean +/- A SE) in the treatment group (placebo group) was 60.7 +/- A 1.1 (61.2 +/- A 1.7) at baseline, and 62.6 +/- A 1.1 (62.1 +/- A 1.9), 64.7 +/- A 1.6 (63.5 +/- A 1.3), 62.6 +/- A 1.6 (61.0 +/- A 1.6) and 63.0 +/- A 1.4 (61.8 +/- A 1.5) at 7.5, 15, 30 and 60 min after bolus application, respectively (p = n.s.). Similarly, no significant changes were found for cardiac output, cardiac index, blood pressure and heart rate. In contrast, gastric pH that was used as a treatment control was significantly increased 60 min after the application of pantoprazole as compared to baseline and to placebo. Pantoprazole as injection is safe in healthy subjects with respect to cardiac contractile function. However, in view of recent reports of negative inotropy of the drug, further studies in heart failure patients are required."],["dc.identifier.doi","10.1007/s00392-009-0012-6"],["dc.identifier.gro","3143105"],["dc.identifier.isi","000267217400008"],["dc.identifier.pmid","19301059"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?goescholar/3460"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/583"],["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","Dr Dietrich Steinkopff Verlag"],["dc.relation.issn","1861-0684"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Recent in vitro findings of negative inotropy of pantoprazole did not translate into clinically relevant effects on left ventricular function in healthy volunteers"],["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.journal","European Heart Journal"],["dc.bibliographiccitation.volume","24"],["dc.contributor.author","Schillinger, Wolfgang"],["dc.contributor.author","Ohler, A."],["dc.contributor.author","Emami, S."],["dc.contributor.author","Mueller, F."],["dc.contributor.author","Koegler, Harald"],["dc.contributor.author","Teucher, N."],["dc.contributor.author","Seidler, Tim"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.date.accessioned","2018-11-07T10:37:12Z"],["dc.date.available","2018-11-07T10:37:12Z"],["dc.date.issued","2003"],["dc.format.extent","58"],["dc.identifier.doi","10.1016/S0195-668X(03)93865-6"],["dc.identifier.isi","000185638800214"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/45507"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","W B Saunders Co Ltd"],["dc.publisher.place","London"],["dc.relation.conference","Congress of the European-Society-of-Cardiology"],["dc.relation.eventlocation","VIENNA, AUSTRIA"],["dc.relation.issn","0195-668X"],["dc.title","The activity of the sarcolemmal Na pump determines the functional consequence of adenoviral Na/Ca exchanger overexpression"],["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","27"],["dc.contributor.author","Teucher, N."],["dc.contributor.author","Sossalla, Samuel T."],["dc.contributor.author","Kettlewell, Sarah"],["dc.contributor.author","Schondube, F. A."],["dc.contributor.author","Smith, Godfrey L."],["dc.contributor.author","Schworer, H."],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Schillinger, Wolfgang"],["dc.date.accessioned","2018-11-07T09:27:53Z"],["dc.date.available","2018-11-07T09:27:53Z"],["dc.date.issued","2006"],["dc.format.extent","343"],["dc.identifier.isi","000240668402202"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/30647"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.publisher.place","Oxford"],["dc.relation.eventlocation","Barcelona, SPAIN"],["dc.relation.issn","1522-9645"],["dc.relation.issn","0195-668X"],["dc.title","Pantoprazole depresses contractile function of human and rabbit myocardium"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","404"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Cardiovascular Research"],["dc.bibliographiccitation.lastpage","412"],["dc.bibliographiccitation.volume","60"],["dc.contributor.author","Wagner, Stefan"],["dc.contributor.author","Seidler, Tim"],["dc.contributor.author","Picht, E."],["dc.contributor.author","Maier, Lars S."],["dc.contributor.author","Kazanski, V"],["dc.contributor.author","Teucher, Niels"],["dc.contributor.author","Schillinger, Wolfgang"],["dc.contributor.author","Pieske, Burkert"],["dc.contributor.author","Isenberg, G."],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Kogler, H."],["dc.date.accessioned","2017-09-07T11:44:09Z"],["dc.date.available","2017-09-07T11:44:09Z"],["dc.date.issued","2003"],["dc.description.abstract","Objective: In heart failure (HF), the generation of reactive oxygen species (ROS) is enhanced. It was shown that failing cardiac myocytes are more susceptible to ROS-induced damage, possibly due to increased expression of the sarcolemmal Na-Ca exchanger (NCX). Methods: We investigated the consequences of increased expression levels of NCX in adult rabbit ventricular cardiomyocytes (via adenovirus-mediated gene transfer, Ad-NCXI-GFP) with respect to tolerance towards ROS. After 48-h incubation, cells were monitored for morphological changes on an inverted microscope. ROS were generated via hydrogen peroxide (H2O2) (100 mumol/l) and Fe3+/nitrilotriacetate (Fe3+/NTA, 100/200 mumol/l) for 4 min and cell morphology was followed over 30 min. [Na+](i) and [Ca2+](i) in native cells were measured using SBFI-AM and Indo l-AM, respectively. Results: In native myocytes, exposure to ROS induced hypercontracture. This was accompanied by a 1.3-fold increase in diastolic Indo l fluorescence ratio (P < 0.05). Overexpression of NCX significantly enhanced development of hypercontracture. After 15 min, the percentage of cells that had undergone hypercontracture (F-hyper) was 85 +/- 4% vs. only 44 +/- 10% in control cells (P < 0.05). Inhibition of NCX-mediated Ca2+ entry with KB-R7943 (5 mumol/l) reduced (F-hyper) to 33 +/- 11% (P < 0.05). [Na+](i) was increased 2.9-fold 1 min prior to hypercontracture (P < 0.05). Conclusions: ROS-induced hypercontracture is due to Ca2+ entry via NCX which could be triggered by a concomitant substantial increase in [Na+]i. Elevated NCX levels predispose to ROS-induced injury, a mechanism likely contributing to myocyte dysfunction and death in heart failure. (C) 2003 European Society of Cardiology. Published by Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.cardiores.2003.08.006"],["dc.identifier.gro","3144041"],["dc.identifier.isi","000186359500025"],["dc.identifier.pmid","14613870"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1621"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","0008-6363"],["dc.title","Na+-Ca2+ exchanger overexpression predisposes to reactive oxygen species-induced injury"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]