Just, Hanjörg

[["dc.bibliographiccitation.firstpage","434"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Circulation Research"],["dc.bibliographiccitation.lastpage","442"],["dc.bibliographiccitation.volume","75"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Reinecke, H."],["dc.contributor.author","Studer, R."],["dc.contributor.author","Meyer, M."],["dc.contributor.author","Pieske, Burkert"],["dc.contributor.author","Holtz, J."],["dc.contributor.author","Holubarsch, Christian"],["dc.contributor.author","Posival, H."],["dc.contributor.author","Just, Hanjörg"],["dc.contributor.author","Drexler, H."],["dc.date.accessioned","2017-09-07T11:52:59Z"],["dc.date.available","2017-09-07T11:52:59Z"],["dc.date.issued","2012"],["dc.identifier.doi","10.1161/01.res.75.3.434"],["dc.identifier.gro","3145001"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/2689"],["dc.notes.intern","Crossref Import"],["dc.notes.status","public"],["dc.publisher","Ovid Technologies (Wolters Kluwer Health)"],["dc.relation.issn","0009-7330"],["dc.title","Relation between myocardial function and expression of sarcoplasmic reticulum Ca(2+)-ATPase in failing and nonfailing human myocardium"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","8"],["dc.bibliographiccitation.journal","European heart journal"],["dc.bibliographiccitation.lastpage","13"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Holubarsch, Christian"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Thierfelder, L."],["dc.contributor.author","Pieske, Burkert"],["dc.contributor.author","Just, Hanjörg"],["dc.date.accessioned","2017-09-07T11:51:53Z"],["dc.date.available","2017-09-07T11:51:53Z"],["dc.date.issued","1991"],["dc.identifier.gro","3144807"],["dc.identifier.isi","A1991GB44200003"],["dc.identifier.pmid","1833195"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/2472"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","W B Saunders Co Ltd"],["dc.relation.issn","0195-668X"],["dc.title","THE HEART IN HEART-FAILURE VENTRICULAR AND MYOCARDIAL ALTERATIONS"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1228"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Circulation"],["dc.bibliographiccitation.lastpage","1237"],["dc.bibliographiccitation.volume","88"],["dc.contributor.author","Holubarsch, Christian"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Schmidt-Schweda, Stephan"],["dc.contributor.author","Knorr, A."],["dc.contributor.author","Pieske, Burkert"],["dc.contributor.author","Ruf, T."],["dc.contributor.author","Fasol, R."],["dc.contributor.author","Just, Hanjörg"],["dc.date.accessioned","2017-09-07T11:53:01Z"],["dc.date.available","2017-09-07T11:53:01Z"],["dc.date.issued","2012"],["dc.identifier.doi","10.1161/01.cir.88.3.1228"],["dc.identifier.gro","3145003"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/2692"],["dc.notes.intern","Crossref Import"],["dc.notes.status","public"],["dc.publisher","Ovid Technologies (Wolters Kluwer Health)"],["dc.relation.issn","0009-7322"],["dc.title","Angiotensin I and II exert inotropic effects in atrial but not in ventricular human myocardium. An in vitro study under physiological experimental conditions"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","17"],["dc.bibliographiccitation.journal","Basic Research in Cardiology"],["dc.bibliographiccitation.lastpage","22"],["dc.bibliographiccitation.volume","91"],["dc.contributor.author","Hasenfuß, G."],["dc.contributor.author","Reinecke, H."],["dc.contributor.author","Studer, R."],["dc.contributor.author","Pieske, B."],["dc.contributor.author","Meyer, M."],["dc.contributor.author","Drexler, H."],["dc.contributor.author","Just, H."],["dc.date.accessioned","2017-09-07T11:51:11Z"],["dc.date.available","2017-09-07T11:51:11Z"],["dc.date.issued","1996"],["dc.description.abstract","Myocardial function, intracellular calcium and levels of calcium cycling proteins were analyzed in failing and nonfailing human myocardium. Myocardial function was evaluated by the isometric force-frequency relation, and intracellular calcium was studied by aequorin light emission. When stimulation frequency was increased above 30 min(-1), there was a continuous increase in isometric tension development in the nonfailing myocardium. In contrast, in failing myocardium, frequency potentiation of contractile force was blunted or inverse. As a consequence, at higher rates of stimulation, twitch tension was reduced significantly in failing compared to nonfailing human myocardium. Aequorin measurements indicated that the contractile deficit in the failing myocardium at higher rates of stimulation is associated with decreased free intracellular calcium concentration. Western blot analysis indicated that in the failing myo cardium protein levels of SR-Ca2+-ATPase are significantly reduced and protein levels of Na+-Ca2+-exchanger are significantly increased. Levels of phospholamban are slightly reduced in the failing myocardium, and ryanodine receptor and calsequestrin protein levels an unchanged. There was a close positive correlation between the protein levels of SR-Ca2+-ATPase and frequency potentiation of contractile force. From these data, we conclude that in failing compared to nonfailing human myocardium 1) force-frequency relation is blunted or inverse. 2) Frequency-dependence of contractile force is closely correlated with frequency-dependence of intracellular calcium cycling. 3) Protein levels of SR-Ca2+-ATPase may determine frequency-dependence of sarcoplasmic reticulum calcium release. 4) Calcium elimination by an increased number of Na+-Ca2+-exchanger molecules may be a compensatory mechanism to prevent diastolic calcium accumulation in failing myocardium with a reduced number of SR calcium pumps."],["dc.identifier.doi","10.1007/BF00795357"],["dc.identifier.gro","3144665"],["dc.identifier.isi","A1996VX75100004"],["dc.identifier.pmid","8957539"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/2314"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0300-8428"],["dc.title","Calcium cycling proteins and force-frequency relationship in heart failure"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","81"],["dc.bibliographiccitation.journal","Basic Research in Cardiology"],["dc.bibliographiccitation.lastpage","92"],["dc.bibliographiccitation.volume","87"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Mulieri, L. A."],["dc.contributor.author","Holubarsch, Christian"],["dc.contributor.author","Pieske, Burkert"],["dc.contributor.author","Just, Hanjörg"],["dc.contributor.author","Alpert, N. R."],["dc.date.accessioned","2017-09-07T11:51:50Z"],["dc.date.available","2017-09-07T11:51:50Z"],["dc.date.issued","1992"],["dc.description.abstract","Using sensitive antimony-bismuth thermopiles, isometric force and heat output were measured in muscle strips from nonfailing human hearts and from failing dilated cardiomyopathic hearts at a stimulation rate of 60 beats per minute (37-degrees-C). This frequency was chosen because analysis of the force-frequency relation showed significant differences in isometric force between failing and nonfailing human myocardium at 60 beats per minute and at higher frequencies, whereas at lower rates of stimulation (30 beats per minute) force of contraction was similar in failing and nonfailing myocardium. The liberated initial heat was partitioned into its two components, tension-dependent heat and tension-independent heat from high-energy phosphate hydrolysis by contractile proteins and excitation-contraction coupling processes, respectively. Tension-dependent heat reflects the total number of cross-bridge interactions, and tension-independent heat is an index of the amount of calcium cycling during the contraction-relaxation cycle. In failing compared to nonfailing human myocardium, peak twitch tension, maximum rate of tension rise and maximum rate of tension fall were reduced significantly. Reduced mechanical performance was associated with reduced liberation of both tension-dependent and tension-independent heat in the failing heart. The reduction of tension-dependent heat by 61 % and of tension-independent heat by 69 % indicate considerable decreases in the number of crossbridge interactions activated and calcium ions cycled during the isometric twitch. In addition, the rate of calcium removal was reduced in the failing human heart as is indicated by a 71 % reduction in tension-independent heat rate. The efficiency of excitation-contraction coupling with respect to crossbridge activation was similar in failing and nonfailing myocardium. These data indicate that impaired myocardial performance in dilated cardiomyopathy may result from disturbed excitation-contraction coupling with reduced amount of calcium cycling and reduced rate of calcium removal."],["dc.identifier.gro","3144799"],["dc.identifier.isi","A1992KQ21200009"],["dc.identifier.pmid","1299212"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/2463"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Dr Dietrich Steinkopff Verlag"],["dc.relation.issn","0300-8428"],["dc.title","ENERGETICS OF CALCIUM CYCLING IN NONFAILING AND FAILING HUMAN MYOCARDIUM"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","86"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Basic Research in Cardiology"],["dc.bibliographiccitation.lastpage","93"],["dc.bibliographiccitation.volume","91"],["dc.contributor.author","Meyer, M"],["dc.contributor.author","Lehnart, Stephan E."],["dc.contributor.author","Pieske, Burkert"],["dc.contributor.author","Schlottauer, K."],["dc.contributor.author","Munk, Axel"],["dc.contributor.author","Holubarsch, Christian"],["dc.contributor.author","Just, Hanjörg"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.date.accessioned","2017-09-07T11:51:11Z"],["dc.date.available","2017-09-07T11:51:11Z"],["dc.date.issued","1996"],["dc.description.abstract","The influence of endothelin 1 on isometrically contracting human atrial muscle strip preparations was investigated under physiological conditions (37 degrees C, 1 Hz, Ca2+ 2.5 mM). Endothelin dose-dependently increased isometric tension from 3x10(-10)M to 1x10(-7)M. At 1x10(-7)M the inotropic effect of endothelin was maximum with isometric tension being increased by 32 +/- 6% (n = 11, p < 0.05). At 1x10(-7)M endothelin the positive inotropic effect was preceded by a transient negative inotropic effect with a decline in tension by - 5 +/- 1% (n = 11, p < 0.05). Endothelin prolonged time from peak tension to 50% relaxation (RT50) by 29 +/- 5%. With BQ123 a competitive antagonist of the ET(A) receptor positive inotropic effect and the prolongation of relaxation was significantly reduced and initial negative inotropic effect was abolished, indicating a ET(A) receptor mediated effect. Preincubation with phorbolmyristateacetate (10(-5)M) to downregulate proteinkinase C (PKC) eliminated the positive inotropic effect of endothelin. Similarly, N-5,5-dimethylamiloride (10(-5)M) which inhibits Na+/H+-exchanger activity, abolished the positive inotropic effect of ET. However, with either PMA or DMA the initial transient negative inotropic effect was still present(- 13 +/- 7%,n = 9, p < 0.05 and - 3 +/- 1%, n = 6, p < 0.05). Furthermore, both substances did not abolish the prolongation of twitch time parameters observed under endothelin. After preincubation with PMA, endothelin prolonged RT50 by 18 +/- 6% and with DMA by 11 +/- 2%. Using the photoprotein aequorin as an indicator for intracellular calcium concentrations showed that the positive inotropic effect was mainly mediated by an increase of systolic intracellular calcium concentrations. Thus, the present data indicate that the positive inotropic effect of endothelin in human atrial myocardium results from activation of PKC with a subsequent activation of the Na+/H+-exchanger. However, the initial negative inotropic effects as well as the prolongation of relaxation seem to result from a different intracellular mechanism of endothelin."],["dc.identifier.gro","3144666"],["dc.identifier.isi","A1996TX89300020"],["dc.identifier.pmid","8660266"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/2315"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Dr Dietrich Steinkopff Verlag"],["dc.relation.issn","0300-8428"],["dc.title","Influence of endothelin 1 on human atrial myocardium - Myocardial function and subcellular pathways"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1802"],["dc.bibliographiccitation.issue","14"],["dc.bibliographiccitation.journal","Circulation"],["dc.bibliographiccitation.lastpage","1809"],["dc.bibliographiccitation.volume","99"],["dc.contributor.author","Pieske, Burkert"],["dc.contributor.author","Beyermann, Beate"],["dc.contributor.author","Breu, Volker"],["dc.contributor.author","Löffler, Bernd M."],["dc.contributor.author","Schlotthauer, Klaus"],["dc.contributor.author","Maier, Lars S."],["dc.contributor.author","Schmidt-Schweda, Stephan"],["dc.contributor.author","Just, Hanjörg"],["dc.contributor.author","Hasenfuss, Gerd"],["dc.date.accessioned","2017-09-07T11:52:39Z"],["dc.date.available","2017-09-07T11:52:39Z"],["dc.date.issued","2012"],["dc.description.abstract","ackground—An activated endothelin (ET) system may be of pathophysiological relevance in human heart failure. We characterized the functional effects of ET-1, ET receptors, and ET-1 peptide concentration in left ventricular myocardium from 10 nonfailing hearts (NF) and 27 hearts in end-stage failure due to idiopathic dilative cardiomyopathy (DCM). Methods and Results—Inotropic effects were characterized in isolated muscle strips (1 Hz; 37°C). ET-1 0.0001 to 0.3 μmol/L significantly (P<0.05) increased twitch force by maximally 59±10% in NF and by 36±11% in DCM (P<0.05 versus NF). Preincubation with propranolol 1 μmol/L and prazosin 0.1 μmol/L did not affect the response to ET-1, but the mixed ET receptor antagonist bosentan and the ETA receptor antagonist BQ-123 shifted the concentration-response curves for ET-1 rightward. The ETB receptor agonist sarafotoxin S6c 0.001 to 0.3 μmol/L had no functional effects. The inotropic response to ET-1 was not associated with increased intracellular Ca2+ transients, as assessed in aequorin-loaded muscle strips. ET receptor density (Bmax; radioligand binding) was 62.5±12.5 fmol/mg protein in NF and 122.4±24.3 fmol/mg protein in DCM (P<0.05 versus NF). The increase in Bmax in DCM resulted from an increase in ETA receptors without change in ETB receptors. ET-1 peptide concentration (radioimmunoassay) was higher in DCM than in NF (14 447±2232 versus 4541±1340 pg/mg protein, P<0.05). Conclusions—ET-1 exerts inotropic effects in human myocardium through ETA receptor–mediated increases in myofibrillar Ca2+ responsiveness. In DCM, functional effects of ET-1 are attenuated, but ETA receptor density and ET-1 peptide concentration are increased, indicating an activated local cardiac ET system and possibly a reduced postreceptor signaling efficiency."],["dc.identifier.doi","10.1161/01.cir.99.14.1802"],["dc.identifier.gro","3144986"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/2672"],["dc.language.iso","en"],["dc.notes.intern","Crossref Import"],["dc.notes.status","final"],["dc.relation.issn","0009-7322"],["dc.title","Functional Effects of Endothelin and Regulation of Endothelin Receptors in Isolated Human Nonfailing and Failing Myocardium"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","778"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Circulation"],["dc.bibliographiccitation.lastpage","784"],["dc.bibliographiccitation.volume","92"],["dc.contributor.author","Meyer, Markus"],["dc.contributor.author","Schillinger, Wolfgang"],["dc.contributor.author","Pieske, Burkert"],["dc.contributor.author","Holubarsch, Christian"],["dc.contributor.author","Heilmann, Claus"],["dc.contributor.author","Posival, Herbert"],["dc.contributor.author","Kuwajima, Goro"],["dc.contributor.author","Mikoshiba, Katsuhiko"],["dc.contributor.author","Just, Hanjörg"],["dc.contributor.author","Hasenfuss, Gerd"],["dc.date.accessioned","2017-09-07T11:52:58Z"],["dc.date.available","2017-09-07T11:52:58Z"],["dc.date.issued","2012"],["dc.description.abstract","Background Previous studies provide considerable evidence that excitation-contraction coupling may be disturbed at the level of the sarcoplasmic reticulum (SR) in the failing human heart. Disturbed SR function may result from altered expression of calcium-handling proteins. Methods and Results Levels of SR proteins involved in calcium release (ryanodine receptor), calcium binding (calsequestrin, calreticulin), and calcium uptake (calcium ATPase, phospholamban) were measured by Western blot analysis in nonfailing human myocardium (n=7) and in end-stage failing myocardium due to dilated cardiomyopathy (n=14). The levels of the ryanodine receptor, calsequestrin, and calreticulin were not significantly different in nonfailing and failing human myocardium. Phospholamban protein levels (pentameric form) normalized per total protein were decreased by 18% in the failing myocardium (P<.05). However, phospholamban protein levels were not significantly different in failing and nonfailing myocardium when normalization was performed per calsequestrin. Protein levels of SR calcium ATPase, normalized per total protein or per calsequestrin, were decreased by 41% (P<.001) or 33% (P<.05), respectively, in the failing myocardium. Furthermore, SR calcium ATPase was decreased relative to ryanodine receptor by 37% (P<.05) and relative to phospholamban by 28% (P<.05). Conclusions Levels of SR proteins involved in calcium binding and release are unchanged in failing dilated cardiomyopathy. In contrast, protein levels of calcium ATPase involved in SR calcium uptake are reduced in the failing myocardium. Moreover, SR calcium ATPase is decreased relative to its inhibitory protein, phospholamban. These findings support the concept that reduced capacity of the SR to accumulate calcium may reflect a major defect in excitation-contraction coupling in human heart failure."],["dc.identifier.doi","10.1161/01.cir.92.4.778"],["dc.identifier.gro","3144999"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/2687"],["dc.language.iso","en"],["dc.notes.intern","Crossref Import"],["dc.notes.status","final"],["dc.relation.issn","0009-7322"],["dc.title","Alterations of Sarcoplasmic Reticulum Proteins in Failing Human Dilated Cardiomyopathy"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","641"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Circulation"],["dc.bibliographiccitation.lastpage","648"],["dc.bibliographiccitation.volume","99"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Schillinger, Wolfgang"],["dc.contributor.author","Lehnart, Stephan E."],["dc.contributor.author","Preuss, Michael"],["dc.contributor.author","Pieske, Burkert"],["dc.contributor.author","Maier, Lars S."],["dc.contributor.author","Prestle, Jürgen"],["dc.contributor.author","Minami, Kazutomo"],["dc.contributor.author","Just, Hanjörg"],["dc.date.accessioned","2022-03-01T11:43:48Z"],["dc.date.available","2022-03-01T11:43:48Z"],["dc.date.issued","1999"],["dc.description.abstract","Background —In the failing human heart, sarcoplasmic reticulum (SR) calcium handling is impaired, and therefore, calcium elimination and diastolic function may depend on the expression of sarcolemmal Na + -Ca 2+ exchanger. Methods and Results —Force-frequency relations were studied in ventricular muscle strip preparations from failing human hearts (n=29). Protein levels of Na + -Ca 2+ exchanger and SR Ca 2+ -ATPase were measured in the same hearts. Hearts were divided into 3 groups by discriminant analysis according to the behavior of diastolic function when stimulation rate of muscle strips was increased from 30 to 180 min −1 . At 180 compared with 30 min −1 , diastolic force was increased by 160%, maximum rate of force decline was decreased by 46%, and relaxation time was unchanged in group III. In contrast, in group I, diastolic force and maximum rate of force decline did not change, and relaxation time decreased by 20%. Na + -Ca 2+ exchanger was 66% higher in group I than in group III. Na + -Ca 2+ exchanger was inversely correlated with the frequency-dependent rise of diastolic force when stimulation rate was increased ( r =−0.74; P <0.001). Compared with nonfailing human hearts (n=6), SR Ca 2+ -ATPase was decreased and Na + -Ca 2+ exchanger unchanged in group III, whereas Na + -Ca 2+ exchanger was increased and SR Ca 2+ -ATPase unchanged in group I. Results with group II hearts were between those of group I and group III hearts. Conclusions —By discriminating failing human hearts according to their diastolic function, we identified different phenotypes. Disturbed diastolic function occurs in hearts with decreased SR Ca 2+ -ATPase and unchanged Na + -Ca 2+ exchanger, whereas increased expression of the Na + -Ca 2+ exchanger is associated with preserved diastolic function."],["dc.description.abstract","Background —In the failing human heart, sarcoplasmic reticulum (SR) calcium handling is impaired, and therefore, calcium elimination and diastolic function may depend on the expression of sarcolemmal Na + -Ca 2+ exchanger. Methods and Results —Force-frequency relations were studied in ventricular muscle strip preparations from failing human hearts (n=29). Protein levels of Na + -Ca 2+ exchanger and SR Ca 2+ -ATPase were measured in the same hearts. Hearts were divided into 3 groups by discriminant analysis according to the behavior of diastolic function when stimulation rate of muscle strips was increased from 30 to 180 min −1 . At 180 compared with 30 min −1 , diastolic force was increased by 160%, maximum rate of force decline was decreased by 46%, and relaxation time was unchanged in group III. In contrast, in group I, diastolic force and maximum rate of force decline did not change, and relaxation time decreased by 20%. Na + -Ca 2+ exchanger was 66% higher in group I than in group III. Na + -Ca 2+ exchanger was inversely correlated with the frequency-dependent rise of diastolic force when stimulation rate was increased ( r =−0.74; P <0.001). Compared with nonfailing human hearts (n=6), SR Ca 2+ -ATPase was decreased and Na + -Ca 2+ exchanger unchanged in group III, whereas Na + -Ca 2+ exchanger was increased and SR Ca 2+ -ATPase unchanged in group I. Results with group II hearts were between those of group I and group III hearts. Conclusions —By discriminating failing human hearts according to their diastolic function, we identified different phenotypes. Disturbed diastolic function occurs in hearts with decreased SR Ca 2+ -ATPase and unchanged Na + -Ca 2+ exchanger, whereas increased expression of the Na + -Ca 2+ exchanger is associated with preserved diastolic function."],["dc.identifier.doi","10.1161/01.CIR.99.5.641"],["dc.identifier.gro","3144987"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/102848"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-531"],["dc.notes.status","final"],["dc.relation.eissn","1524-4539"],["dc.relation.issn","0009-7322"],["dc.title","Relationship Between Na + -Ca 2+ –Exchanger Protein Levels and Diastolic Function of Failing Human Myocardium"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","38"],["dc.bibliographiccitation.issue","Supplement 1"],["dc.bibliographiccitation.journal","Basic Research in Cardiology"],["dc.bibliographiccitation.lastpage","45"],["dc.bibliographiccitation.volume","93"],["dc.contributor.author","Schillinger, W."],["dc.contributor.author","Lehnart, S. E."],["dc.contributor.author","Prestle, J."],["dc.contributor.author","Preuss, M."],["dc.contributor.author","Pieske, B."],["dc.contributor.author","Maier, L. S."],["dc.contributor.author","Meyer, M."],["dc.contributor.author","Just, H."],["dc.contributor.author","Hasenfuss, G."],["dc.date.accessioned","2017-09-07T11:52:38Z"],["dc.date.available","2017-09-07T11:52:38Z"],["dc.date.issued","1998"],["dc.description.abstract","The data presented indicate that altered systolic and diastolic function in failing human hearts may result from altered expression of calcium cycling proteins. Decreased systolic force production and inversion of the force-frequency relation seem to be related to reduced protein levels of SR Ca2+ ATPase and/or to increased protein levels of the Na+-Ca2+ exchanger resulting in an increased ratio of Na+-Ca2+ exchanger to SR Ca2+ ATPase. Impaired diastolic function may result from reduced SR Ca2+ ATPase and is most pronounced in failing hearts with lack of upregulation of the Na+-Ca2+ exchanger. Thus, failing hearts with reduced SR Ca2+ ATPase protein levels and unchanged Na+-Ca2+ exchanger protein levels exhibit severe impairment of both systolic and diastolic function."],["dc.identifier.doi","10.1007/s003950050208"],["dc.identifier.gro","3144991"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/2677"],["dc.language.iso","en"],["dc.notes.intern","Crossref Import"],["dc.notes.status","zu prüfen"],["dc.relation.issn","0300-8428"],["dc.title","Influence of SR Ca2+-ATPase and Na+-Ca2+-exchanger on the force-frequency relation"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]