Just, Hanjörg

[["dc.bibliographiccitation.firstpage","191"],["dc.bibliographiccitation.journal","Basic Research in Cardiology"],["dc.bibliographiccitation.lastpage","196"],["dc.bibliographiccitation.volume","84"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Just, Hanjörg"],["dc.date.accessioned","2017-09-07T11:51:59Z"],["dc.date.available","2017-09-07T11:51:59Z"],["dc.date.issued","1989"],["dc.identifier.doi","10.1007/BF02650359"],["dc.identifier.gro","3144839"],["dc.identifier.isi","A1989CB18400020"],["dc.identifier.pmid","2573341"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/2507"],["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","CLINICAL RELEVANCE OF LONG-TERM THERAPY WITH LEVODOPA AND ORALLY ACTIVE DOPAMINE ANALOGS IN PATIENTS WITH CHRONIC CONGESTIVE 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","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","994"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Cardiovascular Research"],["dc.bibliographiccitation.lastpage","1002"],["dc.bibliographiccitation.volume","28"],["dc.contributor.author","Holubarsch, Christian"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Just, Hanjörg"],["dc.contributor.author","Alpert, N. R."],["dc.date.accessioned","2017-09-07T11:51:25Z"],["dc.date.available","2017-09-07T11:51:25Z"],["dc.date.issued","1994"],["dc.description.abstract","Objective: The aim was to study the effect of three positive inotropic interventions on myocardial force development and heat production in guinea pig papillary muscles in order to investigate the energetic consequences. Methods: The positive inotropic agents used were epinine (beta adrenoceptor stimulation), E-1020 (phosphodiesterase inhibition), and ouabain (sodium-potassium ATPase inhibition). Heat measurements were accomplished using antimony-bismuth thermopiles and initial heat was separated into tension dependent and tension independent heat using the butanedione-monoxime (BDM) and the shortening methods. Results: Optimal concentrations of epinine, E-1020, and ouabain increased peak developed force from 20.0(SD 6.6) to 55.5(9.3) (n = 5; p < 0.01), from 20.9(9.1) to 27.2(7.2) (n = 6; p < 0.05), and from 23.4(9.2) to 44.9(18.0) mN.mm(-2) (n = 6; p < 0.01), respectively. Epinine and E-1020 decreased the tension-time integral per unit initial heat, ie, the economy of isometric contraction, from 5.5(1.4) to 3.6(0.5) (p < 0.01) and from 5.5(1.4) to 3.1(0.9) N.m.s.J(-1) (p < 0.01), respectively; no significant change was observed with ouabain [6.7(1.4) to 8.3(0.5) N.m.s.J(-1)]. The tension independent heat (calcium turnover) was measured in two different ways using BDM or shortening to abolish force production. It was increased significantly by epinine (by 141-243%), E-1020 (by 77-114%), and ouabain (by 23-38%). The first measurement in brackets is the BDM estimate, the second is the shortening estimate. From the tension-time integral and the tension dependent heat the crossbridge force-time integral was analysed: epinine and E-1020 decreased the crossbridge force-time integral from 0.46(0.16) to 0.31(0.06) pN.s (p < 0.01) and from 0.50(0.19) to 0.31(0.08) pN.s (p < 0.01), respectively, while ouabain left the force-time integral unchanged [0.59(0.27) to 0.63(0.20) pN.s]. Conclusions: (1) The inotropic effect of ouabain results from an increase in muscle activation with no change in crossbridge kinetics; (2) epinine and E-1020 increase the tension independent heat and decrease the crossbridge force-time integral, both effects reducing the overall economy; and (3) the shortening and BDM methods for measuring the tension independent heat give qualitatively similar but quantitatively different results."],["dc.identifier.doi","10.1093/cvr/28.7.994"],["dc.identifier.gro","3144727"],["dc.identifier.isi","A1994PA71400009"],["dc.identifier.pmid","7954612"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/2383"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","0008-6363"],["dc.title","POSITIVE INOTROPISM AND MYOCARDIAL ENERGETICS - INFLUENCE OF BETA-RECEPTOR AGONIST STIMULATION, PHOSPHODIESTERASE INHIBITION, AND OUABAIN"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","107"],["dc.bibliographiccitation.lastpage","112"],["dc.bibliographiccitation.volume","86"],["dc.contributor.author","Holubarsch, Christian"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Thierfelder, L."],["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.description.abstract","Vasodilators have been shown to improve hemodynamics of the failing heart as a short-term effect, and to decrease mortality as a long-term result. We, therefore, studied the effects of vasodilators and inotropic agents on myocardial mechanics and energetics in patients with congestive heart failure New York Heart Association (NYHA) classes II-III. In these patients, who underwent routine heart catheterization, myocardial oxygen consumption was measured using the argon method, and LV pressure and geometry were obtained from LV angiography using a Millar microtipped catheter. All data were analyzed for one single heart beat. The best correlation was found between MVO2/beat and the systolic stress-time integral which considers LV pressure, LV wall thickness, and LV geometry. The relation between MVO2/beat and peak systolic wall stress was less relevant. No correlation was found between MVO2/beat and pressure-volume work, dP/dt(max), and mean velocity of circumferential fiber shortening. The intravenous application of nitroprusside and the ACE-inhibitor benazepril decreased both the systolic stress-time integral and the myocardial oxygen consumption in proportion to each other, indicating unchanged economy of myocardial contraction. In contrast, beta1-agonists and phosphodiesterase inhibitors increased myocardial oxygen consumption independently of changes in the stress-time integral. In conclusion, vasodilators decrease LV pressure and chamber size and thereby proportionally reduce MVO2/beat. The reduction of energy needed for myocardial contraction may partially explain the long-term effects of the ACE-inhibitors and combinations of vasodilators. Pure inotropic substances, especially beta-1-agonists, increase myocardial oxygen consumption with only minor changes of systolic stress-time integral. The effect of phosphodiesterase inhibitors on MVO2/beat depends on the balance between the energy-consuming positive inotropic effect and the energy-saving effect of vasodilation. The lack of MVO2 reduction in patients with phosphodiesterase inhibitors or beta-1-agonists may partially explain why mortality is not decreased in long-term treatment."],["dc.identifier.gro","3144812"],["dc.identifier.isi","A1991FB29600014"],["dc.identifier.pmid","1827977"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/2477"],["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.publisher.place","Berlin 33"],["dc.relation.eventlocation","MAASTRICHT, NETHERLANDS"],["dc.relation.ispartof","Basic Research in Cardiology"],["dc.relation.issn","0300-8428"],["dc.title","ENERGETIC CONSEQUENCES OF SUBSTANCES CURRENTLY USED OR RECOMMENDED FOR LONG-TERM TREATMENT OF CHRONIC HEART-FAILURE"],["dc.type","conference_paper"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","257"],["dc.bibliographiccitation.journal","Basic Research in Cardiology"],["dc.bibliographiccitation.lastpage","265"],["dc.bibliographiccitation.volume","84"],["dc.contributor.author","Holubarsch, Christian"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Allgeier, M."],["dc.contributor.author","Heiss, H.Wolfgang"],["dc.contributor.author","Just, Hanjörg"],["dc.date.accessioned","2017-09-07T11:51:59Z"],["dc.date.available","2017-09-07T11:51:59Z"],["dc.date.issued","1989"],["dc.identifier.doi","10.1007/BF02650365"],["dc.identifier.gro","3144841"],["dc.identifier.isi","A1989CB18400026"],["dc.identifier.pmid","2530975"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/2509"],["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","SEPARATION BETWEEN VASODILATION AND POSITIVE INOTROPISM BY ASSESSMENT OF MYOCARDIAL ENERGETICS IN PATIENTS WITH DILATED CARDIOMYOPATHY"],["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","100"],["dc.bibliographiccitation.journal","Zeitschrift für Kardiologie"],["dc.bibliographiccitation.lastpage","104"],["dc.bibliographiccitation.volume","75"],["dc.contributor.author","Holubarsch, Christian"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","KORNER, M"],["dc.contributor.author","Von Herrath, M."],["dc.contributor.author","Bonzel, T."],["dc.contributor.author","TARNOWSKA, R."],["dc.contributor.author","Just, Hanjörg"],["dc.date.accessioned","2017-09-07T11:52:02Z"],["dc.date.available","2017-09-07T11:52:02Z"],["dc.date.issued","1986"],["dc.identifier.gro","3144881"],["dc.identifier.isi","A1986C304500024"],["dc.identifier.pmid","3727668"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/2553"],["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","0300-5860"],["dc.title","MYOCARDIAL PERFORMANCE AND EFFICIENCY AS ASSESSED BY ENERGETIC PARAMETERS DERIVED FROM PRESSURE-VOLUME RELATIONS AND WALL THICKNESS IN HUMAN VENTRICLES"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["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","91"],["dc.bibliographiccitation.lastpage","102"],["dc.bibliographiccitation.volume","88"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Mulieri, L. A."],["dc.contributor.author","Holubarsch, Christian"],["dc.contributor.author","Blanchard, Etienne"],["dc.contributor.author","Just, Hanjörg"],["dc.contributor.author","Alpert, N. R."],["dc.date.accessioned","2017-09-07T11:51:33Z"],["dc.date.available","2017-09-07T11:51:33Z"],["dc.date.issued","1993"],["dc.description.abstract","Myocardial adaptation to stress and development includes reorganization of subcellular systems. Using a myothermal method, changes in the contractile protein system were investigated across species (rat, rabbit, human myocardium) and in consequence of hemodynamic (volume overload human, pressure overload rabbit myocardium) or hormonal stresses (hypothyroid rat, hyperthyroid rabbit myocardium). Mechanical and myothermal measurements were performed in isometrically contracting right or left ventricular muscle strips and the force-time integral of the individual crossbridge cycle was calculated from heat and force data. Within species, crossbridge force-time integral increased by 85% from control human to volume overload human myocardium. Crossbridge force-time integral increased by 100% from control to hypothyroid rat myocardium. In rabbit myocardium, crossbridge force-time integral increased by 164% in pressure overload and decreased by 47% in hyperthyroid compared to control myocardium. Across species, crossbridge force-time integral was smallest in control rat myocardium (0.16+/-0.01 pNs) and increased in the order: control rat < hyperthyroid rabbit < hypothyroid rat, control rabbit < control human < pressure overload rabbit < volume overload human myocardium (0.96+/-0.01 pNs). Within and across species, crossbridge force-time integral was positively correlated with time to peak tension (r=0.86; p<0.05) and negatively correlated with maximum rate of tension rise (r=-0.85; p<0.05) and maximum rate of tension fall (r=-0.78; p<0.05). Furthermore, there were significant correlations between crossbridge force-time integral and total activity related heat (r=-0.81; p<0.05) as well as total activity related heat per tension-time integral (r=-0.89; p<0.005). Thus, the close relationship between crossbridge force-time integral and myocardial function within and across species demonstrates that alterations of crossbridge force-time integral reflect an important mechanism of subcellular adaptation to stress from a mechanical point of view. Moreover, alterations of the crossbridge force-time integral have pronounced effects on energy consumption in the different types of myocardium."],["dc.identifier.gro","3144781"],["dc.identifier.isi","A1993MN67400011"],["dc.identifier.pmid","8147839"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/2442"],["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.publisher.place","Berlin 33"],["dc.relation.eventlocation","KARL FRANZENS UNIV GRAZ, GRAZ, AUSTRIA"],["dc.relation.ispartof","Basic Research in Cardiology"],["dc.relation.issn","0300-8428"],["dc.title","MYOCARDIAL ADAPTATION TO STRESS FROM THE VIEWPOINT OF ADAPTATION AND DEVELOPMENT"],["dc.type","conference_paper"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]