Pieske, Burkert M.

[["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","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","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","91"],["dc.bibliographiccitation.lastpage","100"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Pieske, Burkert"],["dc.contributor.author","Holubarsch, Christian"],["dc.contributor.author","Alpert, Norman R."],["dc.contributor.author","Just, Hanjörg"],["dc.contributor.editor","Sideman, Samuel"],["dc.contributor.editor","Beyar, Rafael"],["dc.date.accessioned","2017-09-07T11:53:01Z"],["dc.date.available","2017-09-07T11:53:01Z"],["dc.date.issued","2011"],["dc.identifier.doi","10.1007/978-1-4615-2946-0_9"],["dc.identifier.gro","3145004"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/2693"],["dc.notes.intern","Crossref Import"],["dc.notes.status","public"],["dc.relation.isbn","978-1-4613-6280-7"],["dc.relation.ispartof","Interactive Phenomena in the Cardiac System"],["dc.title","Excitation-Contraction Coupling and Contractile Protein Function in Failing and Nonfailing Human Myocardium"],["dc.type","book_chapter"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","88"],["dc.bibliographiccitation.issue","Suppl D"],["dc.bibliographiccitation.journal","European heart journal"],["dc.bibliographiccitation.lastpage","91"],["dc.bibliographiccitation.volume","15"],["dc.contributor.author","Holubarsch, Christian"],["dc.contributor.author","Schmidt-Schweda, Stephan"],["dc.contributor.author","Knorr, A."],["dc.contributor.author","DUIS, J"],["dc.contributor.author","Pieske, Burkert"],["dc.contributor.author","Ruf, T."],["dc.contributor.author","Fasol, R."],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Just, Hanjörg"],["dc.date.accessioned","2017-09-07T11:51:23Z"],["dc.date.available","2017-09-07T11:51:23Z"],["dc.date.issued","1994"],["dc.description.abstract","We studied the effects of angiotensin (Ang) I and II in a variety of isolated human cardiac tissues contracting under physiological conditions (37 degrees C, 60 beats.min(-1)). Ang I and II consistently increased the peak developed force of human atrial muscles by 30-40%, an effect that was completely blocked by 10(-6) M saralasine, but not by the combination of prazosin and propranolol. However, neither Ang I or II had significant inotropic effects in right and left ventricular human preparations. We were also able to demonstrate that the positive inotropic effect of Ang II in human right atrial tissue is mediated by the ATI receptor subtype but not the AT(2) receptor subtype."],["dc.identifier.doi","10.1093/eurheartj/15.suppl_d.88"],["dc.identifier.gro","3144706"],["dc.identifier.isi","A1994QA45900016"],["dc.identifier.pmid","7713120"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/2360"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0195-668X"],["dc.relation.issn","0195-668X"],["dc.title","Functional Significance of Angiotensin Receptors in Human Myocardium: Significant Differences Between Atrial and Ventricular Myocardium"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","764"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Journal of Clinical Investigation"],["dc.bibliographiccitation.lastpage","776"],["dc.bibliographiccitation.volume","98"],["dc.contributor.author","Pieske, Burkert"],["dc.contributor.author","Sutterlin, M ."],["dc.contributor.author","Schmidt-Schweda, Stephan"],["dc.contributor.author","Minami, K."],["dc.contributor.author","Meyer, M"],["dc.contributor.author","Olschewski, Manfred"],["dc.contributor.author","Holubarsch, Christian"],["dc.contributor.author","Just, Hanjörg"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.date.accessioned","2017-09-07T11:51:08Z"],["dc.date.available","2017-09-07T11:51:08Z"],["dc.date.issued","1996"],["dc.description.abstract","Post-rest contractile behavior of isolated myocardium indicates the capacity of the sarcoplasmic reticulum (SR) to store and release Ca2+. We investigated post-rest behavior in isolated muscle strips from nonfailing (NF) and endstage failing (dilated cardiomyopathy [DCM]) human hearts. At a basal stimulation frequency of 1 Hz, contractile parameters of the first twitch after increasing rest intervals (2-240 s) were evaluated. In NF (n=9), steady state twitch tension was 13.7+/-1.8 mN/mm(2). With increasing rest intervals, post-rest twitch tension continuously increased to maximally 29.9+/-4.1 mN/mm(2) after 120 s (P <0.05) and to 26.7+/-4.5 mN after 240 s rest, In DCM (n=22), basal twitch tension was 10.0+/-1.5 mN/mm(2) and increased to maximally 13.6+/-2.2 mN/mm(2) after 20 s rest (P <0.05). With longer rest intervals, however, post-rest twitch tension continuously declined (rest decay) to 4.7+/-1.0 mN/mm(2) at 240 s (P <0.05). The rest-dependent changes in twitch tension were associated with parallel changes in intracellular Ca2+ transients in NF and DCM (aequorin method), The relation between rest-induced changes in twitch tension and aequorin light emission was similar in NF and DCM, indicating preserved Ca2+-responsiveness of the myofilaments. Ryanodine (1 mu M) completely abolished post-rest potentiation. Increasing basal stimulation frequency (2 Hz) augmented post-rest potentiation, but did not prevent rest decay after longer rest intervals in DCM. The altered post-rest behavior in failing human myocardium indicates disturbed intracellular Ca2+ handling involving altered function of the SR."],["dc.identifier.doi","10.1172/JCI118849"],["dc.identifier.gro","3144641"],["dc.identifier.isi","A1996VB69800023"],["dc.identifier.pmid","8698869"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/2287"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Rockefeller Univ Press"],["dc.relation.issn","0021-9738"],["dc.title","Diminished post-rest potentiation of contractile force in human dilated cardiomyopathy - Functional evidence for alterations in intracellular Ca2+ handling"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","21"],["dc.bibliographiccitation.lastpage","25"],["dc.bibliographiccitation.volume","83"],["dc.contributor.author","Holubarsch, Christian"],["dc.contributor.author","Pieske, Burkert"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Just, Hanjörg"],["dc.date.accessioned","2017-09-07T11:51:31Z"],["dc.date.available","2017-09-07T11:51:31Z"],["dc.date.issued","1994"],["dc.description.abstract","The phosphodiesterase inhibitor enoximone has both vasodilating and positive inotropic pharmacological properties. The balance between vasodilation and positive inotropism may be different between the various types of heart failure as well as the various stages of heart failure. Therefore, we investigated the effect of intravenous application of enoximone (1 mg/kg body weight) in a cohort of patients (n = 10) suffering from acute or subacute heart failure mainly due to ischemia or hypoxia. All patients had high left ventricular filling pressure, low cardiac output and were pretreated with intravenous dobutamine. Enoximone increased cardiac output from 3.2 +/- 1.2 to 5.5 +/- 2.2 l/min, increased heart rate from 94 +/- 20 to 100 +/- 18 beats/min, decreased systemic peripheral resistance from 1770 +/- 861 to 931 +/- 340 dyn.sec.cm(-5) and decreased pulmonary wedge pressure from 24 +/- 5 to 20 +/- 6 mmHg, significantly. However, systolic aortic pressure, systolic pulmonary pressure and right atrial pressure were not significantly altered. We conclude that in a selected group of patients enoximone - given intravenously and acutely in the intensive care unity - can induce beneficial effects on central hemodynamics without critical falls in perfusion pressure."],["dc.identifier.gro","3144754"],["dc.identifier.isi","A1994NT29300005"],["dc.identifier.pmid","8091821"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/2413"],["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","COLOGNE, GERMANY"],["dc.relation.ispartof","Zeitschrift für Kardiologie"],["dc.relation.issn","0300-5860"],["dc.title","USE OF ENOXIMONE IN PATIENTS WITH ACUTE AND SUBACUTE HEART-FAILURE - AN INTENSIVE-CARE UNIT REPORT"],["dc.type","conference_paper"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]