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Journal articles on the topic 'Langendorff perfused murine heart'

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Published: 4 June 2021
Last updated: 20 February 2023

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1

Liao, Ronglih, Bruno K. Podesser, and Chee Chew Lim. "The continuing evolution of the Langendorff and ejecting murine heart: new advances in cardiac phenotyping." American Journal of Physiology-Heart and Circulatory Physiology 303, no. 2 (July 15, 2012): H156—H167. http://dx.doi.org/10.1152/ajpheart.00333.2012.

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The isolated retrograde-perfused Langendorff heart and the isolated ejecting heart have, over many decades, resulted in fundamental discoveries that form the underpinnings of our current understanding of the biology and physiology of the heart. These two experimental methodologies have proven invaluable in studying pharmacological effects on myocardial function, metabolism, and vascular reactivity and in the investigation of clinically relevant disease states such as ischemia-reperfusion injury, diabetes, obesity, and heart failure. With the advent of the genomics era, the isolated mouse heart preparation has gained prominence as an ex vivo research tool for investigators studying the impact of gene modification in the intact heart. This review summarizes the historical development of the isolated heart and provides a practical guide for the establishment of the Langendorff and ejecting heart preparations with a particular emphasis on the murine heart. In addition, current applications and novel methods of recording cardiovascular parameters in the isolated heart preparation will be discussed. With continued advances in methodological recordings, the isolated mouse heart preparation will remain physiologically relevant for the foreseeable future, serving as an integral bridge between in vitro assays and in vivo approaches.
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2

Ghais, Nina S., Yanmin Zhang, Bina Mistry, Andrew A. Grace, and Christopher L. H. Huang. "Anti-arrhythmic effects of cyclopiazonic acid in Langendorff-perfused murine hearts." Progress in Biophysics and Molecular Biology 98, no. 2-3 (October 2008): 281–88. http://dx.doi.org/10.1016/j.pbiomolbio.2009.01.004.

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3

Ismail, Nur Izzah, Nathaly Anto Michel, Khairunnisa Katwadi, Mim-Mim Lim, To-Kiu Chan, Attaur Rahman, Dachun Xu, Sang-Ging Ong, Derek J. Hausenloy, and Sang-Bing Ong. "Ischemic Preconditioning and Postconditioning Protect the Heart by Preserving the Mitochondrial Network." BioMed Research International 2022 (September 27, 2022): 1–14. http://dx.doi.org/10.1155/2022/6889278.

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Background. Mitochondria fuse to form elongated networks which are more tolerable to stress and injury. Ischemic pre- and postconditioning (IPC and IPost, respectively) are established cardioprotective strategies in the preclinical setting. Whether IPC and IPost modulates mitochondrial morphology is unknown. We hypothesize that the protective effects of IPC and IPost may be conferred via preservation of mitochondrial network. Methods. IPC and IPost were applied to the H9c2 rat myoblast cells, isolated adult primary murine cardiomyocytes, and the Langendorff-isolated perfused rat hearts. The effects of IPC and IPost on cardiac cell death following ischemia-reperfusion injury (IRI), mitochondrial morphology, and gene expression of mitochondrial-shaping proteins were investigated. Results. IPC and IPost successfully reduced cardiac cell death and myocardial infarct size. IPC and IPost maintained the mitochondrial network in both H9c2 and isolated adult primary murine cardiomyocytes. 2D-length measurement of the 3 mitochondrial subpopulations showed that IPC and IPost significantly increased the length of interfibrillar mitochondria (IFM). Gene expression of the pro-fusion protein, Mfn1, was significantly increased by IPC, while the pro-fission protein, Drp1, was significantly reduced by IPost in the H9c2 cells. In the primary cardiomyocytes, gene expression of both Mfn1 and Mfn2 were significantly upregulated by IPC and IPost, while Drp1 was significantly downregulated by IPost. In the Langendorff-isolated perfused heart, gene expression of Drp1 was significantly downregulated by both IPC and IPost. Conclusion. IPC and IPost-mediated upregulation of pro-fusion proteins (Mfn1 and Mfn2) and downregulation of pro-fission (Drp1) promote maintenance of the interconnected mitochondrial network, ultimately conferring cardioprotection against IRI.
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4

Sabir, Ian N., James A. Fraser, Matthew J. Killeen, Andrew A. Grace, and Christopher L. H. Huang. "The contribution of refractoriness to arrhythmic substrate in hypokalemic Langendorff-perfused murine hearts." Pflügers Archiv - European Journal of Physiology 454, no. 2 (February 13, 2007): 209–22. http://dx.doi.org/10.1007/s00424-007-0217-3.

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5

Podobed, Peter, W. Glen Pyle, Suzanne Ackloo, Faisal J. Alibhai, Elena V. Tsimakouridze, William F. Ratcliffe, Allison Mackay, et al. "The day/night proteome in the murine heart." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 307, no. 2 (July 15, 2014): R121—R137. http://dx.doi.org/10.1152/ajpregu.00011.2014.

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Circadian rhythms are essential to cardiovascular health and disease. Temporal coordination of cardiac structure and function has focused primarily at the physiological and gene expression levels, but these analyses are invariably incomplete, not the least because proteins underlie many biological processes. The purpose of this study was to reveal the diurnal cardiac proteome and important contributions to cardiac function. The 24-h day-night murine cardiac proteome was assessed by two-dimensional difference in gel electrophoresis (2D-DIGE) and liquid chromatography-mass spectrometry. Daily variation was considerable, as ∼7.8% (90/1,147) of spots exhibited statistical changes at paired times across the 24-h light- (L) dark (D) cycle. JTK_CYCLE was used to investigate underlying diurnal rhythms in corresponding mRNA. We next revealed that disruption of the L:D cycle altered protein profiles and diurnal variation in cardiac function in Langendorff-perfused hearts, relative to the L:D cycle. To investigate the role of the circadian clock mechanism, we used cardiomyocyte clock mutant (CCM) mice. CCM myofilaments exhibited a loss of time-of-day-dependent maximal calcium-dependent ATP consumption, and altered phosphorylation rhythms. Moreover, the cardiac proteome was significantly altered in CCM hearts, especially enzymes regulating vital metabolic pathways. Lastly, we used a model of pressure overload cardiac hypertrophy to demonstrate the temporal proteome during heart disease. Our studies demonstrate that time of day plays a direct role in cardiac protein abundance and indicate a novel mechanistic contribution of circadian biology to cardiovascular structure and function.
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6

Sabir, Ian N., Matthew J. Killeen, Catharine A. Goddard, Glyn Thomas, Simon Gray, Andrew A. Grace, and Christopher L. H. Huang. "Transient alterations in transmural repolarization gradients and arrhythmogenicity in hypokalaemic Langendorff-perfused murine hearts." Journal of Physiology 581, no. 1 (May 4, 2007): 277–89. http://dx.doi.org/10.1113/jphysiol.2007.128637.

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7

Ghais, Nina S., Yanmin Zhang, Andrew A. Grace, and Christopher L. H. Huang. "Arrhythmogenic actions of the Ca2+channel agonist FPL-64716 in Langendorff-perfused murine hearts." Experimental Physiology 94, no. 2 (January 15, 2009): 240–54. http://dx.doi.org/10.1113/expphysiol.2008.044669.

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8

Olson, Aaron K., Bertrand Bouchard, Wei Zhong Zhu, John C. Chatham, and Christine Des Rosiers. "First characterization of glucose flux through the hexosamine biosynthesis pathway (HBP) in ex vivo mouse heart." Journal of Biological Chemistry 295, no. 7 (January 8, 2020): 2018–33. http://dx.doi.org/10.1074/jbc.ra119.010565.

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The hexosamine biosynthesis pathway (HBP) branches from glycolysis and forms UDP-GlcNAc, the moiety for O-linked β-GlcNAc (O-GlcNAc) post-translational modifications. An inability to directly measure HBP flux has hindered our understanding of the factors regulating protein O-GlcNAcylation. Our goals in this study were to (i) validate a LC-MS method that assesses HBP flux as UDP-GlcNAc (13C)-molar percent enrichment (MPE) and concentration and (ii) determine whether glucose availability or workload regulate cardiac HBP flux. For (i), we perfused isolated murine working hearts with [U-13C6]glucosamine (1, 10, 50, or 100 μm), which bypasses the rate-limiting HBP enzyme. We observed a concentration-dependent increase in UDP-GlcNAc levels and MPE, with the latter reaching a plateau of 56.3 ± 2.9%. For (ii), we perfused isolated working hearts with [U-13C6]glucose (5.5 or 25 mm). Glycolytic efflux doubled with 25 mm [U-13C6]glucose; however, the calculated HBP flux was similar among the glucose concentrations at ∼2.5 nmol/g of heart protein/min, representing ∼0.003–0.006% of glycolysis. Reducing cardiac workload in beating and nonbeating Langendorff perfusions had no effect on the calculated HBP flux at ∼2.3 and 2.5 nmol/g of heart protein/min, respectively. To the best of our knowledge, this is the first direct measurement of glucose flux through the HBP in any organ. We anticipate that these methods will enable foundational analyses of the regulation of HBP flux and protein O-GlcNAcylation. Our results suggest that in the healthy ex vivo perfused heart, HBP flux does not respond to acute changes in glucose availability or cardiac workload.
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9

Zhang, Jimmy, Sergiy M. Nadtochiy, William R. Urciuoli, and Paul S. Brookes. "The cardioprotective compound cloxyquin uncouples mitochondria and induces autophagy." American Journal of Physiology-Heart and Circulatory Physiology 310, no. 1 (January 1, 2016): H29—H38. http://dx.doi.org/10.1152/ajpheart.00926.2014.

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Mitochondrial quality control mechanisms have been implicated in protection against cardiac ischemia-reperfusion (IR) injury. Previously, cloxyquin (5-chloroquinolin-8-ol) was identified via phenotypic screening as a cardioprotective compound. Herein, cloxyquin was identified as a mitochondrial uncoupler in both isolated heart mitochondria and adult cardiomyocytes. Additionally, cardiomyocytes isolated from transgenic mice expressing green fluorescent protein-tagged microtubule-associated protein light chain 3 showed increased autophagosome formation with cloxyquin treatment. The autophagy inhibitor chloroquine abolished cloxyquin-induced cardioprotection in both cellular and perfused heart (Langendorff) models of IR injury. Finally, in an in vivo murine left anterior descending coronary artery occlusion model of IR injury, cloxyquin significantly reduced infarct size from 31.4 ± 3.4% to 16.1 ± 2.2%. In conclusion, the cardioprotective compound cloxyquin simultaneously uncoupled mitochondria and induced autophagy. Importantly, autophagy appears to be required for cloxyquin-induced cardioprotection.
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10

Sabir, Ian N., Lucia M. Li, Andrew A. Grace, and Christopher L. H. Huang. "Restitution analysis of alternans and its relationship to arrhythmogenicity in hypokalaemic Langendorff-perfused murine hearts." Pflügers Archiv - European Journal of Physiology 455, no. 4 (August 18, 2007): 653–66. http://dx.doi.org/10.1007/s00424-007-0327-y.

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11

Talukder, M. A. Hassan, R. Ray Morrison, and S. Jamal Mustafa. "Comparison of the vascular effects of adenosine in isolated mouse heart and aorta." American Journal of Physiology-Heart and Circulatory Physiology 282, no. 1 (January 1, 2002): H49—H57. http://dx.doi.org/10.1152/ajpheart.2002.282.1.h49.

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The present study was designed to characterize and compare the vascular effects of adenosine and its analogs in the murine heart and aorta. Mouse hearts perfused under constant pressure in standard Langendorff fashion demonstrated concentration-dependent increases in coronary flow to adenosine, 2-chloradenosine (CAD), 5′-( N-ethyl-carboxamido)-adenosine (NECA), and 2- p-(2-carboxyethyl)phenethylamino-5′- N-ethylcarboxam-idoadenosine (CGS-21680). All agonists produced comparable increases in coronary flow with the following order of potency: CGS-21680 = NECA ≫ CAD ≥ adenosine. In l-phenylephrine hydrochloride (phenylephrine) precontracted aortic rings, all nonselective agonists (NECA, CAD, and adenosine) produced marked concentration-dependent relaxation, whereas the adenosine A2A selective agonist CGS-21680 did not. Adenosine receptor agonists were >100 times more potent for coronary vasodilation than aortic vasorelaxation. The selective A2A receptor antagonist 5-amino-7-(β-phenylethyl)-2-(8-furyl)pyrazolo-[4,3-e]-1,2,4-triazolo-[1,5-c]pyrimidine (SCH-58261) blocked both CGS-21680- and NECA-induced increases in coronary flow, whereas the A2B receptor antagonist benzo[g]pteridine-2,4(1H,3H)-dione (alloxazine) inhibited NECA-induced aortic relaxation. These data indicate a differential response to adenosine agonists in murine coronary vasculature and aorta where coronary vasodilation is mediated predominantly by activation of A2A adenosine receptors.
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12

Zhang, Yanmin, Christof Schwiening, Matthew J. Killeen, Yanhui Zhang, Aiqun Ma, Ming Lei, Andrew A. Grace, and Christopher L.-H. Huang. "Pharmacological changes in cellular Ca2+homeostasis parallel initiation of atrial arrhythmogenesis in murine langendorff-perfused hearts." Clinical and Experimental Pharmacology and Physiology 36, no. 10 (October 2009): 969–80. http://dx.doi.org/10.1111/j.1440-1681.2009.05170.x.

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13

Knollmann, Björn C., Tilmann Schober, Andreas O. Petersen, Syevda G. Sirenko, and Michael R. Franz. "Action potential characterization in intact mouse heart: steady-state cycle length dependence and electrical restitution." American Journal of Physiology-Heart and Circulatory Physiology 292, no. 1 (January 2007): H614—H621. http://dx.doi.org/10.1152/ajpheart.01085.2005.

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Transgenic mice have been increasingly utilized to investigate the molecular mechanisms of cardiac arrhythmias, yet the rate dependence of the murine action potential duration and the electrical restitution curve (ERC) remain undefined. In the present study, 21 isolated, Langendorff-perfused, and atrioventricular node-ablated mouse hearts were studied. Left ventricular and left atrial action potentials were recorded using a validated miniaturized monophasic action potential probe. Murine action potentials (AP) were measured at 30, 50, 70, and 90% repolarization (APD30–APD90) during steady-state pacing and varied coupling intervals to determine ERCs. Murine APD showed rate adaptation as well as restitution properties. The ERC time course differed dramatically between early and late repolarization: APD30 shortened with increasing S1–S2 intervals, whereas APD90 was prolonged. When fitted with a monoexponential function, APD30 reached plateau values significantly faster than APD90 (τ = 29 ± 2 vs. 78 ± 6 ms, P < 0.01, n = 12). The slope of early APD90 restitution was significantly <1 (0.16 ± 0.02). Atrial myocardium had shorter final repolarization and significantly faster ERCs that were shifted leftward compared with ventricular myocardium. Recovery kinetics of intracellular Ca2+ transients recorded from isolated ventricular myocytes at 37°C (τ = 93 ± 4 ms, n = 18) resembled the APD90 ERC kinetics. We conclude that mouse myocardium shows AP cycle length dependence and electrical restitution properties that are surprisingly similar to those of larger mammals and humans.
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14

Sabir, Ian N., James A. Fraser, Thomas R. Cass, Andrew A. Grace, and Christopher L. H. Huang. "A quantitative analysis of the effect of cycle length on arrhythmogenicity in hypokalaemic Langendorff-perfused murine hearts." Pflügers Archiv - European Journal of Physiology 454, no. 6 (April 17, 2007): 925–36. http://dx.doi.org/10.1007/s00424-007-0255-x.

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15

Ozhathil, Lijo Cherian, Jean-Sébastien Rougier, Prakash Arullampalam, Maria C. Essers, Daniela Ross-Kaschitza, and Hugues Abriel. "Deletion of Trpm4 Alters the Function of the Nav1.5 Channel in Murine Cardiac Myocytes." International Journal of Molecular Sciences 22, no. 7 (March 26, 2021): 3401. http://dx.doi.org/10.3390/ijms22073401.

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Transient receptor potential melastatin member 4 (TRPM4) encodes a Ca2+-activated, non-selective cation channel that is functionally expressed in several tissues, including the heart. Pathogenic mutants in TRPM4 have been reported in patients with inherited cardiac diseases, including conduction blockage and Brugada syndrome. Heterologous expression of mutant channels in cell lines indicates that these mutations can lead to an increase or decrease in TRPM4 expression and function at the cell surface. While the expression and clinical variant studies further stress the importance of TRPM4 in cardiac function, the cardiac electrophysiological phenotypes in Trpm4 knockdown mouse models remain incompletely characterized. To study the functional consequences of Trpm4 deletion on cardiac electrical activity in mice, we performed perforated-patch clamp and immunoblotting studies on isolated atrial and ventricular cardiac myocytes and surfaces, as well as on pseudo- and intracardiac ECGs, either in vivo or in Langendorff-perfused explanted mouse hearts. We observed that TRPM4 is expressed in atrial and ventricular cardiac myocytes and that deletion of Trpm4 unexpectedly reduces the peak Na+ currents in myocytes. Hearts from Trpm4−/− mice presented increased sensitivity towards mexiletine, a Na+ channel blocker, and slower intraventricular conduction, consistent with the reduction of the peak Na+ current observed in the isolated cardiac myocytes. This study suggests that TRPM4 expression impacts the Na+ current in murine cardiac myocytes and points towards a novel function of TRPM4 regulating the Nav1.5 function in murine cardiac myocytes.
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16

Li, Mengye, Sandeep S. Hothi, Samantha C. Salvage, Kamalan Jeevaratnam, Andrew A. Grace, and Christopher L.-H. Huang. "Arrhythmic effects of Epac-mediated ryanodine receptor activation in Langendorff-perfused murine hearts are associated with reduced conduction velocity." Clinical and Experimental Pharmacology and Physiology 44, no. 6 (May 19, 2017): 686–92. http://dx.doi.org/10.1111/1440-1681.12751.

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17

Zhang, Yanmin, JingJing Wu, James H. King, Christopher L. H. Huang, and James A. Fraser. "Measurement and interpretation of electrocardiographic QT intervals in murine hearts." American Journal of Physiology-Heart and Circulatory Physiology 306, no. 11 (June 1, 2014): H1553—H1557. http://dx.doi.org/10.1152/ajpheart.00459.2013.

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Alterations in ECG QT intervals correlate with the risk of potentially fatal arrhythmias, for which transgenic murine hearts are becoming increasingly useful experimental models. However, QT intervals are poorly defined in murine ECGs. As a consequence, several different techniques have been used to measure murine QT intervals. The present work develops a consistent measure of the murine QT interval that correlates with changes in the duration of ventricular myocyte action potentials (APs). Volume-conducted ECGs were compared with simultaneously recorded APs, obtained using floating intracellular microelectrodes in Langendorff-perfused mouse hearts. QT intervals were measured from the onset of the QRS complex. The interval, Q-APR90, measured to the time at 90% AP recovery, was compared with two measures of the QT interval. QT1 was measured to the recovery of the ECG trace to the isoelectric baseline for entirely positive T-waves or to the trough of any negative T-wave undershoot. QT2—used extensively in previous studies—was measured to the return of any ECG trough to the isoelectric baseline. QT1, but not QT2, closely correlated with changes in Q-APR90. These findings were confirmed over a range of pacing rates, in low K+ concentration solutions, and in Scn5a+/Δ KPQ hearts used to model human long QT syndrome. Application of this method in whole anesthetized mice similarly demonstrated a prolonged corrected QT (QTc) in Scn5a+/Δ KPQ hearts. We therefore describe a robust method for the determination of QT and QTc intervals that correlate with the duration of ventricular myocyte APs in murine hearts.
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18

Mohamed, Belal A., Nico Hartmann, Petros Tirilomis, Karolina Sekeres, Wener Li, Stefan Neef, Claudia Richter, et al. "Sarcoplasmic reticulum calcium leak contributes to arrhythmia but not to heart failure progression." Science Translational Medicine 10, no. 458 (September 12, 2018): eaan0724. http://dx.doi.org/10.1126/scitranslmed.aan0724.

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Increased sarcoplasmic reticulum (SR) Ca2+ leak via the cardiac ryanodine receptor (RyR2) has been suggested to play a mechanistic role in the development of heart failure (HF) and cardiac arrhythmia. Mice treated with a selective RyR2 stabilizer, rycal S36, showed normalization of SR Ca2+ leak and improved survival in pressure overload (PO) and myocardial infarction (MI) models. The development of HF, measured by echocardiography and molecular markers, showed no difference in rycal S36– versus placebo-treated mice. Reduction of SR Ca2+ leak in the PO model by the rycal-unrelated RyR2 stabilizer dantrolene did not mitigate HF progression. Development of HF was not aggravated by increased SR Ca2+ leak due to RyR2 mutation (R2474S) in volume overload, an SR Ca2+ leak–independent HF model. Arrhythmia episodes were reduced by rycal S36 treatment in PO and MI mice in vivo and ex vivo in Langendorff-perfused hearts. Isolated cardiomyocytes from murine failing hearts and human ventricular failing and atrial nonfailing myocardium showed reductions in delayed afterdepolarizations, in spontaneous and induced Ca2+ waves, and in triggered activity in rycal S36 versus placebo cells, whereas the Ca2+ transient, SR Ca2+ load, SR Ca2+ adenosine triphosphatase function, and action potential duration were not affected. Rycal S36 treatment of human induced pluripotent stem cells isolated from a patient with catecholaminergic polymorphic ventricular tachycardia could rescue the leaky RyR2 receptor. These results suggest that SR Ca2+ leak does not primarily influence contractile HF progression, whereas rycal S36 treatment markedly reduces ventricular arrhythmias, thereby improving survival in mice.
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19

Matthews, Gareth D. K., Laila Guzadhur, Andrew Grace, and Christopher L.-H. Huang. "Nonlinearity between action potential alternans and restitution, which both predict ventricular arrhythmic properties in Scn5a+/− and wild-type murine hearts." Journal of Applied Physiology 112, no. 11 (June 1, 2012): 1847–63. http://dx.doi.org/10.1152/japplphysiol.00039.2012.

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Electrocardiographic QT- and T-wave alternans, presaging ventricular arrhythmia, reflects compromised adaptation of action potential (AP) duration (APD) to altered heart rate, classically attributed to incomplete Nav1.5 channel recovery prior to subsequent stimulation. The restitution hypothesis suggests a function whose slope directly relates to APD alternans magnitude, predicting a critical instability condition, potentially generating arrhythmia. The present experiments directly test for such correlations among arrhythmia, APD alternans and restitution. Mice haploinsufficient in the Scn5a, cardiac Na+ channel gene ( Scn5a+/−), previously used to replicate Brugada syndrome, were used, owing to their established arrhythmic properties increased by flecainide and decreased by quinidine, particularly in right ventricular (RV) epicardium. Monophasic APs, obtained during pacing with progressively decrementing cycle lengths, were systematically compared at RV and left ventricular epicardial and endocardial recording sites in Langendorff-perfused Scn5a+/− and wild-type hearts before and following flecainide (10 μM) or quinidine (5 μM) application. The extent of alternans was assessed using a novel algorithm. Scn5a+/− hearts showed greater frequencies of arrhythmic endpoints with increased incidences of ventricular tachycardia, diminished by quinidine, and earlier onsets of ventricular fibrillation, particularly following flecainide challenge. These features correlated directly with increased refractory periods, specifically in the RV, and abnormal restitution and alternans properties in the RV epicardium. The latter variables were related by a unique, continuous higher-order function, rather than a linear relationship with an unstable threshold. These findings demonstrate a specific relationship between alternans and restitution, as well as confirming their capacity to predict arrhythmia, but implicate mechanisms additional to the voltage feedback suggested in the restitution hypothesis.
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20

Martin, Claire A., Andrew A. Grace, and Christopher L. H. Huang. "Spatial and temporal heterogeneities are localized to the right ventricular outflow tract in a heterozygotic Scn5a mouse model." American Journal of Physiology-Heart and Circulatory Physiology 300, no. 2 (February 2011): H605—H616. http://dx.doi.org/10.1152/ajpheart.00824.2010.

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Ventricular tachycardia (VT) in Brugada Syndrome patients often originates in the right ventricular outflow tract (RVOT). We explore the physiological basis for this observation using murine whole heart preparations. Ventricular bipolar electrograms and monophasic action potentials were recorded from seven epicardial positions in Langendorff-perfused wild-type and Scn5a+/− hearts. VT first appeared in the RVOT, implicating it as an arrhythmogenic focus in Scn5a+/− hearts. RVOTs showed the greatest heterogeneity in refractory periods, response latencies, and action potential durations, and the most fractionated electrograms. However, incidences of concordant alternans in dynamic pacing protocol recordings were unaffected by the Scn5a+/− mutation or pharmacological intervention. Conversely, particularly at the RVOT, Scn5a+/− hearts showed earlier and more frequent transitions into discordant alternans. This was accentuated by flecainide, but reduced by quinidine, in parallel with their respective pro- and anti-arrhythmic effects. Discordant alternans preceded all episodes of VT. The RVOT of Scn5a+/− hearts also showed steeper restitution curves, with the diastolic interval at which the gradient equaled one strongly correlating with the diastolic interval at which discordant alternans commenced. We attribute the arrhythmic tendency within the RVOT to the greater spatial heterogeneities in baseline electrophysiological properties. These, in turn, give rise to a tendency to drive concordant alternans phenomena into an arrhythmogenic discordant alternans. Our findings may contribute to future work investigating possible pharmacological treatments for a disease in which the current mainstay of treatment is implantable cardioverter defibrillator implantation.
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21

Wafa, Dina, Nóra Koch, Janka Kovács, Margit Kerék, Richard L. Proia, Gábor J. Tigyi, Zoltán Benyó, and Zsuzsanna Miklós. "Opposing Roles of S1P3 Receptors in Myocardial Function." Cells 9, no. 8 (July 24, 2020): 1770. http://dx.doi.org/10.3390/cells9081770.

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Sphingosine-1-phosphate (S1P) is a lysophospholipid mediator with diverse biological function mediated by S1P1–5 receptors. Whereas S1P was shown to protect the heart against ischemia/reperfusion (I/R) injury, other studies highlighted its vasoconstrictor effects. We aimed to separate the beneficial and potentially deleterious cardiac effects of S1P during I/R and identify the signaling pathways involved. Wild type (WT), S1P2-KO and S1P3-KO Langendorff-perfused murine hearts were exposed to intravascular S1P, I/R, or both. S1P induced a 45% decrease of coronary flow (CF) in WT-hearts. The presence of S1P-chaperon albumin did not modify this effect. CF reduction diminished in S1P3-KO but not in S1P2-KO hearts, indicating that in our model S1P3 mediates coronary vasoconstriction. In I/R experiments, S1P3 deficiency had no influence on postischemic CF but diminished functional recovery and increased infarct size, indicating a cardioprotective effect of S1P3. Preischemic S1P exposure resulted in a substantial reduction of postischemic CF and cardiac performance and increased the infarcted area. Although S1P3 deficiency increased postischemic CF, this failed to improve cardiac performance. These results indicate a dual role of S1P3 involving a direct protective action on the myocardium and a cardiosuppressive effect due to coronary vasoconstriction. In acute coronary syndrome when S1P may be released abundantly, intravascular and myocardial S1P production might have competing influences on myocardial function via activation of S1P3 receptors.
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22

Peart, Jason, and John P. Headrick. "Intrinsic A1 adenosine receptor activation during ischemia or reperfusion improves recovery in mouse hearts." American Journal of Physiology-Heart and Circulatory Physiology 279, no. 5 (November 1, 2000): H2166—H2175. http://dx.doi.org/10.1152/ajpheart.2000.279.5.h2166.

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We assessed the role of A1 adenosine receptor (A1AR) activation by endogenous adenosine in the modulation of ischemic contracture and postischemic recovery in Langendorff-perfused mouse hearts subjected to 20 min of total ischemia and 30 min of reperfusion. In control hearts, the rate-pressure product (RPP) and first derivative of pressure development over time (+dP/d t) recovered to 57 ± 3 and 58 ± 3% of preischemia, respectively. Diastolic pressure remained elevated at 20 ± 2 mmHg (compared with 3 ± 1 mmHg preischemia). Interstitial adenosine, assessed by microdialysis, rose from ∼0.3 to 1.9 μM during ischemia compared with ∼15 μM in rat heart. Nonetheless, these levels will near maximally activate A1ARs on the basis of effects of exogenous adenosine and 2-chloroadenosine. Neither A1AR blockade with 200 nM 8-cyclopentyl-1,3-dipropylxanthine (DPCPX) during the ischemic period alone nor A1AR activation with 50 nM N 6-cyclopentyladenosine altered rapidity or extent of ischemic contracture. However, ischemic DPCPX treatment significantly depressed postischemic recovery of RPP and +dP/d t (44 ± 3 and 40 ± 4% of preischemia, respectively). DPCPX treatment during the reperfusion period alone also reduced recovery of RPP and +dP/d t (to 44 ± 2 and 47 ± 2% of preischemia, respectively). These data indicate that 1) interstitial adenosine is lower in mouse versus rat myocardium during ischemia, 2) A1AR activation by endogenous adenosine or exogenous agonists does not modify ischemic contracture in murine myocardium, 3) A1AR activation by endogenous adenosine during ischemia attenuates postischemic stunning, and 4) A1AR activation by endogenous adenosine during the reperfusion period also improves postischemic contractile recovery.
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Sabir, Ian N., Lucia M. Li, Victoria J. Jones, Catharine A. Goddard, Andrew A. Grace, and Christopher L. H. Huang. "Criteria for arrhythmogenicity in genetically-modified Langendorff-perfused murine hearts modelling the congenital long QT syndrome type 3 and the Brugada syndrome." Pflügers Archiv - European Journal of Physiology 455, no. 4 (September 6, 2007): 637–51. http://dx.doi.org/10.1007/s00424-007-0326-z.

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24

Obergassel, Julius, Molly O’Reilly, Laura C. Sommerfeld, S. Nashitha Kabir, Christopher O’Shea, Fahima Syeda, Lars Eckardt, Paulus Kirchhof, and Larissa Fabritz. "Effects of genetic background, sex, and age on murine atrial electrophysiology." EP Europace 23, no. 6 (January 19, 2021): 958–69. http://dx.doi.org/10.1093/europace/euaa369.

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Abstract Aims Genetically altered mice are powerful models to investigate mechanisms of atrial arrhythmias, but normal ranges for murine atrial electrophysiology have not been robustly characterized. Methods and results We analyzed results from 221 electrophysiological (EP) studies in isolated, Langendorff-perfused hearts of wildtype mice (114 female, 107 male) from 2.5 to 17.7 months (mean 7 months) with different genetic backgrounds (C57BL/6, FVB/N, MF1, 129/Sv, Swiss agouti). Left atrial monophasic action potential duration (LA-APD), interatrial activation time (IA-AT), and atrial effective refractory period (ERP) were summarized at different pacing cycle lengths (PCLs). Factors influencing atrial electrophysiology including genetic background, sex, and age were determined. LA-APD70 was 18 ± 0.5 ms, atrial ERP was 27 ± 0.8 ms, and IA-AT was 17 ± 0.5 ms at 100 ms PCL. LA-APD was longer with longer PCL (+17% from 80 to 120 ms PCL for APD70), while IA-AT decreased (−7% from 80 to 120 ms PCL). Female sex was associated with longer ERP (+14% vs. males). Genetic background influenced atrial electrophysiology: LA-APD70 (−20% vs. average) and atrial ERP (−25% vs. average) were shorter in Swiss agouti background compared to others. LA-APD70 (+25% vs. average) and IA-AT (+44% vs. average) were longer in 129/Sv mice. Atrial ERP was longer in FVB/N (+34% vs. average) and in younger experimental groups below 6 months of age. Conclusion This work defines normal ranges for murine atrial EP parameters. Genetic background has a profound effect on these parameters, at least of the magnitude as those of sex and age. These results can inform the experimental design and interpretation of murine atrial electrophysiology.
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Martin, Claire A., Laila Guzadhur, Andrew A. Grace, Ming Lei, and Christopher L. H. Huang. "Mapping of reentrant spontaneous polymorphic ventricular tachycardia in a Scn5a+/− mouse model." American Journal of Physiology-Heart and Circulatory Physiology 300, no. 5 (May 2011): H1853—H1862. http://dx.doi.org/10.1152/ajpheart.00034.2011.

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Two major mechanisms have been postulated for the arrhythmogenic tendency observed in Brugada Syndrome (BrS): delays in conduction or increased heterogeneities in repolarization. We use a contact mapping system to directly investigate the interacting roles of these two mechanisms in arrhythmogenesis using a genetic murine model for BrS for the first time. Electrograms were obtained from a multielectrode recording array placed against the left ventricle and right ventricle (RV) of spontaneously beating Langendorff-perfused wild type (WT) and Scn5a+/− mouse hearts. Scn5a+/− hearts showed activation waves arriving at the epicardial surface consistent with slowed conduction, which was exacerbated in the presence of flecainide. Lines of conduction block across the RV resulting from premature ventricular beats led to the formation of reentrant circuits and polymorphic ventricular tachycardia. WT hearts showed an inverse relationship between activation times and activation recovery intervals measured at the epicardial surface, which resulted in synchronicity of repolarization times. In contrast, Scn5a+/− hearts, despite having smaller mean activation recovery intervals, demonstrated a greater heterogeneity compared with WT. Isochronal maps showed that their normal activation recovery interval gradients at the epicardial surface were disrupted, leading to heterogeneity in repolarization times. We thus directly demonstrate the initiation of arrhythmia in the RV of Scn5a+/− hearts. This occurs as a result of the combination of repolarization heterogeneities leading to lines of conduction block and unidirectional conduction, with conduction slowing allowing the formation of reentrant circuits. The repolarization heterogeneities may also be responsible for the changing pattern of block, leading to the polymorphic character of the resulting ventricular tachycardia.
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Wong, Renee, Angel M. Aponte, Charles Steenbergen, and Elizabeth Murphy. "Cardioprotection leads to novel changes in the mitochondrial proteome." American Journal of Physiology-Heart and Circulatory Physiology 298, no. 1 (January 2010): H75—H91. http://dx.doi.org/10.1152/ajpheart.00515.2009.

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It is proposed that ischemic preconditioning (PC) initiates signaling that converges on mitochondria and results in cardioprotection. The outcome of this signaling on mitochondrial enzyme complexes is yet to be understood. We therefore used proteomic methods to test the hypothesis that PC and pharmacological preconditioning similarly alter mitochondrial signaling complexes. Langendorff-perfused murine hearts were treated with the specific GSK-3 inhibitor AR-A014418 (GSK Inhib VIII) for 10 min or subjected to four cycles of 5-min ischemia-reperfusion (PC) before 20-min global ischemia and 120-min reperfusion. PC and GSK Inhib VIII both improved recovery of postischemic left ventricular developed pressure, decreased infarct size, and reduced lactate production during ischemia compared with their time-matched controls. We used proteomics to examine mitochondrial protein levels/posttranslational modifications that were common between PC and GSK Inhib VIII. Levels of cytochrome- c oxidase subunits Va and VIb, ATP synthase-coupling factor 6, and cytochrome b- c1 complex subunit 6 were increased while cytochrome c was decreased with PC and GSK Inhib VIII. Furthermore, the amount of cytochrome- c oxidase subunit VIb was found to be increased in PC and GSK Inhib VIII mitochondrial supercomplexes, which are comprised of complexes I, III, and IV. This result would suggest that changes in complex subunits associated with cardioprotection may affect supercomplex composition. Thus the ability of PC and GSK inhibition to alter the expression levels of electron transport complexes will have important implications for mitochondrial function.
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Peart, Jason N., and Garrett J. Gross. "Cardioprotective effects of acute and chronic opioid treatment are mediated via different signaling pathways." American Journal of Physiology-Heart and Circulatory Physiology 291, no. 4 (October 2006): H1746—H1753. http://dx.doi.org/10.1152/ajpheart.00233.2006.

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A 5-day exposure to morphine exerts a profound cardioprotective phenotype in murine hearts. In the present study, we examined mechanisms by which morphine generates this effect, exploring the roles of Gi and Gs proteins, PKA, PKC, and β-adrenergic receptors (β-AR) in acute and chronic opioid preconditioning. Langendorff-perfused hearts from placebo, acute morphine (AM; 10 μmol/l)-, or chronic morphine (CM)-treated mice (75-mg pellet, 5 days) underwent 25-min ischemia and 45-min reperfusion. After reperfusion, placebo-treated hearts exhibited marked contractile and diastolic dysfunction [rate-pressure product (RPP), 40 ± 4% baseline; end-diastolic pressure (EDP), 33 ± 3 mmHg], whereas AM hearts showed significant improvement in recovery of RPP and EDP (60 ± 3% and 23 ± 4 mmHg, respectively; P < 0.05 vs. placebo). Furthermore, CM hearts demonstrated a complete return of diastolic function and significantly greater recovery of contractile function (83 ± 3%, P < 0.05 vs. both placebo and AM). Pretreatment with Gi protein inhibitor pertussis toxin abolished AM protection while partially attenuating CM recovery ( P < 0.05 vs. placebo). Treatment with Gs inhibitor NF-449 did not affect AM preconditioning yet completely abrogated CM preconditioning. Similarly, PKA inhibition significantly attenuated the ischemia-tolerant state afforded by CM, whereas it was ineffective in AM hearts. PKC inhibition with chelerythrine was ineffective in CM hearts while completely abrogating AM preconditioning. Moreover, whereas β1-AR blockade with CGP-20712A failed to alter recovery in CM hearts, the β2-AR antagonist ICI-118,551 significantly attenuated postischemic recovery. These data describe novel findings whereby CM preconditioning is mediated by a PKC-independent pathway involving PKA, β2-AR, and Gs proteins, whereas AM preconditioning is mediated via Gi proteins and PKC.
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See Hoe, Louise E., Jan M. Schilling, Emiri Tarbit, Can J. Kiessling, Anna R. Busija, Ingrid R. Niesman, Eugene Du Toit, et al. "Sarcolemmal cholesterol and caveolin-3 dependence of cardiac function, ischemic tolerance, and opioidergic cardioprotection." American Journal of Physiology-Heart and Circulatory Physiology 307, no. 6 (September 15, 2014): H895—H903. http://dx.doi.org/10.1152/ajpheart.00081.2014.

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Cholesterol-rich caveolar microdomains and associated caveolins influence sarcolemmal ion channel and receptor function and protective stress signaling. However, the importance of membrane cholesterol content to cardiovascular function and myocardial responses to ischemia-reperfusion (I/R) and cardioprotective stimuli are unclear. We assessed the effects of graded cholesterol depletion with methyl-β-cyclodextrin (MβCD) and lifelong knockout (KO) or overexpression (OE) of caveolin-3 (Cav-3) on cardiac function, I/R tolerance, and opioid receptor (OR)-mediated protection. Langendorff-perfused hearts from young male C57Bl/6 mice were untreated or treated with 0.02–1.0 mM MβCD for 25 min to deplete membrane cholesterol and disrupt caveolae. Hearts were subjected to 25-min ischemia/45-min reperfusion, and the cardioprotective effects of morphine applied either acutely or chronically [sustained ligand-activated preconditioning (SLP)] were assessed. MβCD concentration dependently reduced normoxic contractile function and postischemic outcomes in association with graded (10–30%) reductions in sarcolemmal cholesterol. Cardioprotection with acute morphine was abolished with ≥20 μM MβCD, whereas SLP was more robust and only inhibited with ≥200 μM MβCD. Deletion of Cav-3 also reduced, whereas Cav-3 OE improved, myocardial I/R tolerance. Protection via SLP remained equally effective in Cav-3 KO mice and was additive with innate protection arising with Cav-3 OE. These data reveal the membrane cholesterol dependence of normoxic myocardial and coronary function, I/R tolerance, and OR-mediated cardioprotection in murine hearts (all declining with cholesterol depletion). In contrast, baseline function appears insensitive to Cav-3, whereas cardiac I/R tolerance parallels Cav-3 expression. Novel SLP appears unique, being less sensitive to cholesterol depletion than acute OR protection and arising independently of Cav-3 expression.
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Ko, Jum-Suk, Shuai Guo, Jonathan Hassel, Patricia Celestino-Soper, Ty C. Lynnes, James E. Tisdale, James J. Zheng, et al. "Ondansetron blocks wild-type and p.F503L variant small-conductance Ca2+-activated K+ channels." American Journal of Physiology-Heart and Circulatory Physiology 315, no. 2 (August 1, 2018): H375—H388. http://dx.doi.org/10.1152/ajpheart.00479.2017.

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Apamin-sensitive small-conductance Ca2+-activated K+ (SK) current ( IKAS) is encoded by Ca2+-activated K+ channel subfamily N ( KCNN) genes. IKAS importantly contributes to cardiac repolarization in conditions associated with reduced repolarization reserve. To test the hypothesis that IKAS inhibition contributes to drug-induced long QT syndrome (diLQTS), we screened for KCNN variants among patients with diLQTS, determined the properties of heterologously expressed wild-type (WT) and variant KCNN channels, and determined if the 5-HT3 receptor antagonist ondansetron blocks IKAS. We searched 2,306,335 records in the Indiana Network for Patient Care and found 11 patients with diLQTS who had DNA available in the Indiana Biobank. DNA sequencing discovered a heterozygous KCNN2 variant (p.F503L) in a 52-yr-old woman presenting with corrected QT interval prolongation at baseline (473 ms) and further corrected QT interval lengthening (601 ms) after oral administration of ondansetron. That patient was also heterozygous for the p.S38G and p.P2835S variants of the QT-controlling genes KCNE1 and ankyrin 2, respectively. Patch-clamp experiments revealed that the p.F503L KCNN2 variant heterologously expressed in human embryonic kidney (HEK)-293 cells augmented Ca2+ sensitivity, increasing IKAS density. The fraction of total F503L-KCNN2 protein retained in the membrane was higher than that of WT KCNN2 protein. Ondansetron at nanomolar concentrations inhibited WT and p.F503L SK2 channels expressed in HEK-293 cells as well as native SK channels in ventricular cardiomyocytes. Ondansetron-induced IKAS inhibition was also demonstrated in Langendorff-perfused murine hearts. In conclusion, the heterozygous p.F503L KCNN2 variant increases Ca2+ sensitivity and IKAS density in transfected HEK-293 cells. Ondansetron at therapeutic (i.e., nanomolar) concentrations is a potent IKAS blocker. NEW & NOTEWORTHY We showed that ondansetron, a 5-HT3 receptor antagonist, blocks small-conductance Ca2+-activated K+ (SK) current. Ondansetron may be useful in controlling arrhythmias in which increased SK current is a likely contributor. However, its SK-blocking effects may also facilitate the development of drug-induced long QT syndrome.
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30

Trouve, R., and G. Nahas. "Cardiac Dynamics of the Langendorff Perfused Heart." Experimental Biology and Medicine 180, no. 2 (November 1, 1985): 303–11. http://dx.doi.org/10.3181/00379727-180-42180.

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31

Mariotti, Erika, Mattia Veronese, Joel T. Dunn, Rodolfo A. Medina, Philip J. Blower, Richard Southworth, and Thomas R. Eykyn. "Assessing radiotracer kinetics in the Langendorff perfused heart." EJNMMI Research 3, no. 1 (2013): 74. http://dx.doi.org/10.1186/2191-219x-3-74.

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32

Zimmer, Heinz-Gerd. "The Isolated Perfused Heart and Its Pioneers." Physiology 13, no. 4 (August 1998): 203–10. http://dx.doi.org/10.1152/physiologyonline.1998.13.4.203.

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In 1866, Carl Ludwig together with Elias Cyon created the first isolated perfused frog heart preparation. Perfusion systems for the isolated mammalian heart were developed by H. Newell Martin in 1883 and by Oscar Langendorff in 1895. In its working mode, the isolated perfused rat heart was established in the 1960s.
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33

Wengrowski, Anastasia M., Sarah Kuzmiak-Glancy, Rafael Jaimes, and Matthew W. Kay. "NADH changes during hypoxia, ischemia, and increased work differ between isolated heart preparations." American Journal of Physiology-Heart and Circulatory Physiology 306, no. 4 (February 15, 2014): H529—H537. http://dx.doi.org/10.1152/ajpheart.00696.2013.

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Langendorff-perfused hearts and working hearts are established isolated heart preparation techniques that are advantageous for studying cardiac physiology and function, especially when fluorescence imaging is a key component. However, oxygen and energy requirements vary widely between isolated heart preparations. When energy supply and demand are not in harmony, such as when oxygen is not adequately available, the imbalance is reflected in NADH fluctuations. As such, NADH imaging can provide insight into the metabolic state of tissue. Hearts from New Zealand white rabbits were prepared as mechanically silenced Langendorff-perfused hearts, Langendorff-perfused hearts, or biventricular working hearts and subjected to sudden changes in workload, instantaneous global ischemia, and gradual hypoxia while heart rate, aortic pressure, and epicardial NADH fluorescence were monitored. Fast pacing resulted in a dip in NADH upon initiation and a spike in NADH when pacing was terminated in biventricular working hearts only, with the magnitude of the changes greatest at the fastest pacing rate. Working hearts were also most susceptible to changes in oxygen supply; NADH was at half-maximum value when perfusate oxygen was at 67.8 ± 13.7%. Langendorff-perfused and mechanically arrested hearts were the least affected by low oxygen supply, with half-maximum NADH occurring at 42.5 ± 5.0% and 23.7 ± 4.6% perfusate oxygen, respectively. Although the biventricular working heart preparation can provide a useful representation of mechanical in vivo heart function, it is not without limitations. Understanding the limitations of isolated heart preparations is crucial when studying cardiac function in the context of energy supply and demand.
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34

Jelicks, L. A., and R. K. Gupta. "Multinuclear NMR studies of the Langendorff perfused rat heart." Journal of Biological Chemistry 264, no. 26 (September 1989): 15230–35. http://dx.doi.org/10.1016/s0021-9258(19)84814-7.

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35

Arad, M., N. Zamir, L. Horowitz, T. Oxman, and B. Rabinowitz. "Release of atrial natriuretic peptide in brief ischemia-reperfusion in isolated rat hearts." American Journal of Physiology-Heart and Circulatory Physiology 266, no. 5 (May 1, 1994): H1971—H1978. http://dx.doi.org/10.1152/ajpheart.1994.266.5.h1971.

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We studied the effects of short-term global ischemia and reperfusion on ANP secretion from Langendorff-perfused rat hearts compared with isolated ventricles. Effects of regional ischemia, with or without increased atrial pressure, were examined in Langendorff-perfused and working heart models. Five minutes of global ischemia were associated with elevated levels of atrial natriuretic peptide (ANP) in the coronary effluent immediately and for approximately 10 min after resumption of reperfusion, resulting in a net hormone excess of 23 +/- 5 ng/g wet wt. The ventricles produced on the average 11% ANP compared with the whole heart, and their contribution of to postischemic ANP overflow was approximately proportional to their basal production. In Langendorff-perfused hearts, regional ischemia increased the concentration of ANP in the coronary effluent 51 +/- 11%, whereas the secretion rate (per minute) decreased 18 +/- 5%. In the presence of atrial distension in the working heart model, a trend for increase in ANP secretion was apparent. We conclude that global ischemia, even of brief duration, has an independent stimulatory effect on ANP release, the ischemic atrium being responsible for most of the excess. Regional ischemia, when not accompanied by atrial distention, reduces the ANP secretion rate during the ischemic period. Heart failure secondary to ischemia stimulates ANP secretion, but this response seems to be both delayed and attenuated compared with atrial stretch alone.
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36

Hildebrandt, E., and M. S. Olson. "Role of activation of myocardial branched-chain 2-oxo acid dehydrogenase complex in the regulation of leucine decarboxylation during cardiac work in vitro." Biochemical Journal 248, no. 2 (December 1, 1987): 423–28. http://dx.doi.org/10.1042/bj2480423.

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The oxidative decarboxylation of L-[1-14C]leucine was measured in the isolated perfused rat heart under both working and non-working conditions. Stimulation of decarboxylation of the labelled substrate was observed in working hearts as cardiac work was increased, and in Langendorff hearts upon increasing the coronary flow rate. The rate of L-[1-14C]leucine decarboxylation was significantly higher (P less than 0.05) in hearts working against moderate afterload pressure when compared to Langendorff hearts perfused at a matching coronary flow rate. The rate of release of 4-methyl-2-oxo[1-14C]pentanoate to the perfusate was high in Langendorff hearts, and was unaffected by changes in coronary flow. In contrast, perfusate levels of 14C-labelled 4-methyl-2-oxopentanoate decreased significantly upon the establishment of the working condition (P less than 0.05). These findings suggested an enhancement in the efficiency of the decarboxylation of the 2-oxo acid in response to cardiac work. The amount of branched-chain 2-oxo acid dehydrogenase complex present in the active form was measured in freeze-clamped hearts. Cardiac work resulted in a rapid activation of the complex (P less than 0.02) within 5 min of work when compared to control Langendorff hearts perfused at matching coronary flow rates. To a lesser extent, increasing the coronary flow rate in Langendorff-perfused hearts also led to activation of the enzyme complex. These studies suggest the following: a) L-leucine oxidation in myocardial tissue can be accelerated by exercise as it is in other tissues; b) this regulatory response can be evoked by the contractile activity of the heart itself, independent of contributions by circulating factors or nervous stimuli; and c) regulation of the activity state of the branched-chain 2-oxo acid dehydrogenase complex is involved in the mechanism by which metabolic flux through this pathway is controlled during cardiac work.
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Pelgrim, Gert Jan, Marco Das, Ulrike Haberland, Cees Slump, Astri Handayani, Sjoerd van Tuijl, Marco Stijnen, et al. "Development of anEx Vivo, Beating Heart Model for CT Myocardial Perfusion." BioMed Research International 2015 (2015): 1–8. http://dx.doi.org/10.1155/2015/412716.

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Objective. To test the feasibility of a CT-compatible,ex vivo, perfused porcine heart model for myocardial perfusion CT imaging.Methods. One porcine heart was perfused according to Langendorff. Dynamic perfusion scanning was performed with a second-generation dual source CT scanner. Circulatory parameters like blood flow, aortic pressure, and heart rate were monitored throughout the experiment. Stenosis was induced in the circumflex artery, controlled by a fractional flow reserve (FFR) pressure wire. CT-derived myocardial perfusion parameters were analysed at FFR of 1 to 0.10/0.0.Results. CT images did not show major artefacts due to interference of the model setup. The pacemaker-induced heart rhythm was generally stable at 70 beats per minute. During most of the experiment, blood flow was 0.9–1.0 L/min, and arterial pressure varied between 80 and 95 mm/Hg. Blood flow decreased and arterial pressure increased by approximately 10% after inducing a stenosis with FFR ≤ 0.50. Dynamic perfusion scanning was possible across the range of stenosis grades. Perfusion parameters of circumflex-perfused myocardial segments were affected at increasing stenosis grades.Conclusion. An adapted Langendorff porcine heart model is feasible in a CT environment. This model provides control over physiological parameters and may allow in-depth validation of quantitative CT perfusion techniques.
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Smith, L. W., S. L. Winbery, L. A. Barker, and K. H. McDonough. "Cardiac function and chronotropic sensitivity to beta-adrenergic stimulation in sepsis." American Journal of Physiology-Heart and Circulatory Physiology 251, no. 2 (August 1, 1986): H405—H412. http://dx.doi.org/10.1152/ajpheart.1986.251.2.h405.

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An organism's cardiovascular response to sepsis is at least partly dependent on hormonal and neural modulation of myocardial function. We have investigated both intrinsic myocardial performance and one aspect of myocardial sensitivity to beta-adrenergic stimulation in a model of sepsis in which animals, at the time studied, exhibited bacteremia, normal arterial blood pressure and cardiac output, elevated heart rate, and elevated plasma catecholamines. Intrinsic myocardial contractile function, studied with the isolated, perfused working heart preparation, was depressed over a range of preloads in septic animals, whereas heart rate was elevated. To determine whether hearts from septic animals could respond normally to beta-adrenergic stimulation, we studied chronotropic responses to isoproterenol in both Langendorff perfused hearts and in isolated right atria. In langendorff perfused hearts from septic animals, basal rates were significantly increased and lower concentrations of isoproterenol elicited greater increases in heart rate. In isolated right atria from septic animals, basal rates were also elevated and the EC50 for the chronotropic response to isoproterenol was significantly less than in atria from control animals. The maximal heart rate response to isoproterenol was not significantly different from control. These results indicate that in sepsis, despite apparently adequate in vivo cardiac performance, intrinsic myocardial function is depressed, but chronotropic sensitivity to beta-adrenergic stimulation is increased.
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Mischke, Karl, Markus Zarse, Christian Knackstedt, and Patrick Schauerte. "Rate Control in Atrial Fibrillation by Cooling: Effect of Temperature on Dromotropy in Perfused Rabbit Hearts." Cardiology Research and Practice 2011 (2011): 1–4. http://dx.doi.org/10.4061/2011/162984.

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Background. Cooling has emerged as a therapeutic option in critically ill patients (especially after cardiac resuscitation) and might also have a negative dromotropic effect in atrial fibrillation. We sought to determine the impact of cooling on electrophysiologic properties of Langendorff-perfused rabbit hearts.Methods and Results. In 20 isolated Langendorff-perfused rabbit hearts, the temperature of the tissue bath was changed between 17 and 42°C. With decreasing temperature, significant increases of the spontaneous sinus cycle length, decreases of the mean ventricular heart rate during atrial fibrillation, and relevant increases of atrial and ventricular refractory periods were observed (ANOVAP<.01).Conclusions. Cardiac hypothermia leads to a significant drop of mean ventricular heart rate during atrial fibrillation. Negative chronotropy and dromotropy induced by moderate cardiac hypothermia might be a feasible therapeutic approach in patients with hemodynamically relevant tachyarrhythmias in a CCU/ICU setting.
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Kennington, Erika J., William Fuller, and Michael J. Shattock. "Beta adrenergic stimulation of the Langendorff-perfused phospholemman knockout mouse heart." Journal of Molecular and Cellular Cardiology 42, no. 6 (June 2007): S27. http://dx.doi.org/10.1016/j.yjmcc.2007.03.075.

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41

Reichelt, Melissa E., Laura Willems, Benjamin A. Hack, Jason N. Peart, and John P. Headrick. "Cardiac and coronary function in the Langendorff-perfused mouse heart model." Experimental Physiology 94, no. 1 (December 22, 2008): 54–70. http://dx.doi.org/10.1113/expphysiol.2008.043554.

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42

Jelicks, L. A., and R. Gupta. "31P-NMR of high-energy phosphates in perfused rat heart during metabolic acidosis." American Journal of Physiology-Heart and Circulatory Physiology 263, no. 3 (September 1, 1992): H903—H909. http://dx.doi.org/10.1152/ajpheart.1992.263.3.h903.

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Intracellular pH (pHi), intracellular free magnesium concentration ([Mg2+]i), and high-energy phosphates in Langendorff perfused rat hearts were evaluated by 31P-nuclear magnetic resonance (NMR) during metabolic acidosis. During acidosis, cardiac pHi approached that of the perfusing solution (pH approximately 6.7) and [Mg2+]i increased. In hearts perfused with glucose as the sole carbon source, the ratio of [phosphocreatine] to [ATP] decreased during acidosis. In contrast, in hearts supplemented with pyruvate (either 2.8 or 10 mM) this ratio increased during acidosis. Oxygen consumption decreased in hearts perfused with glucose only and with pyruvate-glucose. Using the creatine kinase equilibrium constant, we find that [MgADP] is significantly decreased in pyruvate-perfused hearts but is not significantly altered in glucose-perfused hearts during metabolic acidosis. These data indicate that [MgADP] may be the regulator of cardiac oxidative phosphorylation in the presence of excess pyruvate; however, during metabolic acidosis in hearts perfused with glucose only, ATP synthesis appears limited by the availability of pyruvate via glycolysis.
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Gao, BaoXi, Yusheng Qu, Mei Fang, and Hugo Vargas. "Contractility measurements in rat heart: Comparison of isolated myocytes and Langendorff-perfused whole heart." Journal of Pharmacological and Toxicological Methods 68, no. 1 (July 2013): e27. http://dx.doi.org/10.1016/j.vascn.2013.01.102.

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44

Kuzmin, V. S., Yu V. Egorov, and L. V. Rozenshtraukh. "Electrhopysiological Effect of the Polyamine Spermine in Normoxic and Ischemic Ventricular Myocardium." Kardiologiia 59, no. 3 (April 13, 2019): 43–51. http://dx.doi.org/10.18087/cardio.2019.3.10240.

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Cytoplasmic polyamines (PA) are involved in control of many cellular functions and are well known as regulators of so called inward-rectifier potassium ion channels. Nevertheless, functional significance of extracellular PA in the heart is poorly elucidated. Aim of this study was to study effects of endogenous PA spermine in the ventricular myocardium. Effects of the extracellular spermine were investigated in isolated multicellular preparations of rabbit and rat ventricular myocardium. Langendorff-perfused isolated rat and rabbit hearts were also used. Action potential (APs) duration and pattern of excitation in ventricular myocardium were estimated using standard microelectrode technique and optical mapping. Functional refractory periods were assessed in Langendorff perfused hearts with the help of programmedelectrical stimulation of the ventricle. In this study extracellular PA spermine (0.1–5 mM) induced shortening of the APs in multicellular preparations of rat ventricular myocardium registered using sharp microelectrode technique. However, spermine caused only weak effect in preparations of ventricular myocardium from rabbit heart: highest tested concentration of spermine (5 mM) induced 4.7 % APs shortening. Similarly, 0.1–1 mM of spermine was unable to alter substantially ventricular effective refractory periods in isolated perfused rabbit hearts. In two animal species tested (rat and rabbit) 0.1–1 mM of spermine failed to affect conduction velocity and activation pattern in ventricles of isolated Langendorff-perfused hearts under normoxia. However, in the rat no-flow model of ischemia-reperfusion extracellular spermine improved conduction of excitation in ventricles. Our results allow suggesting that extracellular spermine can prevent ischemia-induced proarrhythmic changes in ventricular myocardium probably due to reduction of calcium accumulation, but this effect is significant only when PA is applied in millimolar concentrations. Also, potential anti-ischemic effect of the PA may be species specific.
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45

Headrick, John P., Jason Peart, Ben Hack, Amanda Flood, and G. Paul Matherne. "Functional properties and responses to ischaemia-reperfusion in Langendorff perfused mouse heart." Experimental Physiology 86, no. 6 (November 2001): 703–16. http://dx.doi.org/10.1111/j.1469-445x.2001.tb00035.x.

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46

Gao, Danchen, Li Zhang, Ranvir Dhillon, Ting-Ting Hong, Robin M. Shaw, and Jianhua Zhu. "Dynasore Protects Mitochondria and Improves Cardiac Lusitropy in Langendorff Perfused Mouse Heart." PLoS ONE 8, no. 4 (April 15, 2013): e60967. http://dx.doi.org/10.1371/journal.pone.0060967.

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47

REID, J., L. CARLSSON, and G. DUKER. "Monophasic action potentials recorded from the isolated langendorff-perfused guinea-pig heart." Journal of Molecular and Cellular Cardiology 17 (1985): 12. http://dx.doi.org/10.1016/s0022-2828(85)80179-6.

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48

Morgan, Eric E., Zhichuan Li, Cory Stebal, Aude Belliard, Glen Tennyson, Bijan Salari, Keith D. Garlid, and Sandrine V. Pierre. "Preconditioning by Subinotropic Doses of Ouabain in the Langendorff perfused Rabbit Heart." Journal of Cardiovascular Pharmacology 55, no. 3 (March 2010): 234–39. http://dx.doi.org/10.1097/fjc.0b013e3181ce5e14.

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49

Nygren, A., C. Kondo, R. B. Clark, and W. R. Giles. "Voltage-sensitive dye mapping in Langendorff-perfused rat hearts." American Journal of Physiology-Heart and Circulatory Physiology 284, no. 3 (March 1, 2003): H892—H902. http://dx.doi.org/10.1152/ajpheart.00648.2002.

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Abstract:
An imaging system suitable for recordings from Langendorff-perfused rat hearts using the voltage-sensitive dye 4-[β-[2-(di- n-butylamino)-6-naphthyl]vinyl]pyridinium (di-4-ANEPPS) has been developed. Conduction velocity was measured under hyper- and hypokalemic conditions, as well as at physiological and reduced temperature. Elevation of extracellular [K+] to 9 mM from 5.9 mM caused a slowing of conduction velocity from 0.66 ± 0.08 to 0.43 ± 0.07 mm/ms (35%), and reduction of the temperature to 32°C from 37°C caused a slowing from 0.64 ± 0.07 to 0.46 ± 0.05 mm/ms (28%). Ventricular activation patterns in sinus rhythm showed areas of early activation (breakthrough) in both the right and left ventricle, with breakthrough at a site near the apex of the right ventricle usually occurring first. The effects of mechanically immobilizing the preparation to reduce motion artifact were also characterized. Activation patterns in epicardially paced rhythm were insensitive to this procedure over the range of applied force tested. In sinus rhythm, however, a relatively large immobilizing force caused prolonged PQ intervals as well as altered ventricular activation patterns. The time-dependent effects of the dye on the rat heart were characterized and include 1) a transient vasodilation at the onset of dye perfusion and 2) a long-lasting prolongation of the PQ interval of the electrocardiogram, frequently resulting in brief episodes of atrioventricular block.
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50

Southworth, R., S. C. Blackburn, K. A. B. Davey, G. K. Sharland, and P. B. Garlick. "The low oxygen-carrying capacity of Krebs buffer causes a doubling in ventricular wall thickness in the isolated heart." Canadian Journal of Physiology and Pharmacology 83, no. 2 (February 1, 2005): 174–82. http://dx.doi.org/10.1139/y04-138.

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Abstract:
The buffer-perfused Langendorff heart is significantly vasodilated compared with the in vivo heart. In this study, we employed ultrasound to determine if this vasodilation translated into changes in left ventricular wall thickness (LVWT), and if this effect persisted when these hearts were switched to the "working" mode. To investigate the effects of perfusion pressure, vascular tone, and oxygen availability on cardiac dimensions, we perfused hearts (from male Wistar rats) in the Langendorff mode at 80, 60, and 40 cm H2O pressure, and infused further groups of hearts with either the vasoconstrictor endothelin-1 (ET-1) or the blood substitute FC-43. Buffer perfusion induced a doubling in diastolic LVWT compared with the same hearts in vivo (5.4 ± 0.2 mm vs. 2.6 ± 0.2 mm, p < 0.05) that was not reversed by switching hearts to "working" mode. Perfusion pressures of 60 and 40 cm H2O resulted in an increase in diastolic LVWT. ET-1 infusion caused a dose-dependent decrease in diastolic LVWT (6.6 ± 0.4 to 4.8 ± 0.4 mm at a concentration of 10–9 mol/L, p < 0.05), with a concurrent decrease in coronary flow. FC-43 decreased diastolic LVWT from 6.7 ± 0.5 to 3.8 ± 0.7 mm (p < 0.05), with coronary flow falling from 16.1 ± 0.4 to 8.1 ± 0.4 mL/min (p < 0.05). We conclude that the increased diastolic LVWT observed in buffer-perfused hearts is due to vasodilation induced by the low oxygen-carrying capacity of buffer compared with blood in vivo, and that the inotropic effect of ET-1 in the Langendorff heart may be the result of a reversal of this wall thickening. The implications of these findings are discussed.Key words: ultrasound, endothelin, ventricular wall thickness, vasodilation.
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