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1

Feuvray, D., and M. Karmazyn. "Echangeur Na+/H+ et régulation du pH des myocytes cardiaques : de la physiologie à la physiopathologie." médecine/sciences 15, no. 3 (1999): 322. http://dx.doi.org/10.4267/10608/1341.

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2

Dolber, Paul C., Robert P. Bauman, Judith C. Rembert, and Joseph C. Greenfield. "Are interatrial band myocytes maximally hypertrophied in normal canine hearts?" American Journal of Physiology-Heart and Circulatory Physiology 275, no. 4 (1998): H1225—H1235. http://dx.doi.org/10.1152/ajpheart.1998.275.4.h1225.

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In canine right atrial hypertrophy, the cross-sectional area ( A xs) of right atrial myocytes increases, whereas the A xs of the broader interatrial band myocytes does not. In the current study, myocyte reconstructions showed that right atrial myocyte length increased in proportion to A xs in right atrial hypertrophy. On the other hand, mean interatrial band myocyte length in both normal and right atrial hypertrophy dogs was roughly inversely proportional to mean A xs, as expected if interatrial band myocyte volume was constant. Plotting mean A xs vs. myocyte length for individual interatrial
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3

Krishnan, Anirudh, Emily Chilton, Jaishankar Raman, et al. "Are Interactions between Epicardial Adipose Tissue, Cardiac Fibroblasts and Cardiac Myocytes Instrumental in Atrial Fibrosis and Atrial Fibrillation?" Cells 10, no. 9 (2021): 2501. http://dx.doi.org/10.3390/cells10092501.

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Atrial fibrillation is very common among the elderly and/or obese. While myocardial fibrosis is associated with atrial fibrillation, the exact mechanisms within atrial myocytes and surrounding non-myocytes are not fully understood. This review considers the potential roles of myocardial fibroblasts and myofibroblasts in fibrosis and modulating myocyte electrophysiology through electrotonic interactions. Coupling with (myo)fibroblasts in vitro and in silico prolonged myocyte action potential duration and caused resting depolarization; an optogenetic study has verified in vivo that fibroblasts d
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4

Zhang, Lian-Qin, Xue-Qian Zhang, Timothy I. Musch, Russell L. Moore, and Joseph Y. Cheung. "Sprint training restores normal contractility in postinfarction rat myocytes." Journal of Applied Physiology 89, no. 3 (2000): 1099–105. http://dx.doi.org/10.1152/jappl.2000.89.3.1099.

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The significance of 6–8 wk of high-intensity sprint training (HIST) on contractile abnormalities of myocytes isolated from rat hearts with prior myocardial infarction (MI) was investigated. Compared with the sedentary (Sed) condition, HIST attenuated myocyte hypertrophy observed post-MI primarily by reducing cell lengths but not cell widths. At high extracellular Ca2+ concentration (5 mM) and low pacing frequency (0.1 Hz), conditions that preferentially favored Ca2+ influx over efflux, MI-Sed myocytes shortened less than Sham-Sed myocytes did. HIST significantly improved contraction amplitudes
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5

Li, F., M. R. McNelis, K. Lustig, and A. M. Gerdes. "Hyperplasia and hypertrophy of chicken cardiac myocytes during posthatching development." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 273, no. 2 (1997): R518—R526. http://dx.doi.org/10.1152/ajpregu.1997.273.2.r518.

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For characterization of the growth pattern of cardiac myocytes during posthatching development, cardiac myocytes were enzymatically isolated from the ventricles of 1-, 15-, 29-, and 42-day-old chickens for measurement of myocyte nucleation, length, width, volume, and number, and for immunolabeling of cytoskeletal proteins. Ventricular myocyte number increased 156% from day 1 to day 42. Average cell volume increased more than 400%, and myocytes lengthened 125%, but cell width only increased 53% during this period. All myocytes were mononucleated at day 1. At day 15, 18% of myocytes became binuc
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6

Smolich, J. J., A. M. Walker, G. R. Campbell, and T. M. Adamson. "Left and right ventricular myocardial morphometry in fetal, neonatal, and adult sheep." American Journal of Physiology-Heart and Circulatory Physiology 257, no. 1 (1989): H1—H9. http://dx.doi.org/10.1152/ajpheart.1989.257.1.h1.

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This study has examined left (LV) and right ventricular (RV) myocardial morphometry in perfusion-fixed hearts of late-gestation sheep fetuses, neonatal lambs, and adult sheep. During development, myocyte size, intercapillary distance, and myocyte myofibrillar and mitochondrial volume densities increased, whereas capillary density, the myocyte-to-capillary ratio, and the myocyte matrix volume density decreased. RV myocytes were larger than LV myocytes in cross section in fetuses and 4-day-old lambs. LV and RV myocytes were of similar size in 7-day-old lambs. LV and RV myocytes were of larger in
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7

Barbera, A., G. D. Giraud, M. D. Reller, J. Maylie, M. J. Morton, and K. L. Thornburg. "Right ventricular systolic pressure load alters myocyte maturation in fetal sheep." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 279, no. 4 (2000): R1157—R1164. http://dx.doi.org/10.1152/ajpregu.2000.279.4.r1157.

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The effects of right ventricular (RV) systolic pressure (RVSP) load on fetal myocyte size and maturation were studied. Pulmonary artery (PA) pressure was increased by PA occlusion from mean 47.4 ± 5.0 (±SD) to 71 ± 13.6 mmHg ( P < 0.0001) in eight RVSP-loaded near-term fetal sheep for 10 days. The maximal pressure generated by the RV with acute PA occlusion increased after RVSP load: 78 ± 7 to 101 ± 15 mmHg ( P< 0.005). RVSP-load hearts were heavier (44.7 ± 8.4 g) than five nonloaded hearts (31.8 ± 0.2 g; P < 0.03); heart-to-body weight ratio (10.9 ± 1.1 and 6.5 ± 0.9 g/kg, respective
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8

Wang, Z., R. Mukherjee, C. F. Lam, and F. G. Spinale. "Spatial characterization of contracting cardiac myocytes by computer-assisted, video-based image processing." American Journal of Physiology-Heart and Circulatory Physiology 270, no. 2 (1996): H769—H779. http://dx.doi.org/10.1152/ajpheart.1996.270.2.h769.

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The goals of the present study were to develop and validate a computer-assisted, video-based image processing (CAVIP) system to measure time-dependent changes in isolated myocyte geometry during contraction and to use the CAVIP system to examine spatial characteristics of the myocyte during contraction in normal myocytes and in myocytes after development of dilated cardiomyopathy (DCM). Myocytes were isolated from the left ventricles of five control pigs and five pigs that developed chronic tachycardia (240 beats/min; 3 wk)-induced DCM. Isolated myocytes were stimulated and recorded using a hi
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9

Moore, R. L., T. I. Musch, R. V. Yelamarty, et al. "Chronic exercise alters contractility and morphology of isolated rat cardiac myocytes." American Journal of Physiology-Cell Physiology 264, no. 5 (1993): C1180—C1189. http://dx.doi.org/10.1152/ajpcell.1993.264.5.c1180.

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Chronic exercise training elicits positive adaptations in cardiac contractile function and ventricular dimension. The potential contribution of single myocyte morphological and functional adaptations to these global responses to training was determined in this study. Left ventricular cardiac myocytes were isolated from the hearts of sedentary control (Sed) or exercise-trained (TR) rats. Training elicited an approximately 5% increase in resting myocyte length (Sed, 121.0 +/- 2.0 vs. TR, 126.7 +/- 2.0 microns; P < 0.05), whereas resting sarcomere length and midpoint cell width were unaffected
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10

Chen, Yue-Feng, Suleman Said, Scott E. Campbell, and A. Martin Gerdes. "A method to collect isolated myocytes and whole tissue from the same heart." American Journal of Physiology-Heart and Circulatory Physiology 293, no. 3 (2007): H2004—H2006. http://dx.doi.org/10.1152/ajpheart.00479.2007.

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A technique for isolation of cardiac myocytes and collection of whole heart tissue from individual hearts of adult rats is described in this study. After excision of the apical half of the left ventricle (LV) and cauterization of the cut edge, aortas were cannulated and high-quality isolated cardiac myocytes were collected after collagenase perfusion of the basal portion. Myocyte dimensions from the basal portion of cauterized and noncauterized hearts from matching rats were identical. Additionally, myocyte dimensions from the basal and apical halves of the LV were compared with the use of who
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11

Kajstura, J., W. Cheng, R. Sarangarajan, et al. "Necrotic and apoptotic myocyte cell death in the aging heart of Fischer 344 rats." American Journal of Physiology-Heart and Circulatory Physiology 271, no. 3 (1996): H1215—H1228. http://dx.doi.org/10.1152/ajpheart.1996.271.3.h1215.

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To determine the effects of aging on myocyte cell death, Fischer 344 rats at 3, 7, 12, 16, and 24 mo of age were injected with myosin monoclonal antibody for the localization and quantification of necrotic myocyte cell death in the left ventricle, interventricular septum, and right ventricle. Conversely, the presence of DNA strand breaks in myocyte nuclei, indicative of programmed cell death, was evaluated by the terminal deoxynucleotidyl transferase assay and confirmed by DNA laddering. Myocyte necrosis, which involved nearly 1,000 myocytes in the left ventricular free wall at 3 mo, progressi
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12

Weiss, Harvey R., Gary X. Gong, Michaela Straznicka, Lin Yan, James Tse, and Peter M. Scholz. "Cyclic GMP and cyclic AMP induced changes in control and hypertrophic cardiac myocyte function interact through cyclic GMP affected cyclic-AMP phosphodiesterases." Canadian Journal of Physiology and Pharmacology 77, no. 6 (1999): 422–31. http://dx.doi.org/10.1139/y99-039.

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We tested the hypothesis that the negative functional effects of cyclic GMP (cGMP) would be greater after increasing cyclic AMP (cAMP), because of the action of cGMP-affected cAMP phosphodiesterases in cardiac myocytes and that this effect would be altered in left ventricular hypertrophy (LVH) produced by aortic valve plication. Myocyte shortening data were collected using a video edge detector, and O2 consumption was measured by O2 electrodes during stimulation (5 ms, 1 Hz, in 2 mM Ca2+) from control (n = 7) and LVH (n = 7) dog ventricular myocytes. cAMP and cGMP were determined by a competit
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13

Shiels, Holly A., and Ed White. "Temporal and spatial properties of cellular Ca2+ flux in trout ventricular myocytes." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 288, no. 6 (2005): R1756—R1766. http://dx.doi.org/10.1152/ajpregu.00510.2004.

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Confocal microscopy was used to investigate the temporal and spatial properties of Ca2+ transients and Ca2+ sparks in ventricular myocytes of the rainbow trout ( Oncorhynchus mykiss). Confocal imaging confirmed the absence of T tubules and the long (∼160 μm), thin (∼8 μm) morphology of trout myocytes. Line scan imaging of Ca2+ transients evoked by electrical stimulation in cells loaded with fluo 4 revealed spatial inhomogeneities in the temporal properties of Ca2+ transients across the width of the myocytes. The Ca2+ wavefront initiated faster, rose faster, and reached larger peak amplitudes i
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14

Brady, A. J., J. B. Warren, P. A. Poole-Wilson, T. J. Williams, and S. E. Harding. "Nitric oxide attenuates cardiac myocyte contraction." American Journal of Physiology-Heart and Circulatory Physiology 265, no. 1 (1993): H176—H182. http://dx.doi.org/10.1152/ajpheart.1993.265.1.h176.

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Cardiac muscle fibers have microvessels in close proximity, the distance from the nearest capillary being no greater than 8 microns. We performed experiments on isolated, electrically stimulated, contracting guinea pig cardiac myocytes to test whether NO from endothelium or nitrovasodilators or directly superfused in solution might affect myocyte contractility. In endothelium-myocyte coculture experiments, 10(-7) M bradykinin reduced myocyte shortening by 11 +/- 3.5%. This effect was abolished in the presence of NG-nitro-L-arginine methyl ester and was unaffected by indomethacin. Sodium nitrop
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15

Palmer, Bradley M., Anne M. Thayer, Steven M. Snyder, and Russell L. Moore. "Shortening and [Ca2+] dynamics of left ventricular myocytes isolated from exercise-trained rats." Journal of Applied Physiology 85, no. 6 (1998): 2159–68. http://dx.doi.org/10.1152/jappl.1998.85.6.2159.

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The effects of run endurance training and fura 2 loading on the contractile function and Ca2+ regulation of rat left ventricular myocytes were examined. In myocytes not loaded with fura 2, the maximal extent of myocyte shortening was reduced with training under our pacing conditions [0.5 Hz at 2.0 and 0.75 mM external Ca2+ concentration ([Ca2+]o)], although training had no effect on the temporal characteristics. The “light” loading of myocytes with fura 2 markedly suppressed (∼50%) maximal shortening in the sedentary and trained groups, although the temporal characteristics of myocyte shorteni
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16

Coker, Mytsi L., Melissa A. Doscher, Chadwick V. Thomas, Zorina S. Galis, and Francis G. Spinale. "Matrix metalloproteinase synthesis and expression in isolated LV myocyte preparations." American Journal of Physiology-Heart and Circulatory Physiology 277, no. 2 (1999): H777—H787. http://dx.doi.org/10.1152/ajpheart.1999.277.2.h777.

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In several cardiac disease states, alterations in myocyte and extracellular matrix (ECM) structure occur with left ventricular (LV) remodeling and are associated with changes in matrix metalloproteinase (MMP) activity. Although nonmyocyte cell types have been implicated as sites for synthesis and expression of MMPs within the ECM, whether the LV myocyte itself expresses specific types and active forms of MMPs remains unknown. Accordingly, isolated Ca2+-tolerant LV porcine myocytes (105 cells/ml) in which selective disaggregation and resuspension was performed (13 independent experiments) were
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17

Li, P., C. Park, R. Micheletti, et al. "Myocyte performance during evolution of myocardial infarction in rats: effects of propionyl-L-carnitine." American Journal of Physiology-Heart and Circulatory Physiology 268, no. 4 (1995): H1702—H1713. http://dx.doi.org/10.1152/ajpheart.1995.268.4.h1702.

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To determine whether alterations in the mechanical properties and calcium transients of myocytes are important factors in the evolution of the postinfarcted heart, these physiological parameters were measured in the viable muscle cells of the left ventricle 6 h, 2–3 days, 1 wk, and 1 mo after coronary artery occlusion and the documentation of left ventricular failure. In addition, the effects of propionyl-L-carnitine (PLC) on shortening properties and calcium dynamics of single myocytes were established to demonstrate whether the potential increase in ATP generation by this intervention improv
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18

Shen, Jian-Bing, Robin Shutt, Mariela Agosto, Achilles Pappano, and Bruce T. Liang. "Reversal of cardiac myocyte dysfunction as a unique mechanism of rescue by P2X4 receptors in cardiomyopathy." American Journal of Physiology-Heart and Circulatory Physiology 296, no. 4 (2009): H1089—H1095. http://dx.doi.org/10.1152/ajpheart.01316.2008.

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Binary cardiac transgenic (Tg) overexpression of P2X4 receptors (P2X4R) improved the survival of the cardiomyopathic calsequestrin (CSQ) mice. Here we studied the mechanism of rescue using binary P2X4R/CSQ Tg and CSQ Tg mice as models. Cellular and intact heart properties were determined by simultaneous sarcomere shortening (SS) and Ca2+ transients in vitro and echocardiography in vivo. Similar to a delay in death, binary mice exhibited a slowed heart failure progression with a greater left ventricular (LV) fractional shortening (FS) and thickness and a concomitant lesser degree of LV dilatati
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19

O'Connell, T. D., J. E. Berry, A. K. Jarvis, M. J. Somerman, and R. U. Simpson. "1,25-Dihydroxyvitamin D3 regulation of cardiac myocyte proliferation and hypertrophy." American Journal of Physiology-Heart and Circulatory Physiology 272, no. 4 (1997): H1751—H1758. http://dx.doi.org/10.1152/ajpheart.1997.272.4.h1751.

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We previously demonstrated that 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] inhibits myocyte maturation (T. D. O'Connell, D. A. Giacherio, A. K. Jarvis, and R. U. Simpson. Endocrinology 136: 482-488, 1995). To define further the role of 1,25(OH)2D3 in regulating myocardial development, we examined the effects of 1,25(OH)2D3 on proliferation and growth of primary cultures of ventricular myocytes isolated from neonatal rat hearts. When neonatal myocytes were grown in a serum-supplemented medium, cell number approximately doubled, and treating these myocytes with 1,25(OH)2D3 inhibited their proliferat
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20

Samuel, J. L., F. Marotte, C. Delcayre, and L. Rappaport. "Microtubule reorganization is related to rate of heart myocyte hypertrophy in rat." American Journal of Physiology-Heart and Circulatory Physiology 251, no. 6 (1986): H1118—H1125. http://dx.doi.org/10.1152/ajpheart.1986.251.6.h1118.

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Since stimulation of heart hypertrophy by pressure overload was previously shown to be accompanied by a densification of microtubule network in rat heart myocytes, we verified that similar process occurred during postnatal growth in euthyroid rats and in hypothyroid rats whose growth was stimulated by 4 micrograms/day L-thyroxine (T4). For this purpose, tubulin, the constituent protein of microtubules, was immunolabeled in myocytes isolated at various times after birth. Myocyte hypertrophy was evaluated by myocyte size, the number of nuclei per cell and isomyosin expression. In hypothyroid rat
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21

Korte, F. Steven, Todd J. Herron, Michael J. Rovetto, and Kerry S. McDonald. "Power output is linearly related to MyHC content in rat skinned myocytes and isolated working hearts." American Journal of Physiology-Heart and Circulatory Physiology 289, no. 2 (2005): H801—H812. http://dx.doi.org/10.1152/ajpheart.01227.2004.

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The amount of work the heart can perform during ejection is governed by the inherent contractile properties of individual myocytes. One way to alter contractile properties is to alter contractile proteins such as myosin heavy chain (MyHC), which is known to demonstrate isoform plasticity in response to disease states. The purpose of this study was to examine myocyte functionality over the complete range of MyHC expression in heart, from 100% α-MyHC to 100% β-MyHC, using euthyroid and hypothyroid rats. Peak power output in skinned cardiac myocytes decreased as a nearly linear function of β-MyHC
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22

Zhang, Xue-Qian, Timothy I. Musch, Robert Zelis, and Joseph Y. Cheung. "Effects of impaired Ca2+homeostasis on contraction in postinfarction myocytes." Journal of Applied Physiology 86, no. 3 (1999): 943–50. http://dx.doi.org/10.1152/jappl.1999.86.3.943.

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The significance of altered Ca2+ influx and efflux pathways on contractile abnormalities of myocytes isolated from rat hearts 3 wk after myocardial infarction (MI) was investigated by varying extracellular Ca2+concentration ([Ca2+]o, 0.6–5.0 mM) and pacing frequency (0.1–5.0 Hz). Myocytes isolated from 3-wk MI hearts were significantly longer than those from sham-treated (Sham) hearts (125 ± 1 vs. 114 ± 1 μm, P < 0.0001). At high [Ca2+]oand low pacing frequency, conditions that preferentially favored Ca2+ influx over efflux, Sham myocytes shortened to a greater extent than 3-wk MI myocytes.
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23

Jonker, Sonnet S., J. Job Faber, Debra F. Anderson, Kent L. Thornburg, Samantha Louey, and George D. Giraud. "Sequential growth of fetal sheep cardiac myocytes in response to simultaneous arterial and venous hypertension." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 292, no. 2 (2007): R913—R919. http://dx.doi.org/10.1152/ajpregu.00484.2006.

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While the fetal heart grows by myocyte enlargement and proliferation, myocytes lose their capacity for proliferation in the perinatal period after terminal differentiation. The relationship between myocyte enlargement, proliferation, and terminal differentiation has not been studied under conditions of combined arterial and venous hypertension, as occurs in some clinical conditions. We hypothesize that fetal arterial and venous hypertension initially leads to cardiomyocyte proliferation, followed by myocyte enlargement. Two groups of fetal sheep received intravascular plasma infusions for 4 or
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24

Xu, Hu, Yongwei Yao, Zhaoliang Su та ін. "Endogenous HMGB1 contributes to ischemia-reperfusion-induced myocardial apoptosis by potentiating the effect of TNF-α/JNK". American Journal of Physiology-Heart and Circulatory Physiology 300, № 3 (2011): H913—H921. http://dx.doi.org/10.1152/ajpheart.00703.2010.

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High-mobility group box 1 (HMGB1) is a nuclear protein that has been implicated in the myocardial inflammation and injury induced by ischemia-reperfusion (I/R). The purpose of the present study was to assess the role of HMGB1 in myocardial apoptosis induced by I/R. In vivo, myocardial I/R induced an increase in myocardial HMGB1 expression and apoptosis. Inhibition of HMGB1 (A-box) ameliorated the I/R-induced myocardial apoptosis. In vitro, isolated cardiac myocytes were challenged with anoxia-reoxygenation (A/R; in vitro correlate to I/R). A/R-challenged myocytes also generated HMGB1 and under
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25

Wang, Wei, Hongyu Zhang, Hui Gao та ін. "β1-Adrenergic receptor activation induces mouse cardiac myocyte death through both L-type calcium channel-dependent and -independent pathways". American Journal of Physiology-Heart and Circulatory Physiology 299, № 2 (2010): H322—H331. http://dx.doi.org/10.1152/ajpheart.00392.2010.

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Cardiac diseases persistently increase the contractility demands of cardiac myocytes, which require activation of the sympathetic nervous system and subsequent increases in myocyte Ca2+ transients. Persistent exposure to sympathetic and/or Ca2+ stress is associated with myocyte death. This study examined the respective roles of persistent β-adrenergic receptor (β-AR) agonist exposure and high Ca2+ concentration in myocyte death. Ventricular myocytes (VMs) were isolated from transgenic (TG) mice with cardiac-specific and inducible expression of the β2a-subunit of the L-type Ca2+ channel (LTCC).
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26

Liang, B. T. "Direct preconditioning of cardiac ventricular myocytes via adenosine A1 receptor and KATP channel." American Journal of Physiology-Heart and Circulatory Physiology 271, no. 5 (1996): H1769—H1777. http://dx.doi.org/10.1152/ajpheart.1996.271.5.h1769.

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Both adenosine receptor and ATP-sensitive K (KATP) channel mediate the protective effect of ischemic preconditioning in the intact heart. The objective of the present study was to determine the role of adenosine receptor and KATP channel as well as their interaction in simulating and mediating preconditioning of the cardiac myocyte. Cardiac ventricular myocytes cultured from chick embryos 14 days in ovo were developed as a myocyte model of preconditioning. Myocytes were preconditioned by exposing them to 5-min hypoxia, termed preconditioning hypoxia, before a second 90-min hypoxia. Preconditio
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27

Lefroy, D. C., T. Crake, F. Del Monte, et al. "Angiotensin II and contraction of isolated myocytes from human, guinea pig, and infarcted rat hearts." American Journal of Physiology-Heart and Circulatory Physiology 270, no. 6 (1996): H2060—H2069. http://dx.doi.org/10.1152/ajpheart.1996.270.6.h2060.

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The effects of angiotensin II on myocardial contractility were assessed in isolated cardiac myocyte preparations, using video microscopy with a computerized edge-detection system. Angiotensin II (1 nM-10 microM) did not affect the contraction of rat (n = 10), guinea pig (n = 11), or human ventricular myocytes (n = 8) or of human atrial myocytes (n = 12). Isoproterenol or raised extracellular calcium increased the contraction amplitude of the cardiac myocytes to a maximum of between 150 and 560% above basal, and there were corresponding increases in the velocities of contraction and relaxation.
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28

Kumar, Anand, Rupinder Brar, Peter Wang, et al. "Role of nitric oxide and cGMP in human septic serum-induced depression of cardiac myocyte contractility." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 276, no. 1 (1999): R265—R276. http://dx.doi.org/10.1152/ajpregu.1999.276.1.r265.

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Previous studies have demonstrated the existence of a circulating myocardial depressant substance during human septic shock. We have recently identified this substance as a synergistic combination of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β). This study utilized an in vitro cardiac myocyte assay to evaluate the potential mechanistic role of nitric oxide (NO) and cGMP in depression of myocyte contractility induced by TNF-α, IL-1β, TNF-α + IL-1β (at low concentrations), and human septic shock serum (HSS). TNF-α, IL-1β, TNF-α + IL-1β, and each of 5 sera from patients with acute s
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29

Rook, M. B., A. C. van Ginneken, B. de Jonge, A. el Aoumari, D. Gros, and H. J. Jongsma. "Differences in gap junction channels between cardiac myocytes, fibroblasts, and heterologous pairs." American Journal of Physiology-Cell Physiology 263, no. 5 (1992): C959—C977. http://dx.doi.org/10.1152/ajpcell.1992.263.5.c959.

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Cultures of neonatal rat heart cells contain predominantly myocytes and fibroblastic cells. Most abundant are groups of synchronously contracting myocytes, which are electrically well coupled through large gap junctions. Cardiac fibroblasts may be electrically coupled to each other and to adjacent myocytes, be it with low intercellular conductances. Nevertheless, synchronously beating myocytes interconnected via a fibroblast were present, demonstrating that nonexcitable cardiac cells are capable of passive impulse conduction. In fibroblast pairs as well as in myocyte-fibroblast cell pairs, no
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30

Huang, Ming-He, Paul R. Knight, and Joseph L. Izzo. "Ca2+-induced Ca2+ release involved in positive inotropic effect mediated by CGRP in ventricular myocytes." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 276, no. 1 (1999): R259—R264. http://dx.doi.org/10.1152/ajpregu.1999.276.1.r259.

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To investigate the effects and mechanisms of calcitonin gene-related peptide (CGRP) on ventricular contractility, ventricular myocytes isolated from adult rat and mouse hearts were exposed to CGRP. Myocyte contractility was assessed by a video edge motion detector, and the intracellular [Ca2+] transients were measured by a spectroflurophotometer in fura 2-loaded myocytes. CGRP exerted a potent concentration-dependent (10 pM–10 nM, EC50 = 44.1 pM) positive inotropism on rat ventricular myocytes. CGRP (1 nM) increased cell shortening during contraction by 140 ± 40% above baselines and increased
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31

Hershman, Kenneth M., та Edwin S. Levitan. "RPTPμ and protein tyrosine phosphorylation regulate K+channel mRNA expression in adult cardiac myocytes". American Journal of Physiology-Cell Physiology 278, № 2 (2000): C397—C403. http://dx.doi.org/10.1152/ajpcell.2000.278.2.c397.

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Previously, we reported that cell-cell contact regulates K+channel mRNA expression in cultured adult rat cardiac myocytes. Here we show that exposing cardiac myocytes to tyrosine kinase inhibitors (genistein, tyrphostin A25), but not inactive analogs, prevents downregulation of Kv1.5 mRNA and upregulation of Kv4.2 mRNA normally observed when they are cultured under low-density conditions. Furthermore, cardiac myocytes cocultured with cells that endogenously (Mv 1 Lu) or heterologously (Chinese hamster ovary cells) express the receptor-type protein tyrosine phosphatase μ (RPTPμ) display Kv1.5 m
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32

Coker, Mytsi L., Jennifer R. Jolly, Cassandra Joffs, et al. "Matrix metalloproteinase expression and activity in isolated myocytes after neurohormonal stimulation." American Journal of Physiology-Heart and Circulatory Physiology 281, no. 2 (2001): H543—H551. http://dx.doi.org/10.1152/ajpheart.2001.281.2.h543.

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Changes in myocardial matrix metalloproteinase (MMP) activity and expression have been associated with left ventricular (LV) remodeling. A recent study demonstrated that LV myocytes synthesize and release MMPs, which suggests that LV myocytes may participate in myocardial remodeling. However, extracellular stimuli that may potentially influence LV myocyte MMP production remains to be defined. In the present study MMP activity and expression were measured in porcine LV myocyte preparations (105 total cells; n = 6) following incubation (6 h) with endothelin-1 (ET-1;50 pM), angiotensin II (ANG II
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33

Chen, Hua, Xueyin N. Huang, Alexandre F. R. Stewart, and Jorge L. Sepulveda. "Gene expression changes associated with fibronectin-induced cardiac myocyte hypertrophy." Physiological Genomics 18, no. 3 (2004): 273–83. http://dx.doi.org/10.1152/physiolgenomics.00104.2004.

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Fibronectin (FN) is an extracellular matrix protein that binds to integrin receptors and couples cardiac myocytes to the basal lamina. Cardiac FN expression is elevated in models of pressure overload, and FN causes cultured cardiac myocytes to hypertrophy by a mechanism that has not been characterized in detail. In this study, we analyzed the gene expression changes induced by FN in purified rat neonatal ventricular myocytes using the Affymetrix RAE230A microarray, to understand how FN affects gene expression in cardiac myocytes and to separate the effects contributed by cardiac nonmyocytes in
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34

Pitts, Kelly R., and Christopher F. Toombs. "Coverslip hypoxia: a novel method for studying cardiac myocyte hypoxia and ischemia in vitro." American Journal of Physiology-Heart and Circulatory Physiology 287, no. 4 (2004): H1801—H1812. http://dx.doi.org/10.1152/ajpheart.00232.2004.

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In vitro experimental models designed to study the effects of hypoxia and ischemia typically employ oxygen-depleted media and/or hypoxic chambers. These approaches, however, allow for metabolites to diffuse away into a large volume and may not replicate the high local concentrations that occur in ischemic myocardium in vivo. We describe herein a novel and simple method for creating regional hypoxic and ischemic conditions in neonatal rat cardiac myocyte monolayers. This method consists of creating a localized diffusion barrier by placing a glass coverslip over a portion of the monolayer. The c
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35

Haddad, J., M. L. Decker, L. C. Hsieh, M. Lesch, A. M. Samarel, and R. S. Decker. "Attachment and maintenance of adult rabbit cardiac myocytes in primary cell culture." American Journal of Physiology-Cell Physiology 255, no. 1 (1988): C19—C27. http://dx.doi.org/10.1152/ajpcell.1988.255.1.c19.

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The present observations demonstrate that quiescent calcium-tolerant adult rabbit cardiac myocytes can be isolated by collagenase-hyaluronidase perfusion and maintained in primary culture for at least 2 wk. Culturing large numbers of myocytes requires that the freshly isolated cells be attached to a suitable substratum such as laminin, type IV collagen, or fetal bovine serum. The cultured myocytes retain their rod-like morphology for approximately 7 days before gradually spreading into a flattened conformation by 14 days. During the 1st wk of culture, contaminating interstitial cells rapidly p
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36

Ren, J., and A. J. Davidoff. "Diabetes rapidly induces contractile dysfunctions in isolated ventricular myocytes." American Journal of Physiology-Heart and Circulatory Physiology 272, no. 1 (1997): H148—H158. http://dx.doi.org/10.1152/ajpheart.1997.272.1.h148.

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To determine whether diabetes-induced cardiac dysfunction is due to contractile dysfunction at the single-cell level, mechanical properties and Ca2+ transients were evaluated in ventricular myocytes isolated from diabetic rats. Rats were made diabetic by injection with streptozotocin and killed either 4-6 days or 8 wk after treatment. Shortening and relengthening (twitch) properties were evaluated in isolated myocytes with a high-resolution (120-Hz) video-based edge-detection system during electrical stimulation between 0.1 and 5 Hz. A separate cohort of myocytes was loaded with fura 2 to asse
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37

Hershman, Kenneth M., and Edwin S. Levitan. "Cell-cell contact between adult rat cardiac myocytes regulates Kv1.5 and Kv4.2 K+channel mRNA expression." American Journal of Physiology-Cell Physiology 275, no. 6 (1998): C1473—C1480. http://dx.doi.org/10.1152/ajpcell.1998.275.6.c1473.

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Regulation of voltage-gated K+channel genes represents an important mechanism for modulating cardiac excitability. Here we demonstrate that expression of two K+channel mRNAs is reciprocally controlled by cell-cell interactions between adult cardiac myocytes. It is shown that culturing acutely dissociated rat ventricular myocytes for 3 h results in a dramatic downregulation of Kv1.5 mRNA and a modest upregulation of Kv4.2 mRNA. These effects are specific, because similar changes are not detected with other channel mRNAs. Increasing myocyte density promotes maintenance of Kv1.5 gene expression,
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38

Ahuja, Preeti, Patima Sdek, and W. Robb MacLellan. "Cardiac Myocyte Cell Cycle Control in Development, Disease, and Regeneration." Physiological Reviews 87, no. 2 (2007): 521–44. http://dx.doi.org/10.1152/physrev.00032.2006.

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Cardiac myocytes rapidly proliferate during fetal life but exit the cell cycle soon after birth in mammals. Although the extent to which adult cardiac myocytes are capable of cell cycle reentry is controversial and species-specific differences may exist, it appears that for the vast majority of adult cardiac myocytes the predominant form of growth postnatally is an increase in cell size (hypertrophy) not number. Unfortunately, this limits the ability of the heart to restore function after any significant injury. Interest in novel regenerative therapies has led to the accumulation of much infor
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39

Berger, H. J., S. K. Prasad, A. J. Davidoff, et al. "Continual electric field stimulation preserves contractile function of adult ventricular myocytes in primary culture." American Journal of Physiology-Heart and Circulatory Physiology 266, no. 1 (1994): H341—H349. http://dx.doi.org/10.1152/ajpheart.1994.266.1.h341.

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To model with greater fidelity the electromechanical function of freshly isolated heart muscle cells in primary culture, we describe a technique for the continual electrical stimulation of adult myocytes at physiological frequencies for several days. A reusable plastic cover was constructed to fit standard, disposable 175-cm2 tissue culture flasks and to hold parallel graphite electrodes along the long axis of each flask, which treated a uniform electric field that resulted in a capture efficiency of ventricular myocytes of 75–80%. Computer-controlled amplifiers were designed to be capable of
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40

Zhang, Qihang, Michael Lazar, Bruno Molino, et al. "Reduction in interaction between cGMP and cAMP in dog ventricular myocytes with hypertrophic failure." American Journal of Physiology-Heart and Circulatory Physiology 289, no. 3 (2005): H1251—H1257. http://dx.doi.org/10.1152/ajpheart.01234.2003.

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Baseline function and signal transduction are depressed in hearts with hypertrophic failure. We tested the hypothesis that the effects of cGMP and its interaction with cAMP would be reduced in cardiac myocytes from hypertrophic failing hearts. Ventricular myocytes were isolated from control dogs, dogs with aortic valve stenosis hypertrophy, and dogs with pacing hypertrophic failure. Myocyte function was measured using a video edge detector. Cell contraction data were obtained at baseline, with 8-bromo-cGMP (10−7, 10−6, and 10−5 M), with erythro-9-(2-hydroxy-3-nonyl)adenine [EHNA; a cAMP phosph
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41

Myrmel, Truls, Terje K. Steigen, Erling Bjordal, and Terje S. Larsen. "Phosphatidylcholine metabolism in hypoxic and phospholipase C exposed rat ventricular myocytes." Canadian Journal of Physiology and Pharmacology 71, no. 10-11 (1993): 840–47. http://dx.doi.org/10.1139/y93-126.

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A phospholipase C specific for choline and ethanolamine acyl and plasmalogen glycerophospholipids (PC-PLC) has been described in myocardial tissue. In the present study we investigated whether an endogenous PC-PLC is activated in hypoxic, substrate-free incubations of rat ventricular myocytes. The phosphatidylcholine pool of the myocytes was prelabelled with [14C]choline during a 4-h preincubation (pulse) period. The myocytes were subsequently washed and incubated for another 2 h (chase period) in normoxic, hypoxic, or hypoxic buffer supplemented with PC-PLC from Bacillus cereus. We hypothesiz
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42

Miyazaki, Koji, Satoshi Komatsu, Mitsuo Ikebe, Richard A. Fenton та James G. Dobson. "Protein kinase Cε and the antiadrenergic action of adenosine in rat ventricular myocytes". American Journal of Physiology-Heart and Circulatory Physiology 287, № 4 (2004): H1721—H1729. http://dx.doi.org/10.1152/ajpheart.00224.2004.

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Adenosine-induced antiadrenergic effects in the heart are mediated by adenosine A1 receptors (A1R). The role of PKCε in the antiadrenergic action of adenosine was explored with adult rat ventricular myocytes in which PKCε was overexpressed. Myocytes were transfected with a pEGFP-N1 vector in the presence or absence of a PKCε construct and compared with normal myocytes. The extent of myocyte shortening elicited by electrical stimulation of quiescent normal and transfected myocytes was recorded with video imaging. PKCε was found localized primarily in transverse tubules. The A1R agonist chlorocy
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43

Su, Jun, Peter M. Scholz, James Tse, and Harvey R. Weiss. "Effects of cyclic GMP and its protein kinase on the contraction of ventricular myocytes from hearts after cardiopulmonary arrest." Canadian Journal of Physiology and Pharmacology 82, no. 11 (2004): 986–92. http://dx.doi.org/10.1139/y04-105.

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Hearts undergoing cardiopulmonary arrest and resuscitation have depressed function and may have changes in signal transduction. We hypothesized that the cyclic GMP (cGMP) signaling pathway would be altered in the post-resuscitation heart. This was studied in ventricular myocytes from 7 anesthetized open-chest rabbits. Cardiopulmonary arrest was achieved for 10 min through ventricular fibrillation and respirator shutdown. After cardiopulmonary arrest, respiration was resumed, the heart was defibrillated, and the heart recovered for 15 min. Seven additional rabbits served as controls. Myocyte fu
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44

Hinken, Aaron C., F. Steven Korte, and Kerry S. McDonald. "Porcine cardiac myocyte power output is increased after chronic exercise training." Journal of Applied Physiology 101, no. 1 (2006): 40–46. http://dx.doi.org/10.1152/japplphysiol.00798.2005.

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Chronic exercise training increases the functional capacity of the heart, perhaps by increased myocyte contractile function, as has been observed in rodent exercise models. We examined whether cardiac myocyte function is enhanced after chronic exercise training in Yucatan miniature swine, whose heart characteristics are similar to humans. Animals were designated as either sedentary (Sed), i.e., cage confined, or exercise trained (Ex), i.e., underwent 16–20 wk of progressive treadmill training. Exercise training efficacy was shown with significantly increased heart weight-to-body weight ratios,
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45

Liu, Lijun, Xiaochen Zhao, Sandrine V. Pierre, and Amir Askari. "Association of PI3K-Akt signaling pathway with digitalis-induced hypertrophy of cardiac myocytes." American Journal of Physiology-Cell Physiology 293, no. 5 (2007): C1489—C1497. http://dx.doi.org/10.1152/ajpcell.00158.2007.

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Our previous studies on cardiac myocytes showed that positive inotropic concentrations of the digitalis drug ouabain activated signaling pathways linked to Na+-K+-ATPase through Src and epidermal growth factor receptor (EGFR) and led to myocyte hypertrophy. In view of the known involvement of phosphatidylinositol 3-kinase (PI3K)-Akt pathways in cardiac hypertrophy, the aim of the present study was to determine whether these pathways are also linked to cardiac Na+-K+-ATPase and, if so, to assess their role in ouabain-induced myocyte growth. In a dose- and time-dependent manner, ouabain activate
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46

Kim, Song-Jung, Maha Abdellatif, Sharat Koul, and George J. Crystal. "Chronic treatment with insulin-like growth factor I enhances myocyte contraction by upregulation of Akt-SERCA2a signaling pathway." American Journal of Physiology-Heart and Circulatory Physiology 295, no. 1 (2008): H130—H135. http://dx.doi.org/10.1152/ajpheart.00298.2008.

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Chronic treatment with insulin-like growth factor I (IGF-I) improves contractile function in congestive heart failure and ischemic cardiomyopathy. The present study investigated the effect of chronic treatment with IGF-I on intrinsic myocyte function and the role of the phosphatidylinositol (PI)3-kinase-Akt-sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA)2a signaling cascade in these responses. Myocytes were isolated from 23 adult rats and cultured with and without IGF-I (10−6 M). After 48 h of treatment, myocyte function was evaluated. IGF-I increased contractile function (percent contraction
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47

Henry, R. A., S. Y. Boyce, T. Kurz, and R. A. Wolf. "Stimulation and binding of myocardial phospholipase C by phosphatidic acid." American Journal of Physiology-Cell Physiology 269, no. 2 (1995): C349—C358. http://dx.doi.org/10.1152/ajpcell.1995.269.2.c349.

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Exposure of adult ventricular myocytes to exogenous natural phosphatidic acid results in the production of inositol phosphates by unknown mechanism(s). We characterized stimulation of myocytic phosphoinositide-specific phospholipase C (PLC) by synthetic dioleoyl phosphatidic acid (PA) as a potential mechanism for modulation of inositol phosphate production. Our data demonstrate that exogenous PA, at 10(-8)-10(-5) M, caused a concentration-dependent increase in inositol 1,4,5-trisphosphate in adult rabbit ventricular myocytes. PA also caused a concentration-dependent increase in in vitro activi
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48

L'Ecuyer, Thomas, Sanjeev Sanjeev, Ronald Thomas, et al. "DNA damage is an early event in doxorubicin-induced cardiac myocyte death." American Journal of Physiology-Heart and Circulatory Physiology 291, no. 3 (2006): H1273—H1280. http://dx.doi.org/10.1152/ajpheart.00738.2005.

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Anthracyclines are antitumor agents the main clinical limitation of which is cardiac toxicity. The mechanism of this cardiotoxicity is thought to be related to generation of oxidative stress, causing lethal injury to cardiac myocytes. Although protein and lipid oxidation have been documented in anthracycline-treated cardiac myocytes, DNA damage has not been directly demonstrated. This study was undertaken to determine whether anthracyclines induce cardiac myocyte DNA damage and whether this damage is linked to a signaling pathway culminating in cell death. H9c2 cardiac myocytes were treated wi
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49

Kawai, Kentaro, Tomoko Kawai, Justin T. Sambol, et al. "Cellular mechanisms of burn-related changes in contractility and its prevention by mesenteric lymph ligation." American Journal of Physiology-Heart and Circulatory Physiology 292, no. 5 (2007): H2475—H2484. http://dx.doi.org/10.1152/ajpheart.01164.2006.

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Major burn injury results in impairment of left ventricular (LV) contractile function. There is strong evidence to support the involvement of gut-derived factor(s) transported in mesenteric lymph in the development of burn-related contractile dysfunction; i.e., mesenteric lymph duct ligation (LDL) prevents burn-related contractile depression. However, the cellular mechanisms for altered myocardial contractility of postburn hearts are largely unknown, and the cellular basis for the salutary effects of LDL on cardiac function have not been investigated. We examined contractility, Ca2+ transients
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50

Hinken, Aaron C., та Kerry S. McDonald. "β-Myosin heavy chain myocytes are more resistant to changes in power output induced by ischemic conditions". American Journal of Physiology-Heart and Circulatory Physiology 290, № 2 (2006): H869—H877. http://dx.doi.org/10.1152/ajpheart.00221.2005.

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During ischemia intracellular concentrations of Pi and H+ increase. Also, changes in myosin heavy chain (MHC) isoform toward β-MHC have been reported after ischemia and infarction associated with coronary artery disease. The purpose of this study was to investigate the effects of myoplasmic changes of Pi and H+ on the loaded shortening velocity and power output of cardiac myocytes expressing either α- or β-MHC. Skinned cardiac myocyte preparations were obtained from adult male Sprague-Dawley rats (control or treated with 5- n-propyl-2-thiouracil to induce β-MHC) and mounted between a force tra
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