The Effects of Metabolic Inhibitors on Cultured Rat Heart Cells

Orloff, Kenneth G.; McCarl, Richard L.

doi:10.1083/jcb.57.1.225

Cited by 9 publications

(3 citation statements)

References 17 publications

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“…The present study demonstrated, for the first time, that the MEA system could be used to study metabolic inhibition using cardiomyocytes derived from the HL-1 cell line, and the results revealed that PIN may have advantages over SDZ under acute metabolically compromised conditions. In previous studies, metabolic inhibitors and KCOs have already been shown to reduce the beat frequency of cardiomyocytes (Hasin and Barry 1984, Orloff and McCarl 1973, Yeung et al 2007. The close correlation between the beat frequency and exAP amplitude suggests that similar concentrations of drugs are needed in order to reduce these parameters to the same extent, and that these observed physiological changes are intricately linked.…”

Section: Discussionmentioning

confidence: 84%

“…In previous studies, metabolic inhibitors and KCOs have already been shown to reduce the beat frequency of cardiomyocytes (Hasin and Barry 1984, Orloff and McCarl 1973, Yeung et al 2007. The close correlation between the beat frequency and exAP amplitude suggests that similar concentrations of drugs are needed in order to reduce these parameters to the same extent, and that these observed physiological changes are intricately linked.…”

Section: Discussionmentioning

confidence: 84%

“…Sodium azide (NaN 3 ) or 2-deoxyglucose (2-DG) was used to elicit two different acute metabolically inhibited conditions. NaN 3 is an inhibitor of mitochondrial oxidative phosphorylation (Inomata and Tanaka 2003), whereas 2-DG is an inhibitor of glycolysis (Orloff and McCarl 1973).…”

Section: Solutions and Reagentsmentioning

confidence: 99%

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The use of microelectrode array (MEA) to study the protective effects of potassium channel openers on metabolically compromised HL-1 cardiomyocytes

Law

Yeung

Hofmann³

et al. 2009

Physiol. Meas.

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The microelectrode array (MEA) was used to evaluate the cardioprotective effects of adenosine triphosphate sensitive potassium (K(ATP)) channel activation using potassium channel openers (KCOs) on HL-1 cardiomyocytes subjected to acute chemically induced metabolic inhibition. Beat frequency and extracellular action potential (exAP) amplitude were measured in the presence of metabolic inhibitors (sodium azide (NaN(3)) or 2-deoxyglucose (2-DG)) or KCOs (pinacidil (PIN, a cyanoguanidine derivative, activates sarcolemmal K(ATP) channels) or SDZ PCO400 (SDZ, a benzopyran derivative, activates mitochondrial K(ATP) channels)). The protective effects of these KCOs on metabolically inhibited HL-1 cells were subsequently investigated. Signal shapes indicated that NaN(3) and 2-DG reduced the rate of the sodium (Na(+)) influx signal as reflected by a reduction in beat frequency. PIN and SDZ appeared to reduce both rate of depolarization and extent of the Na(+) influx signals. Pre-treating cardiomyocytes with PIN (0.1 mM), but not SDZ, prevented the reduction of beat frequency associated with NaN(3)- or 2-DG-induced metabolic inhibition. The exAP amplitude was not affected by either KCO. The cardioprotective effect of PIN relative to SDZ may be due to the opening of different K(ATP) channels. This metabolic inhibition model on the MEA may provide a stable platform for the study of cardiac pathophysiology in the future.

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Section: Discussionmentioning

confidence: 84%

Section: Discussionmentioning

confidence: 84%

See 1 more Smart Citation

The use of microelectrode array (MEA) to study the protective effects of potassium channel openers on metabolically compromised HL-1 cardiomyocytes

Law

Yeung

Hofmann³

et al. 2009

Physiol. Meas.

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Energy Metabolism and Transport in Neonatal Heart Cells in Culture

Pinson¹,

Huizer²

1988

Developments in Cardiovascular Medicine

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Fatty acids and phospholipids of adult and newborn rat hearts and of cultured, beating neonatal rat myocardial cells

Rogers¹

1974

Lipids

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Fatty acids and phospholipids of adult and newborn rat hearts and of cultured, neonatal rat heart cells were determined by gas liquid and thin layer chromatographies. In adult heart, the proportion of linoleic acid was higher and that of palmitic acid lower than in newborn hearts or in cultured cells. The relative amounts of linoleic and arachidonic acids in adult heart were affected by the source and amount of dietary fat. In heart cells, after 3 days in culture, the proportion of arachidonic acid resembled that in the newborn and adult rat hearts but showed a gradual and significant decline with age. The gradual shift in fatty acid composition as the cells aged in culture was attributed to outgrowth of mesenchymal cells (fibroblasts and endothelioid cells) characterized by a low relative proportion of arachidonic acid. The amounts of phospholipids in heart cells after 3 days in culture differed from those in the newborn or adult rat hearts. Phosphatidylethanolamine was highest in adult heart (34% of lipid phosphorus) and lowest in cells (26%); lecithin was higher in newborn heart (43%) than in adult heart (37%) or in cells (39%), while sphingomyelin was higher in cells (8%) than in newborn (5%) or adult heart (3%). Phospholipid levels in cultured heart cells were unrelated to those of serum in the growth medium. The absence of a significant change in phospholipid composition after continued incubation of the heart cell cultures for periods up to 3 weeks reflected the major structural role of these lipid components in cell membranes.

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The Effects of Metabolic Inhibitors on Cultured Rat Heart Cells

Cited by 9 publications

References 17 publications

The use of microelectrode array (MEA) to study the protective effects of potassium channel openers on metabolically compromised HL-1 cardiomyocytes

The use of microelectrode array (MEA) to study the protective effects of potassium channel openers on metabolically compromised HL-1 cardiomyocytes

Energy Metabolism and Transport in Neonatal Heart Cells in Culture

Fatty acids and phospholipids of adult and newborn rat hearts and of cultured, beating neonatal rat myocardial cells

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