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Specific electromechanical responses of cardiomyocytes to individual and combined components of ischemia

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The main factors of myocardial ischemia are hypoxia, substrate deprivation, acidosis, and high extracellular potassium concentration ([K+]e), but the influence of each of these factors has not yet been evaluated in a cardiomyocyte (CM) culture system. Electromechanical responses to the individual and combined components of ischemia were studied in CM cultured from newborn rat ventricles. Action potentials (APs) were recorded using glass microelectrodes and contractions were monitored photometrically. Glucose-free hypoxia initially reduced AP duration, amplitude, and rate and altered excitation–contraction coupling, but AP upstroke velocity (max) remained unaffected. Early afterdepolarizations appeared, leading to bursts of high-rate triggered impulses before the complete arrest of electromechanical activity after 120 min. Acidosis reduced max, whereas AP amplitude and rate were moderately decreased. Combining acidosis and substrate-free hypoxia also decreased max but attenuated the effects of substrate-free hypoxia on APs and delayed the cessation of the electrical activity (180 min). Raising [K+]e reduced the maximal diastolic potential and max. Total ischemia (substrate deletion, hypoxia, acidosis, and high [K+]e) decreased AP amplitude and max without changing AP duration. Moreover, delayed afterdepolarizations appeared, initiating triggered activity. Ultimately, 120 min of total ischemia blocked APs and contractions. To conclude, glucose-free hypoxia caused severe functional defects, acidosis delayed the changes induced by substrate-free hypoxia, and total ischemia induced specific dysfunctions differing from those caused by the former conditions. Heart-cell cultures thus represent a valuable tool to scrutinize the individual and combined components of ischemia on CMs. Key words: cell culture, cardiomyocytes, membrane potential, cell contraction, ischemia.

Les principales causes de l'ischémie myocardique sont l'hypoxie, l'absence de substrat, l'acidose et l'élévation de la concentration du potassium extracellulaire ([K+]e), mais l'influence de chacun de ces facteurs n'a pas encore été évaluée dans un même modèle de cardiomyocytes (CM) en culture. Les effets électromécaniques des composantes individuelles et combinées de l'ischémie ont été étudiés dans des cultures de CM de ventricules de rat nouveau-nés. Les potentiels d'action (PA) ont été dérivés avec des microélectrodes de verre et les contractions ont été enregistrées photoélectriquement. Initialement, l'hypoxie sans glucose réduit l'amplitude, la durée et la fréquence des PA et altère le couplage excitation–contraction, mais la vitesse de dépolarisation des PA (max) est inchangée. Des postdépolarisations apparaissent, déterminant des salves d'impulsions à haute fréquence, avant l'arrêt de l'activité électromécanique après 120 min. L'acidose ralentie max, tandis que l'amplitude et la fréquence des PA sont modérément diminuées. L'association de l'acidose à l'hypoxie sans substrat diminue aussi max mais atténue les effets de l'hypoxie sans substrat sur les PA et retarde la disparition de l'activité électrique (180 min). L'augmentation de [K+]e réduit le potentiel maximal diastolique et max. L'ischémie totale (absence de substrat, hypoxie, acidose et [K+]e élevé) diminue l'amplitude des PA et max sans changement de durée des PA.

Keywords: cardiomyocytes; cell contraction; cell culture; contraction cellulaire; culture de cellules; ischemia; ischémie; membrane potential; potentiel action

Document Type: Research Article

Publication date: 2002-12-01

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