Key result
Total ischemia (substrate deletion, hypoxia, acidosis, and high [K+]e) decreased action potential amplitude and upstroke velocity, blocking action potentials and contractions after 120 minutes.
In cultured newborn rat ventricular cardiomyocytes, individual components of ischemia produce distinct electromechanical dysfunctions compared to total combined ischemia.
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Differentiates total versus component ischemia effects in neonatal cardiomyocytes; extends mechanistic insights but leaves open clinical translation.
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 (Vmax) 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 Vmax whereas AP amplitude and rate were moderately decreased. Combining acidosis and substrate-free hypoxia also decreased Vmax 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 Vmax. Total ischemia (substrate deletion, hypoxia, acidosis, and high [K+]e) decreased AP amplitude and Vmax 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.
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Tissier et al. (2002) studied Myocardial ischemia (in vitro model). Ischemia components (hypoxia, substrate deprivation, acidosis, high [K+]e) was evaluated on Electromechanical responses (action potentials and contractions). Total ischemia (substrate deletion, hypoxia, acidosis, and high [K+]e) decreased action potential amplitude and upstroke velocity, blocking action potentials and contractions after 120 minutes.
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