Key result
HOE642 reduces rigor contracture by ~49% in rat cardiomyocytes during metabolic inhibition.
Why the study?
The effect of Na+-H+ exchange and HCO3--Na+ symport inhibition on the development of rigor contracture in cardiomyocytes during metabolic inhibition was unclear.
Does HOE642 reduce the development of rigor contracture in adult rat cardiomyocytes during metabolic inhibition?
Population
Freshly isolated adult rat cardiomyocytes
Comparison
Perfusion with HOE642 (NHE inhibitor) vs without HOE642 in HCO3- or HCO3--free buffer
Design
Preclinical experimental study
Follow-up
60 min metabolic inhibition and 5 min re-energization
Authors
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HOE642 may attenuate rigor in energy-deprived rat cardiomyocytes when HCO3--dependent transport is blocked; hypothesis-generating and requires in vivo confirmation.
Does HOE642 reduce the development of rigor contracture in adult rat cardiomyocytes during metabolic inhibition?
Absolute Event Rate: 40% vs 79%
p-value: p=< 0.001
HOE642 protects against rigor contracture during energy deprivation in rat cardiomyocytes, but only when HCO3--dependent transporters are inhibited.
Ruiz‐Meana et al. (2000) studied Rigor contracture during metabolic inhibition. HOE642 vs. Without HOE642 was evaluated on Percentage of cells developing rigor during metabolic inhibition in HCO3--free conditions (p=< 0.001). In HCO3--free conditions, HOE642 reduced the percentage of rat cardiomyocytes developing rigor during metabolic inhibition from 79% to 40% (P < 0.001).
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