Key result
In a rat heart model of calcium paradox, the Na+/Ca2+ exchanger inhibitor KB-R7943 reduced contracture and improved contractile function more effectively than the calpain inhibitor MDL28170, suggesting contracture causes contractile dysfunction while calpain mediates cell death.
Population
Isolated Langendorff-perfused hearts from Sprague-Dawley male rats subjected to Ca2+ paradox, n=54.
Comparison
KB-R7943 or MDL28170 administered 1 min before… vs Control hearts perfused with normal KH solution…
Design
Preclinical, The experiments were randomly divided into 9 groups., Individuals…
Follow-up
30 min of Ca2+ repletion
Authors
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Preclinical distinction of contracture versus calpain pathways; leaves open whether NCX inhibition offers clinical benefit in calcium-mediated cardiac injury.
This preclinical study suggests that in calcium paradox-induced heart injury, contracture primarily causes contractile dysfunction while calpain activation mediates cell death.
Zhang et al. (2012) studied Calcium paradox-induced heart injury (n=54). KB-R7943 and MDL28170 vs. Vehicle/Control (Ca2+ paradox without drug) was evaluated on Left ventricular end-diastolic pressure (LVEDP), left ventricular developed pressure (LVDP), and tissue survival. In a rat heart model of calcium paradox, the Na+/Ca2+ exchanger inhibitor KB-R7943 reduced contracture and improved contractile function more effectively than the calpain inhibitor MDL28170, suggesting contracture causes contractile dysfunction while calpain mediates cell death.
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