Key result
R(+)-bupivacaine induced a significantly larger inhibition of the cardiac sodium current during long depolarizations compared to S(-)-bupivacaine (72% vs 58%, P<0.01) in guinea pig myocytes.
Why the study?
Does S(-)-bupivacaine exhibit less potent block of cardiac sodium channels compared to R(+)-bupivacaine in isolated guinea pig ventricular myocytes?
Population
Isolated guinea pig ventricular myocytes
Comparison
10 mumol/L R(+)-bupivacaine and S(-)-bupivacaine vs Control and direct comparison between enantiomers
Design
Preclinical
Authors
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Supports further preclinical exploration of enantiomer-specific cardiotoxicity; leaves open human translation and practice change.
Does S(-)-bupivacaine exhibit less potent block of cardiac sodium channels compared to R(+)-bupivacaine in isolated guinea pig ventricular myocytes?
Absolute Event Rate: 72% vs 58%
p-value: p=< .01
R(+)-bupivacaine blocks the inactivated state of cardiac sodium channels more potently and faster than S(-)-bupivacaine, providing a mechanistic basis for the reduced cardiac toxicity of the S(-)-enantiomer.
Valenzuela et al. (1995) studied this question. R(+)-bupivacaine vs. S(-)-bupivacaine was evaluated on Inhibition of cardiac sodium current (INa) during long depolarizations (p=< .01). R(+)-bupivacaine induced a significantly larger inhibition of the cardiac sodium current during long depolarizations compared to S(-)-bupivacaine (72% vs 58%, P<0.01) in guinea pig myocytes.
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