Why the study?
Does acute exposure to thyroid hormone alter sodium currents and action potentials in neonatal rat myocytes?
Does acute exposure to thyroid hormone alter sodium currents and action potentials in neonatal rat myocytes?
Thyroid hormone acutely interacts with the myocyte membrane, slowing the inactivation of sodium channels and prolonging action potential duration.
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Alerts to potential proarrhythmic effects of acute thyroid hormone in neonates; leaves open translation from rat myocytes to clinical practice.
Sodium currents and action potentials were recorded from myocytes of neonatal rats during acute exposure to thyroid hormone (5-20 nM). One to 5 minutes after addition of thyroid hormone to the bath, decay from peak Na current was slowed, with the fractional current flowing 20 ms after onset (relative to peak current) increasing from 6 +/- 5% to 17 +/- 13% (p less than 0.01, n = 12). Action potential durations were increased from 55 +/- 14 to 86 +/- 36 msec (p less than 0.05, n = 6). The effects of thyroid hormone were partially reversed by lidocaine (60 microM, n = 5), a specific blocker of a slow sub-population of Na channels. Thus thyroid hormone interacts directly with myocyte membrane, probably by slowing of inactivation of Na channels.
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Craelius et al. (1990) studied this question.
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