Key result
Halothane reversibly inhibited the sodium-calcium exchange current in neonatal rabbit ventricular myocytes, decreasing it by 49% at 1.5% concentration and by 66% at 3% concentration.
Halothane reversibly inhibits the sodium-calcium exchange current in neonatal myocardium, which could theoretically ameliorate reperfusion injury.
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No clinical implications for neonatal anesthesia; hypothesis-generating for halothane in myocardial reperfusion injury.
Neonatal myocardium is distinctly more sensitive to extracellular calcium levels than is mature myocardium. This has been ascribed to the poorly developed sarcoplasmic reticulum of neonatal myocardium. Recent evidence has suggested that there is an increased dependence of neonatal myocardium on the sodium-calcium exchange current, and that sodium-calcium exchange may be a major source of calcium influx in neonatal myocardial cells. We determined the effect of halothane on the sodium-calcium exchange current on single neonatal (2- to 5-day-old) rabbit ventricular myocytes by means of the whole cell voltage clamp. Lower (1.5%) halothane decreased sodium-calcium exchange current by 49%, from 29 +/- 3 to 15 +/- 6 pA. Higher (3%) halothane decreased this current by 66%, from 50 +/- 9 to 17 +/- 9 pA. Thus halothane has a reversible inhibition of sodium-calcium exchange current in neonatal myocardium. Inhibition of sodium-calcium exchange current would be expected to have a magnified effect on contractility in neonatal as opposed to adult myocardium, and could theoretically ameliorate reperfusion injury due to influx of calcium via the sodium-calcium exchanger.
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Baum et al. (1994) studied Neonatal myocardium. Halothane vs. Baseline was evaluated on Sodium-calcium exchange current. Halothane reversibly inhibited the sodium-calcium exchange current in neonatal rabbit ventricular myocytes, decreasing it by 49% at 1.5% concentration and by 66% at 3% concentration.
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