期刊
ANESTHESIA AND ANALGESIA
卷 92, 期 5, 页码 1192-1198出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/00000539-200105000-00021
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Propofol decreases muscle tone in the absence of neuromuscular blocking drugs. This effect probably cannot be attributed solely to central nervous depression. We studied the effects of propofol on heterologously expressed skeletal muscle sodium channels. Our hypothesis was that the decrease in muscle tone may partly be attributed to an interaction of propofol with sarcolemmal sodium channels. Cells were voltage clamped and whole-cell sodium inward currents were recorded in the absence and presence of propofol. When depolarizing pulses to 0 mV were started from a holding potential close to the normal resting potential of muscle (-70 mV), or when a 2.5s prepulse inducing slow inactivation was applied before the test pulse at -100 mV, a significant reduction in the peak current amplitude was achieved by 10 and 5 muM propofol, respectively (P < 0.001). Half-maximum blocking concentrations with these protocols were 23 and 22 M. Blocking potency increased at depolarized membrane potentials with the fraction of inactivated channels; the estimated dissociation constant K, from the inactivated state was 4.6 muM. These results suggest that propofol significantly blocks sarcolemmal sodium channels at clinically relevant concentrations while maintaining potentials close to the physiological resting potential.
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