Abstract

The depressant effect of general anaesthetics such as halothane and ethanol in the nervous system is well documented. It is also clear that high doses of ethanol depress the maximum velocity of the upstroke, the total amplitude and duration of the action potential, and the force of contraction of cardiac muscle. Also, many agents with a local anaesthetic effect on nerves have a class 1 antiarrhythmic action on myocardium, which is associated with a negative inotropic effect. In both tissues, such agents reduce the maximum rate of depolarization as a consequence of inhibition of the fast sodium channel. The resting and rate-dependent depression of this channel has been carefully characterized, and the sodium-channel blockade by these agents has been modelled in the modulated receptor hypothesis (Hondeghem and Katzung 1984) and the guarded receptor hypothesis (Starmer and Grant 1985).

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