ABSTRACT
Ethanol and cocaine have opposite pharmacologic effects. Ethanol is a central nervous system depressant. Low amounts of alcoholic beverages increase sociability, while higher levels impair cognitive ability and depress sensorimotor function. The acute in vivo cardiovascular response to moderate levels of ethanol intake involves sympathetic activation, probably due to peripheral vasodilatation, and usually results in an increase in heart rate and maintained or elevated cardiac output [3]. Cardiac arrhythmia seems to be more prevalent. Delbridge et al.’s recent findings report identifying ethanol at 0.05%(v/v) as a modulator of cardiac contractility. Kinetic analyses indicate that the mechanism of action involves disturbance of sarcoplasmic reticulum function and this may contribute to arrhythmogenic vulnerability – especially in an in vivo context of heightened compensatory sympathetic drive [3]. The study goes on to state that the stabilizing effects of ethanol on intracellular Ca2+ stores may be the cellular basis for the arrhythmogenic response to acute ethanol exposure – a response which is more evident in the normal than in the myopathic myocardium [3].
