The effects of smoking on electrocortical arousal in coronary prone (type A) and non-coronary prone (type B) subjects.

Abstract

Twenty-nine Type A subjects, (greater than 75 percentile on the Jenkins Activity Survey) and 28 Type Bs (less than 25 percentile of the survey) were asked to smoke one cigarette (1.0 mg nicotine, 16 mg tar, 14 mg CO) using a standardized smoking procedure. Significant differences between baseline and smoking conditions were noted in the distribution of electrocortical activity for both groups. In addition, a shift from EEG low frequency high amplitude (alpha) events to high frequency low amplitude activity (beta) was noted for the As, while the Bs showed enhanced very low frequency high amplitude (theta) activity. A striking parallel was observed between the behavioral predisposition of the subject (A/B) and the possible function of the underlying neurological structure mediating the observed EEG changes. It is suggested that the electrocortical changes observed for the As during smoking are mediated by reticular (ARS I) arousal. Enhanced reticular activity may coincide with an increased rate of information processing, attention and vigilance. On the other hand, the electrocortical changes observed for the Type Bs may represent enhanced activity of the limbic system (ARS II) with could coincide with stimulation of the reward/pleasure centers. Smoking may produce a pattern of neurophysiological arousal which parallels the behavioral tempo of the individual. Possible differences in in vivo regulation of nicotine cholinergic binding sites are also discussed.