The acute effect of cigarette smoking on pattern visual evoked potentials.
ABSTRACT Reports of tobacco-induced electrocortical activation and decrements in ocular blood flow in the acute phase indicated that this effect is mediated via nicotine's action or neuronal systems. In this study, pattern visual evoked potentials were investigated in a group of male smokers (22 right eyes of 22 subjects) in separate real smoking and sham smoking sessions. On each session, pattern visual evoked potentials were recorded before smoking, immediately after smoking, and five minutes after smoking. Latency and amplitude values for P100 peaks were assessed and analyzed in each smoking condition for both real smoking and sham smoking sessions. Real smoking significantly decreased P100 latency values (p value related to difference between pre-smoking and immediately after smoking conditions is 0.009) and increased P100 amplitude values (p value related to difference between pre-smoking and fifth minute after smoking is 0.039). Statistically no significant difference was observed in sham smoking sessions. Our results are consistent with smoking-induced stimulant effects on pattern visual evoked potentials.
- [show abstract] [hide abstract]
ABSTRACT: SUMMARY1. Auditory and visual evoked potentials produced by five intensities of tones and light flashes were recorded in twelve young men who were habitual smokers.2. The subjects attended the laboratory on four occasions. Two recordings were made on each of the last three of these visits. They were made (i) before and after smoking, (ii) without smoking, (iii) before and after smoking after 12 h abstinence from smoking.3. Smoking was associated with increases in the amplitudes of the components V-VI, VI-VII in the visual system and a decrease in the amplitude of N2P2 in the auditory system. Abstinence from smoking produced effects in the opposite direction.4. These findings are consistent with the possibility that smoking has different and perhaps opposite effects on the visual and auditory system.5. The findings may be helpful in re-evaluating some of the apparently conflicting reports on the effects of smoking on perceptual processes.Clinical and Experimental Pharmacology and Physiology 11/1980; 7(6):609 - 615. · 2.16 Impact Factor
- [show abstract] [hide abstract]
ABSTRACT: 1. Effects of nicotine, cigarette smoke and carbon monoxide have been compared in the cat encéphale isolé preparation, exhibiting a synchronized electrocorticogram (ECoG) and behavioural sleep.2. 2 ml samples of smoke, containing approximately 7 mug nicotine (approximately 2 mug nicotine/kg for a 3 kg cat), introduced into the lungs at 30 s intervals from a smoking simulator, caused desynchronization of the ECoG and behavioural arousal.3. Effects of smoke were matched in the same experiments by intravenous injections of nicotine, 2 mug/kg every 30 s.4. The use of specific nicotine antagonists, for example mecamylamine, and filters for removing nicotine, indicated the presence in smoke of other agents capable of exerting a pharmacological response.5. Cigarette smoke contains approximately 5.0% carbon monoxide. Introduced into the lungs of cats pretreated with mecamylamine (2 mg/kg), 2 ml samples of 5% carbon monoxide caused changes in the ECoG similar to those caused by smoke.6. Effects of nicotine or smoke were not modified by pretreatment with chlorpromazine (2.0-4.0 mg/kg). Atropine (0.3 mg/kg), however, prevented the cortical activation, but not the behavioural arousal.7. 2 ml samples of smoke applied to the nostrils caused the occurrence in the olfactory bulb of a discharge or burst of "induced" waves. This discharge was sometimes accompanied by a transient period of cortical activation.8. These studies demonstrate that in cats, nicotine is the principal pharmacological constituent of tobacco smoke as far as effects on the central nervous system are concerned, although other constituents of smoke may play a contributory role.British Journal of Pharmacology 03/1970; 38(2):271-86. · 5.07 Impact Factor
- [show abstract] [hide abstract]
ABSTRACT: The effects of caffeine, nitrazepam and cigarette smoking on the contingent negative variation (CNV) in man were studied. In 13 subjects who took caffeine citrate (300 mg), the mean magnitude of the CNV was significantly increased 35–42 min after taking the drug; in 12 subjects who took nitrazepam (2.5 mg), the mean magnitude of the CNV was significantly decreased 35–42 min after drug administration. In 22 smokers, significant changes in CNV magnitude were also observed after smoking one cigarette. However, the direction of change in CNV size following smoking differed in different smokers beyond the variation expected by chance. Some smokers showed consistent increases and others consistent decreases in CNV magnitude immediately after smoking. These changes were interpreted as reflecting stimulant and depressant effects. Correlations of the percentage change in CNV magnitude with rate of nicotine intake and with degree of extraversion suggested that the rate of nicotine intake in extraverted smokers was slower and associated with a stimulant effect while in introverted smokers the rate was faster and associated with a depressant effect in terms of changes in CNV magnitude. There was a significant negative correlation in the smokers between reaction time and CNV magnitude.The amplitude of the N1-P2 component of the visual evoked response (VER) was increased after caffeine and decreased after nitrazepam but showed no consistent changes after cigarette smoking and there was no significant overall correlation between VER amplitude and CNV magnitude.RésuméLes effets de la caféïne, du nitrazepam et de l'action de fumer une cigarette sur la variation contingente négative (VCN) on été étudiés chez l'homme. Chez 13 sujets ayant absorbé du citrate de caféine (300 mg), l'amplitude moyenne des VCN a augmenté de façon significative 35 à 42 min après la prise de la drogue. Chez 12 sujets ayant pris du nitrazepam (2,5 mg) la valeur moyenne des VCN a diminué de façon significative 35 à 42 min après l'administration de la drogue. Chez 22 fumeurs, des changements significatifs des VCN ont été également observés après avoir fumé une cigarette-standard; toutefois, ces dernières variations d'amplitude des VCN ont différé selon les fumeurs au-delà de celles résultant du hazard. Certains fumeurs présentaient systématiquement de larges augmentations d'amplitude et d'autres de larges diminutions immédiatement après avoir fumé. Ces modifications ont été interpretées comme traduisant des effets respectivement stimulants et dépresseurs. Des corrélations établies entre le pourcentage de changement de la valeur moyenne des VCN et la vitesse d'inhalation de la nicotine ainsi que le degré d'extraversion du sujet suggérent que l'inhalation de la nicotine chez les fumeurs extraverti était moins rapide et associée à un effet stimulant alors que chez les fumeurs introvertis cette vitesse était plus rapide et l'inhalation associée à un effet dépressif, estimé par la valeur moyenne des VCN. Une corrélation négative significative a d'autre part été établie, pour les sujets fumeurs, entre le temps de réaction et la valeur moyenne des VCN.L'amplitude des composantes N1-P2 de la réponse visuelle évoquée a augmenté avec la caféïne et diminué avec nitrazepam mais n'a présenté aucun changement consistant après la consommation de la cigarette. Il n'existait pas de corrélation significative entre l'amplitude de la réponse évoquée et la valeur moyenne des VCN.Electroencephalography and Clinical Neurophysiology 08/1974; 37(1):59-71.