Rapid physiologic effects of nicotine in humans and selective blockade of behavioral effects by mecamylamine.

Je, Henninfield; Miyasato, K; Re, Johnson; Dr, Jasinski

doi:10.1037/e469622004-001

Cited by 8 publications

(10 citation statements)

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“…Previous research has shown doserelated blockade of nicotine effects in humans (Henningfield et al 1983c;. The increased smoking observed in the present study is analogous to the results of animal studies, which have shown increases in opioid self-administration in animals pretreated with the opioid antagonist naloxone on an acute basis (Goldberg et al 1969;Woods et al 1975;Griffiths et al 1981).…”

Section: Discussionsupporting

confidence: 80%

“…Mecamylamine would appear to be a viable canditate for such a treatment approach to cigarette smoking. Mecamylamine pretreatment attenuates the effects of IV nicotine (Henningfield et al 1983c). Furthermore, a preliminary study of IV nicotine self-administration by a human volunteer showed that preference for nicotine, as compared to placebo, was reduced by pretreatment with mecamylamine .…”

Section: Discussionmentioning

confidence: 99%

“…review by Henningfield and Goldberg 1983). One study with human volunteers confirmed that mecamylamine blocks certain subjective and physiological responses to nicotine (Henningfield et al 1983c). Another study examined the effect of mecamylamine pretreatment on cigarette smoking in human volunteers (Stolerman et al 1973).…”

mentioning

confidence: 99%

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Effects of mecamylamine on human cigarette smoking and subjective ratings

1986

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Multiple measures of cigarette smoking, subjective effect and physiological effect were collected during 90-min test sessions in normal volunteers. Before sessions subjects received oral doses of mecamylamine (2.5, 5.0, 10, 20 mg) or placebo. Each dose and placebo was given three times in a randomized block sequence. Mecamylamine increased several measures of cigarette smoking, including number of cigarettes, number of puffs per cigarette, and expired air carbon monoxide level. Mecamylamine also produced modest, dose-related decreases in standing blood pressure and increases in standing heart rate. The subjective effects produced by mecamylamine were not characteristic of those of psychoactive drugs. Mecamylamine appears to have increased cigarette smoking by decreasing the effective dose level of nicotine available from cigarette smoking.

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Section: Discussionsupporting

confidence: 80%

Section: Discussionmentioning

confidence: 99%

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Effects of mecamylamine on human cigarette smoking and subjective ratings

1986

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“…However, there is no consensus on the effects of smoking tobacco cigarettes on the human pupil. Increases of pupil diameter have been reported either after inhalations in smokers who had abstained from smoking for 2 h [9] or dose-dependently after intravenous nicotine in smokers who had abstained from smoking for about 6 h [10] . Decreases in pupil diameter have also been reported in smokers asked to abstain from smoking for at least 8 h [13] or following 12 h of abstinence prior to the experiment [11] .…”

Section: Discussionmentioning

confidence: 99%

“…Nicotine markedly infl uences ANS function, affecting various physiological parameters such as heart rate, blood pressure, the electroencephalogram, and the patellar and Hoffman refl exes [6][7][8] . Surprisingly, there are few studies on the effects of nicotine or tobacco smoking in the human pupil, and results differ greatly [9][10][11][12][13] .…”

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confidence: 99%

Effects of Tobacco Smoking on the Kinetics of the Pupillary Light Reflex: A Comparison between Smokers and Non-Smokers

Morte¹,

Benito²,

Grasa³

et al. 2005

Neuropsychobiology

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Background: The time course of the pupillary light reflex (PLR) is determined by the successive activation of parasympathetic and sympathetic innervations of the iris, latency and amplitude reflecting parasympathetic activity and recovery time showing mainly sympathetic activity. Objective: To determine the effects of tobacco cigarette smoking on the PLR in smokers after an abstinence period of at least 12 h. Methods: Ten smokers (mean 15.7 cigarettes/day) and 10 non-smokers participated in a randomised, non-intervention controlled, cross-over study that included a parallel control group. Smokers underwent two sessions with a time interval between 3 and 8 days; two recordings were taken at each session, separated by 20 min: session 1, without smoking, and session 2, smoking 3 cigarettes within a 30-min period. Non-smokers underwent one session; two recordings were taken separated by 20 min. At each recording, in both groups, PLR was elicited with four light flashes of increasing luminance. Results: The relationship between PLR parameters and light intensity was linear in each subject. The slope of the regression line for relative amplitude increase versus intensity was significantly flatter in abstinent smokers than in non-smokers (p = 0.033); the slope returned significantly after smoking (p = 0.043). No other significant effects were obtained. Conclusions: Kinetic parameters of PLR provide a sensitive pharmacological test to detect cholinergic neurotransmission manipulation effects, as they seem to detect changes in moderate smokers after 12 h of abstinence, and their reversal on return to smoking. These results suggest an enhancement in the suppression of the parasympathetic oculomotor reflex arc rather than a facilitation of the sympathetic drive to the iris.

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