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Biomedical subjects

O F Pomerleau

Publications and source records attributed to O F Pomerleau.

At least 19 recordsLinked to original sources
PubMed1992

Nicotine and the central nervous system: biobehavioral effects of cigarette smoking.

The effects of nicotine, like those of other drugs with potential for abuse and dependence, are centrally mediated. The impact of nicotine on the central nervous system is neuroregulatory in nature, affecting biochemical and physiological functions in a manner that reinforces drug-taking behavior. Dose-dependent neurotransmitter and neuroendocrine effects occur as plasma nicotine levels rise when a cigarette is smoked. Circulating levels of norepinephrine and epinephrine increase, and the bioavailability of dopamine is altered as well. Among the neuroendocrine effects are release of arginine vasopressin, beta-endorphin, adrenocorticotropic hormone, and cortisol. Notably, several of these neurochemicals are psychoactive and/or known to modulate behavior. Thus, affective states or cognitive demands may be favorably modified (at least temporarily) by nicotine intake. When nicotine is inhaled, the neuroregulatory effects just described are immediately available and the reinforcing effects of the drug are maximized. On the other hand, nicotine gum and most other nicotine replacement vehicles in current use have a slower onset of action, resulting in less reinforcement value. Recent data suggest that smoking cessation rates may be optimized by tailoring the dose of nicotine replacement (for example, 2 or 5 mg of nicotine gum) to the individual degree of nicotine dependence. In view of the dynamic interactions between the neuroregulatory effects of nicotine and a host of environmental conditions, nicotine replacement therapy is best carried out in combination with behavior modification techniques.

Behavior↗
PubMed1992

Euphoriant effects of nicotine in smokers.

Two studies were conducted to replicate and extend previous demonstrations of smoking-induced, dose-related reports of euphoria, and to confirm this relationship using measures of plasma nicotine. In experiment 1, overnight-deprived subjects, in three different sessions, smoked ultralow-, high-nicotine, and usual-brand cigarettes. In experiment 2, ultralow-, medium-, and high-nicotine cigarettes were used, and plasma nicotine was measured. In both studies, subjects were asked to depress a button during euphoric sensations. Number of sensations for the ultralow-nicotine cigarette was significantly lower than for the high-nicotine cigarette in the first study, and than for both the medium- and high-nicotine conditions in the second; a significant linear trend was observed for number of sensations as a function of plasma nicotine level in the second study. For the high-nicotine cigarette, 19 of 22 subjects experienced at least one sensation (mean around three), starting around 2.5 min after lighting up. Together, these studies support the existence of a dose-response relationship for nicotine-induced euphoric sensations; suggest that they are more pronounced following overnight abstinence than following minimal deprivation, and in more dependent smokers; and characterize in detail the temporal features of these sensations.

Adult↗
PubMed1992

Controlled dosing of nicotine via an Intranasal Nicotine Aerosol Delivery Device (INADD).

The present report describes an Intranasal Nicotine Aerosol Delivery Device (INADD) employing an artist's airbrush as aerosolizer and precise, electromechanical control of spray duration. It was designed for the administration of controlled doses of nicotine in a laboratory setting and has been used successfully in over 30 smokers and nonsmokers of both genders. In the present study, nicotine was administered to 12 male smokers at three different doses (0.05 mg, 1.00 mg, and 2.00 mg), and at the same dose (1 mg) on three different occasions. The low dose produced a minimal change in plasma nicotine, while the high dose produced a peak increment of around 16 ng/ml. The medium dose reliably produced a peak increment of around 8-9 ng/ml on all three occasions. Nicotine in plasma showed a sharp rise followed by a slower decline, mimicking the pattern associated with cigarette smoking. Physiological and biochemical responses showed significant dose-response relationships. Subjective reports suggested that aerosol dosing was somewhat aversive, but it is unclear whether this effect is intrinsic to the method or due to other factors. The device described in this report answers the need for a safe and easy means of controlling nicotine dose. Moreover, since nicotine administration via aerosol is novel for both smokers and non-smokers, minimizing the contributions of behavioral tolerance and habituation to the dosing vehicle, it lends itself to the comparison of the pharmacological effects of nicotine between experienced and naive subjects.

Administration, Intranasal↗
PubMed1992

Cotinine in an ultrafiltrate of saliva.

BACKGROUND: We have developed a device for the simplified collection of a prepurified sample of saliva in the mouth. METHOD: The device is based on the principle of an osmotic pump and accumulated about 1.2 ml of an ultrafiltrate of saliva within 8 min. We have investigated the ultrafiltrate for its utility as a biological medium in the evaluation of cigarette smoking status. RESULTS: (a) In 58 matched samples from 13 subjects, the correlation coefficient for the cotinine concentration in the saliva and the ultrafiltrate was 0.95; (b) in matched plasma and ultrafiltrate samples from 27 smokers, the correlation coefficient for the cotinine concentrations was 0.96 with plasma containing 1.2 times the ultrafiltrate mean; (c) in a nonsmoker, elevated cotinine levels could be detected in the ultrafiltrate more than 24 hr after smoking 2 cigarettes, and the pattern of rise and decrease reflected that in whole saliva; and (d) in a habitual smoker; the mean cotinine concentration in the ultrafiltrate was 157 ng/ml (SD +/- 25.7 ng/ml) during a period of smoking 15 cigarettes per day and dropped to a mean of 47 ng/ml (SD +/- 10.5) when smoking was reduced to 5 cigarettes per day; after cessation of smoking, detectable concentrations of cotinine persisted for up to 5 days. CONCLUSION: The device facilitated the aesthetic, noninvasive collection of a biological sample useful in the validation of smoking status.

Adult↗
PubMed1992

The effects of menstrual phase and nicotine abstinence on nicotine intake and on biochemical and subjective measures in women smokers: a preliminary report.

Nicotine intake, menstrual and smoking withdrawal symptomatology, and baseline cortisol and MHPG were assessed in nine women smokers under conditions of ad lib smoking and overnight abstinence in three menstrual phases (early follicular, mid-to-late follicular, and late luteal). A trend towards higher nicotine intake (p < 0.10) was observed in the mid-to-late follicular phase. Although menstrual symptomatology was not significantly elevated during the smoking abstinence condition overall, abstinence appeared to prevent the normal reduction in symptomatology during the mid-to-late follicular phase that occurred under conditions of ad lib smoking. Menstrual and withdrawal symptoms were highly correlated, and both were most pronounced during the late luteal/abstinence condition. The smoking-specific item "craving" reflected this pattern, though in attenuated form, suggesting that the observed exacerbation of withdrawal symptomatology was not simply due to generalized dysphoria, as queried in both instruments. MHPG was significantly elevated in the late luteal phase, whereas cortisol was significantly higher during ad lib smoking than during abstinence and tended to be highest in the mid-to-late follicular phase. Further investigation will be needed to determine the functional significance of these findings for understanding and treating smoking in women.

Adult↗
PubMed1992

Relationship of Tridimensional Personality Questionnaire scores and smoking variables in female and male smokers.

The Tridimensional Personality Questionnaire (TPQ) was developed by Cloninger (1986) to measure heritable variation in three patterns of response to environmental stimuli: novelty seeking, harm avoidance, and reward dependence. Cloninger (1987) used the TPQ to identify two types of alcoholism: Type 1 (low novelty seeking, high harm avoidance and reward dependence; both male and female) and Type 2 (high novelty seeking, low harm avoidance and reward dependence; predominantly male). To determine whether characteristic patterns exist in smokers, we administered the TPQ to 119 female and 121 male smokers, along with the Fagerstrom Tolerance Questionnaire (FTQ, a measure of nicotine dependence), the Russell Motives for Smoking Questionnaire (RMSQ), and the Spielberger State-Trait Anxiety Inventory (STAI/trait). Compared with a normative sample, our sample exhibited elevated scores on the Novelty-Seeking scale; female smokers were somewhat overrepresented in the highest quartile of the Harm-Avoidance scale; both genders tended to be clustered in the lower quartiles of the Sentimentality-Attachment-Dependence subscale of the Reward-Dependence scale and in the highest quartile of the Persistence subscale. Female smokers showed a significant positive association between Harm Avoidance and FTQ scores, and Harm Avoidance was positively correlated with several RMSQ factors (including Additive smoking) in both genders. These findings suggest that the likelihood of becoming a smoker may be a function of novelty seeking and reward dependence, whereas degree of dependence or addiction once the habit is entrained may be linked to harm avoidance. Our observations establish the potential utility of the TPQ as a tool for examining environmental and heritable variation in smoking behavior and may contribute to improved strategies for prevention and treatment of smoking.

Adult↗
PubMed1992

National working conference on smoking and body weight. Task Force 1: Mechanisms relevant to the relations between cigarette smoking and body weight.

Careful, comprehensive, and empirical observations provide the building blocks of the sciences, whereas theory and mechanisms provide the "cement" to hold the blocks together and serve as blueprints to direct future building. This article resulted from several days of discussion regarding theories that may underlie the relation between cigarette smoking and body weight and the relation between smoking cessation and body weight. The working group composed of social and biological scientists who addressed this assignment considered what is already known within the smoking and body weight literature and also considered relevant findings from studies of smoking or body weight regulation that have not directly addressed the interaction of these variables. As expected, we were successful at listing some of what is not known and what is worth knowing. We also tried to identify fruitful possibilities for research activity that might clarify mechanisms of action and eventually lead to theoretical development. Because we do not believe that the present state of our deliberations merits the label of theories, we decided, instead, to report the summary of these deliberations as potential mechanisms relevant to the relation between smoking and body weight.

Adult↗
PubMed1991

Sweet taste preference in women smokers: comparison with nonsmokers and effects of menstrual phase and nicotine abstinence.

Cigarette smokers weigh less than comparably aged nonsmokers, and many gain weight following cessation. Though some evidence suggests that nicotine reduces food intake, with a selective effect on sweet-tasting foods, the issue remains unresolved. In the current study, 64 women (20 smokers, 26 never-smokers, and 18 ex-smokers) were tested for sweet taste preference; 9 of these smokers were studied under conditions of both ad lib smoking and overnight abstinence, in three hormonally verified menstrual phases. 1) Although no overall differences were detected in taste preference among the three groups, significantly more smokers than nonsmokers preferred the higher sucrose concentrations. 2) No significant differences due to menstrual phase were observed. 3) Although preference ratings did not differ significantly between overnight abstinence and ad lib smoking, a subset of smokers who preferred higher sucrose concentrations rated their preference for the solutions significantly higher during the ad lib smoking sessions. Our findings suggest that smoking and nonsmoking women differ with respect to taste preference and that, at least in a subset of female smokers, preference is affected by nicotine abstinence/acute dosing.

Adolescent↗
PubMed1991

Effects of fluoxetine on weight gain and food intake in smokers who reduce nicotine intake.

The effect of fluoxetine hydrochloride, a 5-HT uptake inhibitor (60 mg/day PO), in preventing weight gain associated with nicotine reduction was investigated in participants in a double-blind, placebo-controlled smoking-cessation trial. A lunch of cheese pizza and chocolate bars was offered, and caloric intake was monitored. The analysis focused on subjects (placebo: n = 11; fluoxetine: n = 10) who succeeded in reaching cotinine levels of less than 50% of their starting cotinine levels (signifying a stringent reduction in nicotine intake) and who participated in pre- and post-nicotine reduction lunch sessions 70 days apart. Subjects on placebo gained significantly more weight (mean +/- SEM = +3.3 +/- 0.7 kg) than subjects on fluoxetine (-0.6 +/- 1.2 kg). In fluoxetine-treated subjects, weight gain/loss was strongly correlated with initial body mass index, with higher BMI being associated with greater decreases in weight. A trend towards decreased caloric intake in the fluoxetine group was observed; the change in total calories at lunch was significantly correlated with weight change, an association accounted for principally by change in pizza intake. We conclude that fluoxetine treatment effectively prevents the weight gain that accompanies nicotine reduction and that this phenomenon is mediated, at least in part, by diminished caloric intake.

Adult↗
PubMed1991

Biobehavioral research on nicotine use in women.

More American women are taking up smoking than men and fewer are quitting; if current trends continue, rates for women will surpass those for men by the mid-1990's. But ironically, much of what is known about the biobehavioural aspects of smoking is based on research using male subjects. The present paper reviews evidence suggesting that: (1) women may differ from men with regard to nicotine intake and/or effects; (2) nicotine intake and effects may be influenced by menstrual cycle phase; (3) oral contraceptive use and estrogen replacement therapy may affect intake and effects of nicotine; (4) the effects of chronic nicotine use on female reproductive endocrinology may have implications for the reinforcement of smoking; and (5) pharmacological agents used to treat smoking may have different effects in women than in men. Guidelines and suggestions are presented by future biobehavioural research in women, including standardization of assessment procedures, attention to the use of appropriate controls, and use of pharmacological probes.

Arousal↗
PubMed1991

Research on stress and smoking: progress and problems.

Despite evidence that smoking behaviour increases in the context of stress, there has yet to be a clear-cut demonstration that nicotine intake is similarly enhanced. Although nicotine intake has been shown to reduce reported anxiety in the context of stress, the controlling conditions (type of stressor, intensity, temporal relationships, etc.) need further exploration. Recent findings involving nicotine's effects on the hypophyseal-adrenal axis provide a new perspective on these issues, in that increased nicotine intake during exposure to a stressor may represent, at least in part, behavioral compensation for diminished sensitivity to nicotine brought about by nicotine-stimulated corticosteroid release. Corticosteroids may decrease central nervous system excitability in a way that could account for anxiety reduction; on the other hand, anxiety reduction may be an epiphenomenon with respect to the reinforcement of smoking behaviour. The integration of behavioural, physiological, and biochemical research exemplified by the above approach should lead to a better understanding of stress and smoking.

Animals↗
PubMed1990

Behavioural studies in humans: anxiety, stress and smoking.

Numerous observers have reported that smokers smoke more under stressful conditions. The most frequent explanation is that nicotine reduces anxiety, an intervening variable identified as a negative reinforcer for smoking behaviour. The conditions under which anxiety reduction occurs in response to smoking, however, have not been well defined, nor are underlying mechanisms well understood. There are several possible explanations, including Schachter's theory based on stress-induced changes in urinary pH and the hypothesis of endogenous opioid involvement. The work of Collins and his associates in animals has shown that genetic variations in corticosteroid responsiveness to nicotine are associated with differences in sensitivity to nicotine. Research in our laboratory has extended to humans Collins' findings that sensitivity to nicotine is inversely related to corticosteroid activity. We also found that the combination of a psychological stressor and smoking produced additive effects on cortisol release in humans. These findings suggest a novel way of explaining the interaction between smoking and stress, in that increased nicotine intake in the context of stress may in part reflect behavioural compensation for diminished sensitivity to nicotine when corticosteroid activity is enhanced by the stressor.

Anxiety↗
PubMed1990

Dexamethasone attenuation of the cortisol response to nicotine in smokers.

The effect of corticosteroids upon the cortisol response to nicotine from smoking was investigated in five heavy smokers. Corticosteroid activity was manipulated by administering dexamethasone, a synthetic glucocorticoid (1 mg orally, 14 h before), in a double-blind, placebo-controlled procedure. Testing took place in the middle of the day and involved the smoking of two high-nicotine (2.87 mg) research cigarettes over a 15-min period. The dexamethasone condition was characterized by a pronounced suppression of baseline plasma cortisol, as expected, and by a significant dampening of the cortisol response to nicotine, indicating diminished sensitivity to nicotine under conditions of enhanced corticosteroid activity.

Adult↗
PubMed1990

Cortisol response to a psychological stressor and/or nicotine.

The effects of a psychological stressor and nicotine upon corticosteroid release were investigated using a full factorial, repeated-measures design in eight moderate smokers. Sessions involved the presentation of either competitive mental arithmetic or reading aloud and either smoking a usual cigarette or sham smoking. Self-reported anxiety increased after exposure to competitive mental arithmetic, confirming the stressfulness of the procedure. Cortisol levels increased significantly in response to psychological stress and showed a trend towards a significant elevation over time in response to nicotine self-administration. The two manipulations in combination produced additive effects upon plasma cortisol. These findings underscore the usefulness of the corticosteroid response as a marker of the impact of different procedures and suggest that it may provide an indicator for exploring the mechanisms by which nicotine-stress interactions are mediated. Systematic research that varies temporal and other parameters involving nicotine and various stressors will be needed to resolve inconsistencies in the literature on smoking and anxiety in the context of stress.

Adult↗
PubMed1990

Relationship between nicotine tolerance questionnaire scores and plasma cotinine.

The Fagerström Tolerance Questionnaire (TQ) is often used in both research and treatment contexts to evaluate nicotine tolerance and physiological dependence in cigarette smokers. Recently, however, questions about its validity and its usefulness in comparison to other easily collected measures have been raised. In the present study, 100 male subjects reporting for experimental sessions (Sample I) and 50 male and female subjects entering a smoking cessation clinic program (Sample II) were administered the TQ and determinations of plasma cotinine during ad libitum smoking were made. TQ scores were found to be correlated with cotinine levels in both samples, and several of the individual items proved to have statistically significant discriminatory value. Other schemes for determining degree of dependence were considered and found not to be superior to the TQ. Suggestions for further refining the TQ are reviewed.

Adult↗
PubMed1990

Aerobic physical training and alterations in pressor response during norepinephrine infusion: a controlled single-subject experiment.

To test the influence of aerobic physical training on pressor response to infused norepinephrine, the present study utilized a single subject A-B-A-B withdrawal design consisting of 9-week alternating sedentary and aerobic phases (S1, A1, S2, A2). During each 9-week phase the subject underwent infusions every 3 weeks, consisting of saline, low-dose and high-dose norepinephrine (Low-NE, High-NE). Heart rate and mean arterial blood pressure were monitored continuously; resting platelet and plasma catecholamines were also measured. Infusions were conducted 48 h from the most recent exercise bout to minimize residual effects of acute exercise. Fitness level was confirmed by VO2max during graded exercise testing at the conclusion of each 9-week phase. Blood pressure during saline did not differ between aerobic and sedentary phases. However, in all but one comparison, aerobic fitness was associated with a highly significant reduction in pressor response during Low-NE as well as High-NE. Plasma norepinephrine was higher during the two aerobic phases; platelet catecholamines and plasma epinephrine showed no reliable association with fitness. Results for this subject support an attenuation of pressor response associated with aerobic conditioning.

Adult↗
PubMed1990

Discordance of physiological and biochemical response to smoking and to psychological stress.

Both smoking and psychological stress produce marked effects upon cardiovascular function, and several studies have demonstrated that in combination they produce additive or potentiating effects. More recently, it has been reported that individuals strongly reactive to psychological stress are also strongly reactive to nicotine. In an attempt to replicate and extend those findings, we examined reactivity to smoking and competitive mental arithmetic across several physiological and biochemical variables. Despite stable responding across mental arithmetic trials, we were unable to demonstrate significant correlations between reactivity to smoking and to a psychological stressor. We further observed that anxiety level, when low, was a poor predictor of desire to smoke and of withdrawal, whereas higher anxiety levels were more tightly linked to these measures. These findings have implications for the identification of individuals at risk of cardiovascular disease as well as for the design of smoking treatment and relapse prevention programs.

Adult↗