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Query: UMLS:C0027497 (nausea)
 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Experimental evidence indicates that arginine vasopressin (AVP) contributes to the release of ACTH under certain conditions. The present study investigates the role of vasopressin as a secretagogue of ACTH during cigarette smoking or nicotine infusion with additional injection of corticotropin releasing hormone (CRH) and using the specific AVP antagonist d(CH2)5Tyr(Me)-AVP. We first tested the effect of the AVP antagonist (10 micrograms/kg body weight i.v.) on ACTH and cortisol release following cigarette smoking in 15 healthy young male smokers. Smoking led to marked increments in plasma nicotine and to a small rise in plasma ACTH and cortisol. Mean plasma ACTH and cortisol levels were at no time significantly altered by the antagonist. This might be due to a slight agonistic effect of the AVP antagonist, to high interindividual variability of the ACTH and cortisol responses after smoking or to a negligible role of AVP in smoking-induced ACTH release. In a second study we performed the following tests in six healthy male non-smokers: (1) nicotine infusion (1.0 micrograms/kg body weight per min); (2) CRH i.v. (100 micrograms); (3) AVP antagonist i.v. (5 micrograms/kg); (4) nicotine infusion plus CRH i.v.; (5) nicotine infusion plus AVP antagonist i.v.; (6) nicotine infusion plus CRH and AVP antagonist i.v.; and (7) sham infusion. Nicotine infusion led to greater increments of AVP, ACTH and cortisol than smoking without causing nausea. Peak nicotine levels after nicotine infusion were lower than after smoking. The AVP antagonist in the reduced dosage given alone had no effect on hormone levels. However, it slightly attenuated the effect of nicotine on ACTH and cortisol (P less than 0.05, ANOVA).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The role of vasopressin in the nicotine-induced stimulation of ACTH and cortisol in men. 132 53

Nicotine was found to markedly potentiate haloperidol-induced hypokinesia in rats. Nicotine alone was without effect. Subsequently, concurrent administration of 2 mg nicotine gum to 10 Tourette syndrome patients being treated with haloperidol produced a substantial decrease in tics and improvement of concentration and attention span. Nicotine gum alone was without effect. While 80% of children showed improvement with nicotine gum, 70% completely discontinued the gum because of side-effects, primarily involving nausea and bitter taste. Nicotine may prove useful for treating other neuroleptic responsive disorders, such as schizophrenia and Huntington's disease.
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PMID:Nicotine potentiates the effects of haloperidol in animals and in patients with Tourette syndrome. 273 Sep 49

The potential role of nicotine in tobacco dependence was investigated using the strategies of abuse liability assessment. Eight male volunteer cigarette smokers with histories of drug abuse resided on a research ward for the duration of the study. Each subject was tested with three doses of i.v. nicotine (0.75, 1.5 and 3.0 mg/10-sec infusion) and placebo each test day, and with three doses of inhaled nicotine, in the form of research cigarette smoke (0.4, 1.4 and 2.9 mg estimated yield) and placebo (sham-smoking), given on alternate test days. Each subject was tested on 4 days with both routes of administration, according to identical experimental protocols. Physiologic, subjective and observer data were collected at intervals ranging from 15 sec to 10 min beginning 10 min before drug administration and continuing for 30 min after administration. Both i.v. and inhaled nicotine produced dose-related increases in heart rate and blood pressure, and i.v. nicotine produced a transient bradycardia in four subjects during the first 30 sec after drug administration. Skin temperature was decreased by nicotine and pupil diameter was not consistently changed. Ratings of drug dose "strength" and drug "liking" were directly related to dose level whereas "desire to smoke cigarettes" was inversely related. Scores on the Morphine-Benzedrine Group (or Euphoria) scale of the Addiction Research Center Inventory were elevated by nicotine, and i.v. doses were identified frequently as cocaine. Signs and symptoms were similar for nicotine across the two routes of administration and included coughing, dizziness, nausea and relaxed feelings. Nicotine shared the pharmacologic profile of prototypic drugs of abuse. The study supports the hypothesis that the role of nicotine in tobacco dependence is equivalent to the role of other psychoactive drugs in substance abuse, e.g., to the role of cocaine in coca leaf use.
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PMID:Abuse liability and pharmacodynamic characteristics of intravenous and inhaled nicotine. 400 94

Nicotine chewing gum (Nicorette 4 mg) and an identical placebo gum were administered on different days, in a double-blind cross over fashion, to 4 men, aged 25-52 years, and 4 women, aged 21-49 years, all healthy non-smokers. The subjects chewed the gum for 30 min and heart rate, blood pressure, electrocardiogram, finger tip temperature, calf and hand blood flow and whole blood nicotine levels were measured for 240 min in the supine position, under indirect body heating. 72% -96% of the nicotine was absorbed. Only heart rate showed a significant increase (10%-12%) during the study as compared to placebo. The mean peak nicotine level was 6.5 ng/ml, which occurred at 15-60 min and roughly coincided with the peak heart rate, and then levelled off to around 3 ng/l at 120-240 min. All subjects complained of nausea, dizziness or anxiety to varying degrees. It is concluded that if healthy non-smokers chew Nicorette gum 4 mg by mistake, they would probably suffer more from generally unpleasant symptoms than from any cardiovascular upset.
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PMID:Cardiovascular effect of nicotine chewing gum in healthy non-smokers. 717

Smoking has been associated with a decreased frequency of UC. Currently, the role of nicotine for the treatment of UC is not established. Several studies have evaluated nicotine gum and transdermal patches as supplemental therapy for stable UC, but nicotine has not been compared with other treatment modalities. Nicotine dosages in the studies have varied from 5 to 30 mg/d without apparent dose-related therapeutic effects, and many patients have found relief from placebo treatment. Patients often do not tolerate nicotine therapy's adverse effects, which can include nausea, light-headedness, and headache. Due to the cyclic disease course of UC and the potential addictiveness of nicotine, further large studies are warranted to assess the benefits of nicotine therapy for UC. These studies should be conducted using a randomized, double-blind design with an extensive follow-up period. Until further trials are conducted, nicotine should generally not be recommended for UC treatment.
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PMID:Nicotine therapy for ulcerative colitis. 887 66

Discriminative stimulus properties of low nicotine doses administered in the form of chewing gum in combination with caffeine have been evaluated in humans, using established behavioural drug discrimination procedures. Twenty-one smokers who were also regular coffee drinkers were trained to discriminate 0 versus 1 mg nicotine chewing gum. Twenty subjects (11 men and nine women) were able to reach criterion performance (at least 80% correct). Generalization of responding across nicotine doses of 0, 0.25, 0.5 and 1 mg was then examined. Subjects were randomly allocated to receive either 50 mg caffeine or placebo before testing. Nicotine-appropriate responding was linearly related to dose, demonstrating that smokers can accurately discriminate nicotine from placebo and between relatively small doses of nicotine. Nicotine-appropriate responding was high at the 0 mg nicotine dose in the caffeine group demonstrating a partial generalization. Subjective effects assessed concurrently with behavioural discrimination revealed that nicotine discrimination was guided by the interoceptive cues of 'sensations in mouth', 'taste', 'heart rate', 'stimulated', 'alert' 'jittery' and 'nausea'. Caffeine increased self-ratings of 'stimulated' and 'alert' (at the 0 mg nicotine dose) and 'jittery' at the 0.5 and 1.0 mg nicotine dose. Relationships between nicotine-appropriate responding and subjective feelings induced by caffeine suggested that feelings of 'stimulated' and 'alert' were guiding discrimination behaviour. These data are discussed in terms of interoceptive nicotine cues and their importance at different doses and after caffeine preload.
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PMID:Discriminative stimulus properties of nicotine at low doses: the effects of caffeine preload. 983 36

Smoking is protective against developing ulcerative colitis. Nicotine may be the cause of this protective effect. Controlled trials have demonstrated efficacy of transdermal nicotine for active ulcerative colitis. Side effects observed with transdermal nicotine include contact dermatitis, nausea, and lightheadedness. Topical administration of nicotine to the colon reduces nicotine blood concentrations and side effects, and may be of clinical benefit.
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PMID:Nicotine therapy for ulcerative colitis: a review of rationale, mechanisms, pharmacology, and clinical results. 1023 87

Nicotine, a rapid-acting poison, is present in environmental tobacco smoke and has been used as a greenhouse insecticide. Due to its toxicity, several health hazard evaluations (HHE) have resulted from potential nicotine exposures to casino workers, airline flight attendants, and greenhouse employees. Exposure to nicotine can occur by inhalation, skin adsorption, and ingestion, resulting in such adverse health effects as nausea, vomiting, headache, dizziness, tachycardia, hypertension, convulsions, and cardiac arrhythmia. The development of an improved sampling and analytical methodology for nicotine was required to accommodate the broad concentration of nicotine levels and varying sampling scenarios presented by the differing HHE requests. A XAD-4 sorbent tube was selected for the collection of airborne nicotine. Analytical methodology for the separation, identification, and quantitation of nicotine by both gas chromatography-flame ionization detection and gas chromatography-nitrogen/ phosphorous detection is described. The limit of detection for nicotine was 0.013 microg/sample. The desorption efficiency for nicotine was determined over the range of study and ranged from 90.9% (0.096 microg) to 93.7% (24.0 microg). Nicotine exhibited storage stability for 30 days at 5 degrees C and for 14 days at ambient temperature. Based on the results of this research study, the new method for nicotine was published in the NIOSH Manual of Analytical Methods (NMAM 2551).
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PMID:Development of a versatile method for the detection of nicotine in air. 1176 27

Transdermal nicotine delivery systems are widely used in smoking cessation. The purpose of this study was to determine whether common symptoms of pyrosis and dyspepsia associated with these patches are related to gastroesophageal reflux or esophageal dysmotility. Twenty-seven paid volunteer cigarette smokers (> 15 cigarettes/day) without symptomatic gastroesophageal reflux disease participated in this single-blinded, placebo-controlled study. Twenty subjects completed the study. Subjects underwent three sequential 24-h intraesophageal pH/motor studies (Synectics model T32342084, Shore View, MN). The pH/motility probe was positioned 5 cm above the manometrically determined LES. A placebo patch was applied for the first 24-h study and a 15-mg nicotine patch (Nicotrol) was applied for the initial 16 h (removed for remaining 8 h) of the second 24-h period. A 21-mg nicotine patch (Nicoderm) was applied for another 24-h study period. All subjects consumed an identical, defined diet documented by meal receipts, and refrained from smoking and tobacco use throughout the study periods (CO breath test confirmation). The Wilcoxon, paired t-test, exact McNemar statistical methods were used. The results showed that there were no significant differences in reflux symptoms (pyrosis, chest pain, nausea, dysphagia), supine gastroesophageal reflux (number of episodes, duration, or cumulative acid exposure), or the total number of reflux episodes between placebo and nicotine patch treatment periods. The number of post-prandial upright acid reflux episodes (p = 004) and number of upright acid reflux episodes lasting more than 5 min (p = 0.007) were statistically higher with the placebo patch compared to the active nicotine patches. No differences in intraesophageal pH or motility indices were noted between the two transdermal nicotine patches (Nicotrol, Nicoderm). It was concluded that dyspeptic symptoms in subjects utilizing transdermal nicotine patches are not related to gastroesophageal reflux or to esophageal motor abnormalities.
Nicotine Tob Res 1999 Dec
PMID:Transdermal nicotine patches do not cause clinically significant gastroesophageal reflux or esophageal motor disorders. 1107 35

We utilized cluster analysis to identify individual differences in response to the initial effects of smoking following overnight abstinence among 183 regular smokers. Participants smoked three cigarettes (1 mg nicotine, spaced 30 min apart) in standardized fashion and completed questionnaires about their subjective responses to each cigarette. Heart rate was monitored throughout the procedure. Participants were grouped into two clusters based on their reported subjective effects and heart rate changes to the first cigarette. Clusters differed in terms of greater increases in heart rate, reports of dizziness, sweating, unpleasantness, nausea, and buzzing sensations in one group compared to the other group. The smokers showing increased responses developed greater acute tolerance to the effects of smoking subsequent cigarettes on subjective negative effects and heart rate, and experienced greater negative affect after quitting. These results are partially consistent with a nicotine sensitivity interpretation or a tolerance model of the effects of initial smoking.
Nicotine Tob Res 2001 Feb
PMID:Individual differences in responses to the first cigarette following overnight abstinence in regular smokers. 1126 Aug 9


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