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An Sist Sanit Navar. 1997 May;20(2):191-9.
[Giving up the tobacco habit through the application of the smoker's aid program in the Chantrea Health Centre]

[Article in Spanish]

Nuin M, Fuertes C, Ancizu P, Espelosin G, Royo C, Sarasa I.

Unidad de Programacion y Docencia de Atencion Primaria, Plaza de la Paz, s/n, 31002 Pamplona, Spain.

INTRODUCTION: This is a prospective descriptive study of intervention without aleatory assignation, carried out in the Chantrea Health Centre. Its aim is to determine the characteristics of the smokers who are taking part in two interventions by the Smokers' Aid Program (Programa de Ayuda al Fumador - PAF), and to evaluate the factors that influence the latter's success. MATERIAL AND METHODS: The characteristics of 100 smokers were analyzed. They were offered one of the two PAF interventions: Minimal Intervention 1 (MN1): they are given a support brochure in the first consultations, contacted by telephone after one month and called to consultation after 6 months to measure CO. Minimal Intervention 2 (MN2): the smoker makes 5 consultations of support in giving up smoking (+ or - nicotine patches) with the doctor, nurse or social worker indiscriminately. The factors that were influential in abandoning the habit with 65 subjects were evaluated. RESULTS: 60% of the subjects were male with an average age of 41 (DE 29). 29% showed a pathology related to tobacco, with no relation found between this and the success of the interventions. Those who chose MN2 (38%) had started tobacco consumption at an earlier age and were more dependent on nicotine. Of the 65 smokers who completed the program, 37% continued not to smoke after 6 months. Those who managed to give up smoking were of a greater average age, had spent more years smoking and belonged above all to the MN1 intervention. DISCUSSION: Notable successes are achieved if the actions are carried out by the First Aid Team. We find no significant differences between the characteristics of those who give up smoking and those who do not. Not even a serious pathology, related to tobacco, is predictive of success. The smoker's dependence on nicotine must be taken into account in the intervention.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12891446&dopt=Abstract [PubMed - in process]

Eur J Pharmacol. 2003 Jul 25;473(2-3):217-23.
Extrahypothalamic corticotropin-releasing hormone mediates (-)-nicotine-induced elevation of plasma corticosterone in rats.

Okada S, Shimizu T, Yokotani K.

Department of Pharmacology, Kochi Medical School, Nankoku, Kochi 783-8505, Japan.

(-)-Nicotine activates the hypothalamic-pituitary-adrenal axis via an activation of the brainstem catecholaminergic neurons in rats. The present study was undertaken to clarify the mechanisms involved in the (-)-nicotine-induced activation of brainstem catecholaminergic neurons in anesthetized rats. Physostigmine (a cholinesterase inhibitor) (0.31 and 0.77 micromol/animal, i.p.) dose-dependently elevated plasma corticosterone in the presence of scopolamine (a muscarinic receptor antagonist) (2.3 micromol/animal, i.p.). (-)-Nicotine (250 and 500 nmol/animal, i.c.v.) dose-dependently elevated plasma corticosterone with concomitant noradrenaline release in the hypothalamic paraventricular nucleus. The (-)-nicotine (500 nmol/animal, i.c.v.)-induced elevation of corticosterone was abolished by phentolamine (an alpha-adrenoceptor antagonist) (0.66 micromol/animal, i.c.v.), and attenuated by (+/-)-sotalol (a beta-adrenoceptor antagonist) (0.97 micromol/animal, i.c.v.). The (-)-nicotine-induced increases of plasma corticosterone and hypothalamic noradrenaline release were abolished either by hexamethonium (a nicotinic acetylcholine receptor antagonist) (1.8 micromol/animal, i.c.v.), CP-154,526 (butyl-ethyl-[2,5-dimethyl-7-(2,4,6-trimethylphenyl)-7H-pyrrolo[2,3-d]pyrimidin-4-yl]amine) (a selective CRF-1 receptor antagonist) (1.3 micromol/animal, i.c.v.) or indomethacin (a cyclooxygenase inhibitor) (1.2 micromol/animal, i.c.v.). These results suggest that (-)-nicotine elevates plasma corticosterone by CRF-1 receptor- and prostaglandin-mediated noradrenaline release in the paraventricular nucleus in rats.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12892841&dopt=Abstract [PubMed - in process]

Addict Biol. 1996;1(4):333-48.
Alcoholism and the dopaminergic system: a review.

Noble E.

Alcohol Research Center, Department of Psychiatry and Biobehavioral Sciences and the Brain Research Institute, University of California, California, USA.

Alcohol as well as other substances of abuse are reinforcing substances which manifest their effects through activation of the mesolimbic dopaminergic reward pathways of the brain. In animal genetic models of alcoholism, reduced dopamine levels and D2 dopamine receptor (DRD2) numbers have been found in the brains of alcohol-preferring animals. Dopamine receptor agonists reduce alcohol consumption, whereas antagonists, in general, show the opposite effect. Moreover, quantitative trait loci studies in animals suggest the DRD2 gene and the region proximate to this locus is a chromosomal "hot spot" for alcohol-related behaviors. Human studies provide additional support for connection between alcohol dependence and CNS dopaminergic function. In endocrinological studies, using dopamine receptor agonists, reduced dopaminergic activity has been found in more severe and more genetic types of alcoholics. Brain imaging studies are similarly revealing a diminished dopaminergic tone in alcoholics. Treatment of alcoholics with dopamine receptor agonists shows reduced alcohol consumption and improvements in other outcome measures. Molecular genetic studies in humans have identified an association of the Al allele of the DRD2 gene with alcoholism. Moreover, a diminished central dopaminergic function has been found in DRD2 A1 allele subjects using pharmacological, electrophysiological and neuropsychological studies. Further, treatment of alcoholics with a dopamine receptor agonist showed more salutary effects on alcoholics who carry than those who do not carry the DRD2 A1 allele. The A1 allele has also been associated with substance use disorders other than alcoholism, including and cocaine and nicotine dependence and polysubstance abuse. The emerging evidence suggests that the DRD2 is a reinforcement or reward gene. It could represent one of the most prominent single-gene determinants of susceptibility to severe substance abuse. However, the environment and other genes, when combined, still play the larger role.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12893451&dopt=Abstract [PubMed - in process]

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