58 resultados para Crack Cocaine
Resumo:
This paper reports the study of drug consumption carried out within the population of undergraduate students from 2 colleges of Alfenas, in the state of Minas Gerais state. Both licit and illicit drugs were studied, including alcohol, tobacco, marijuana, cocaine, heroin, crack, inhalants, glue, tranquilizers, stimulants, and others. METHODOLOGY: The research included a wide bibliographical search and the application of a questionnaire to approximately 23% of the students (total of 6500 students). RESULTS: A total of 1500 students participated in this investigation. The results demonstrated that there was a significant consumption of both licit and illicit drugs. The pattern of drug consumption in the research sample was similar to other investigations conducted in Brazil and in other countries. DISCUSSION: It was observed that 55% of the university students use drugs. However, the most surprising finding was that most of the students (88%) answered "yes" to the inquiry, "Have you already tried any type of drug, including alcohol and cigarettes?" The students revealed that they had taken drugs even prior to the admission to the university. The results suggest clearly that the university environment does not necessarily represent the starting point for student drug consumption.
Resumo:
OBJETIVOS: O objetivo deste estudo foi identificar, sob a ótica de usuários de crack, quais são as estratégias que eles utilizam para minimizar ou evitar os riscos decorrentes do consumo de crack. MÉTODO: Utilizou-se método qualitativo de pesquisa, desenvolvido mediante entrevistas semiestruturadas em profundidade. Foi entrevistada uma amostra intencional por critérios, composta por 30 usuários de crack, selecionados por meio de informantes-chave e distribuídos em oito diferentes cadeias. As entrevistas foram transcritas literalmente, inseridas e analisadas no software NVivo 8, com exploração dos dados mediante a técnica de análise de conteúdo. RESULTADOS: Os entrevistados acreditam que os maiores riscos decorrentes da dependência do crack sejam os relacionados aos efeitos psíquicos da droga, como fissura, sintomas paranoides transitórios e sintomas depressivos, assim como os decorrentes da ilegalidade dela, como a polícia e as questões referentes ao tráfico. Entretanto, os riscos de complicações físicas do consumo quase não foram apontados. As estratégias se concentraram no controle dos efeitos psíquicos, principalmente pelo consumo de álcool e maconha. Para lidar com as consequências da ilegalidade da droga, mostraram se preocupar com a postura que adotam perante o traficante e a polícia. CONCLUSÕES: As estratégias desenvolvidas pelos usuários focam na tentativa de se autoprotegerem principalmente dos episódios de violência e no alívio de sintomas desagradáveis causados pela droga - principalmente fissura e sintomas paranoides transitórios. Essas estratégias podem parecer efetivas a curto prazo, porém apresentaram riscos de longo prazo, tais como dependência de álcool e maconha.
Resumo:
OBJETIVO: Verificar a ocorrência de trauma e transtorno de estresse pós-traumático (TEPT) em uma amostra de mulheres dependentes de cocaína tipo crack. MÉTODO: A amostra foi composta por 99 mulheres, entre 18 e 52 anos, internadas em uma unidade de desintoxicação e extensamente avaliadas por meio da SCID-I e a ASI-6. RESULTADOS: Verificou-se uma taxa de exposição a trauma de 86,9% entre mulheres dependentes de cocaína tipo crack. A taxa de TEPT na amostra foi de 15,1%. Os clusters de revivescência e hiperexcitabilidade foram os mais frequentes - 24,4% e 20,9% respectivamente. Entre os tipos de eventos relatados, os mais frequentes foram sofrer agressão/abuso físico e ser testemunha de violência a outros. CONCLUSÃO: Os resultados sugerem uma frequente exposição a eventos traumáticos. Com relação à idade da experiência traumática, sugere-se que as usuárias expostas a trauma durante a infância e adolescência apresentam um início do uso de drogas em idades mais precoces que aquelas cujo trauma ocorreu na vida adulta.
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OBJETIVOS: Investigar se há associação entre intensidade e frequência de uso de crack e o nível econômico de dependentes da droga e verificar se há relação entre classe econômica e intensidade e frequência de uso de crack em homens adultos em internação psiquiátrica. MÉTODO: Estudo transversal quantitativo. Instrumentos: entrevista estruturada, Critérios de Classificação Econômica Brasil e Miniexame do Estado Mental. Tratamento estatístico: análises descritivas e inferenciais (testes de Kolmogorov-Smirnov, Mann-Whitney e Kruskal-Wallis - nível de significância de 5%). RESULTADOS: Duzentos e vinte e um participantes foram divididos em dois grupos: (1) Grupo de maior nível econômico (classes A e B) e (2) Grupo de menor nível econômico (Classes C, D e E). Não houve diferença significativa (p = 0,893 - teste de Mann-Whitney) entre os grupos quanto à intensidade e à frequência de uso de crack. Também não houve relação significativa (p = 0,549 - teste de Kruskal-Wallis) entre classe econômica (A, B, C, D e E) e intensidade e frequência de uso de crack. CONCLUSÃO: Os dependentes de crack de maior e de menor poder aquisitivo não diferiram de forma significativa com relação à intensidade e à frequência de uso da droga. Não houve relação entre classe econômica e intensidade e frequência de uso de crack nesta amostra.
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OBJETIVOS: Verificar as alterações da composição corporal e de parâmetros antropométricos de dependentes de crack internados para tratamento da adição. MÉTODOS: Estudo de coorte prospectivo, com 40 voluntários masculinos dependentes de crack, de 18 a 60 anos, em tratamento. Foram aferidos parâmetros antropométricos e de composição corporal, por meio de bioimpedância elétrica, na internação e alta hospitalar. RESULTADOS: Com idade média de 29,3 ± 6,9 anos, os pacientes tiveram, durante a abstinência, aumento de peso de 7,6 ± 3,7 kg; 11,6 ± 6,4% do peso corporal; 5,6 ± 4,2 cm de circunferência de cintura. Houve aumento de 4,2 ± 3,2 kg de gordura, 3,5 ± 3,0 kg de massa magra e de 2,5 ± 2,6 litros de água. Ao se internarem, 75% estavam eutróficos, 17,5% apresentavam sobrepeso e 5% apresentavam desnutrição, valores que, na alta, se alteraram para 50% de eutrofia e 47,6% de sobrepeso (IMC - Índice de Massa Corporal). Observou-se que a média de ganho de peso foi maior nas duas primeiras semanas de internação. CONCLUSÃO: Ao longo da internação, foram identificados ganho de peso e alterações de composição corporal e nos parâmetros antropométricos dos pacientes, refletindo em migração da eutrofia para o sobrepeso em parcela expressiva deles.
Resumo:
Objetivo Dimensionar a contribuição de características de grupos familiares de usuários de crack tanto em situações de consumo quanto na promoção da cessação do uso da substância. Métodos Estudo observacional, transversal, misto, com delineamento quantitativo (estatísticas descritiva e analítica, por regressão de Poisson robusta) e qualitativo (análise temática de conteúdos de entrevistas individuais semiestruturadas). Resultados Foram analisados dados oriundos de entrevistas com 519 usuários de crack, dos quais 48,3% referiram já ter feito uso compartilhado com algum familiar. A relação mais referida para compartilhamento do crack foi a conjugal, indicada por 30,6% dos entrevistados. A estimativa das razões de prevalência do desfecho abstinência na data da entrevista, por regressão de Poisson robusta controlada para fatores de confusão, para usuários de crack que referiram uso compartilhado com irmãos, foi de 0,940 (IC95%: 0,885-0,999; p = 0,045), tendo os que não referiram como referência. Na dimensão qualitativa, 20 entrevistados expuseram livremente modalidades de envolvimento dos familiares com o uso da droga, alguns indicando oposição ao consumo, outros estímulo, ou oferta, além da influência recíproca entre consumo de crack e conflitos familiares ou um ambiente considerado negativo. Além disso, os entrevistados que informaram ter familiares em tratamento em saúde mental tiveram 9% mais probabilidade de estar em uso cessado por 12 semanas ou mais (RP = 1,09; IC95%: 1,03-1,15; p = 0,005). Conclusão Os grupos familiares aparecem não somente como fator de proteção, mas também como importante fator de risco para o uso do crack, e sua inclusão como grupo primário de atendimento se justifica com essas evidências.
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OBJECTIVE: To characterize the cardiac electrophysiologic effects of cocaine. METHODS: In 8 dogs (9-13 kg), electrophysiologic parameters and programmed stimulation were undertaken using transvenous catheters at baseline, and after cocaine intravenous infusion (12 mg/kg bolus followed by 0.22 mg/kg/min for 25 minutes). RESULTS: Cocaine plasma levels (n=5) rose to 6.73± 0.56 mg/mL. Cocaine did not affect sinus cycle length and arterial pressure. Cocaine prolonged P wave duration (54±6 vs 73±4 ms, P<0.001), PR interval (115±17 vs 164±15 ms, P<0.001), QRS duration (62±10 vs 88±14 ms, P<0.001), and QTc interval (344±28 vs 403±62 ms, P=0.03) but not JT interval (193±35 vs 226±53 ms, NS). Cocaine prolonged PA (9±6 vs 23±8 ms, P<0.001), AH (73±16 vs 92±15 ms; P=0.03), and HV (35±5 vs 45±3ms; P<0.001) intervals and Wenckebach point (247±26 vs 280±28 ms, P=0.04). An increase occurred in atrial (138±8 vs 184± 20 ms; P<0.001) and ventricular (160±15 vs 187±25 ms; P=0.03) refractoriness at a cycle length of 300 ms. Atrial arrhythmias were not induced in any dog. Ventricular fibrillation (VF) was induced in 2/8 dogs at baseline and 4/8 dogs after cocaine. CONCLUSION: High doses of cocaine exert significant class I effects and seem to enhance inducibility of VF but not of atrial arrhythmias.
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The presence of illicit drugs such as cocaine and marijuana in US paper currency is very well demonstrated. However, there is no published study describing the presence of cocaine and/or other illicit drugs in Brazilian paper currency. In this study, Brazilian banknotes were collected from nine cities, extracted and analyzed by capillary gas chromatography/mass spectrometry, in order to investigate the presence of cocaine. Bills were extracted with deionized water followed by ethyl acetate. Results showed that 93% of the bills presented cocaine in a concentration range of 2.38-275.10 µg/bill.
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The thermal elimination of benzoic acid from (-)-cocaine is shown to be temperature-dependent. In the temperature range of 200-500 °C only a trans-elimination is observed leading to methylecgonidine. Above ca. 500 °C a second mechanism, the cis-elimination, comes up yielding a novel alkaloid methylisoecgonidine which has been characterized by means of mass spectrometry. At 600 °C the cis-elimination predominates. The trans-elimination is postulated a two-step process consisting of a 1,7- and a 1,5-hydrogen shift. The chemistry of cocaine base smoking is explained using the theory of chemical activation.
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Cocaine-induced behavioral sensitization and weight loss were investigated in periadolescent Wistar rats kept with their mothers or subjected to repeated maternal separation. Litters allocated to the separation procedure were placed in a temperature-controlled (33ºC) chamber for 3 h per day from postnatal day 6 (P6) to P20. Non-handled rats were left undisturbed until weaning. Treatments were started on P30-31 and the test was performed on P36-37. Animals received injections of saline or cocaine (10 mg/kg, sc) twice daily for 5 days. On day 6 all animals received saline. On day 7 animals were challenged with 10 mg/kg cocaine and their locomotion was evaluated in activity cages. A third group received saline throughout the 7-day period. Body weights were recorded on P30-31 and P36-37. Two-way ANOVA on body weights showed a main effect of treatment group (F(1,35) = 10.446, P = 0.003; N = 10-12). Non-handled rats treated with cocaine for 5 days gained significantly less weight, while no significant effect was observed in maternally separated rats. Two-way ANOVA revealed a main effect of drug treatment on locomotor activity (F(2,32) = 15.209, P<0.001; N = 6-8), but not on rearing condition (F(1,32)<0.001, P = 0.998). Animals pretreated with cocaine showed a clear behavioral sensitization relative to the saline group. No difference in the magnitude of sensitization was found between separated and non-handled animals. Only the effect of cocaine on weight gain was significantly affected by repeated episodes of early maternal separation during the pre-weaning period.
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The objective of the present study was to determine if the acute behavioral effects of cocaine acutely administered intraperitoneally (ip) at doses of 5, 10 and 20 mg/kg on white male CF1 mice, 90 days of age, would be influenced by leptin acutely administered ip (at doses of 5, 10 and 20 µg/kg) or by endogenous leptin production enhanced by a high-fat diet. The acute behavioral effects of cocaine were evaluated in open-field, elevated plus-maze and forced swimming tests. Results were compared between a group of 80 mice consuming a balanced diet and a high-fat diet, and a group of 80 mice fed a commercially available rodent chow formula (Ralston Purina) but receiving recombinant leptin (rLeptin) or saline ip. Both the high-fat-fed and rLeptin-treated mice showed decreased locomotion in the open-field test, spent more time in the open arms of the elevated plus-maze and showed less immobility time in the forced swimming test (F(1,68) = 7.834, P = 0.007). There was an interaction between diets and cocaine/saline treatments in locomotion (F(3,34) = 3.751, P = 0.020) and exploration (F(3,34) = 3.581, P = 0.024). These results suggest that anxiolytic effects and increased general activity were induced by leptin in cocaine-treated mice and that low leptin levels are associated with behavioral depression. Chronic changes in diet composition producing high leptin levels or rLeptin treatment may result in an altered response to cocaine in ethologic tests that measure degrees of anxiety and depression, which could be attributed to an antagonistic effect of leptin.
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Sleep loss is both common and critically relevant to our society and might lead to the abuse of psychostimulants such as amphetamines, cocaine and modafinil. Since psychoactive substance abuse often occurs within a scenario of sleep deficit, the purpose of this investigation was to compare the sleep patterns of rats challenged with cocaine (7 mg/kg, ip), methamphetamine (7 mg/kg, ip), or modafinil (100 mg/kg, ip) subsequent to paradoxical sleep deprivation (PSD) for 96 h. Our results show that, immediately after 96 h of PSD, rats (10 per group) that were injected with a psychostimulant presented lower percentages of paradoxical sleep compared to those injected with saline (P < 0.01). Regarding slow wave sleep (SWS), rats injected with psychostimulants after PSD presented a late rebound (on the second night subsequent to the injection) in the percentage of this phase of sleep when compared to PSD rats injected with saline (P < 0.05). In addition, the current study has produced evidence of the characteristic effect of each drug on sleep architecture. Home cage control rats injected with modafinil and methamphetamine showed a reduction in SWS compared with the saline group. Methamphetamine affected sleep patterns most, since it significantly reduced paradoxical sleep, SWS and sleep efficiency before and after PSD compared to control (P < 0.05). Cocaine was the psychostimulant causing the least changes in sleep pattern in relation to those observed after saline injection. Therefore, our results suggest that abuse of these psychostimulants in a PSD paradigm aggravates their impact on sleep patterns.
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Female rats are intensely affected by cocaine, with estrogen probably playing an important role in this effect. Progesterone modulates the GABA system and attenuates the effects of cocaine; however, there is no information about its relevance in changing GABA synthesis pathways after cocaine administration to female rats. Our objective was to investigate the influence of progesterone on the effects of repeated cocaine administration on the isoenzymes of glutamic acid decarboxylase (GAD65 and GAD67) mRNA in brain areas involved in the addiction circuitry. Ovariectomized, intact and progesterone replacement-treated female rats received saline or cocaine (30 mg/kg, ip) acutely or repeatedly. GAD isoenzyme mRNA levels were determined in the dorsolateral striatum (dSTR) and prefrontal cortex (PFC) by RT-PCR, showing that repeated, but not acute, cocaine decreased GADs/β-actin mRNA ratio in the dSTR irrespective of the hormonal condition (GAD65: P < 0.001; and GAD67: P = 0.004). In the PFC, repeated cocaine decreased GAD65 and increased GAD67 mRNA ratio (P < 0.05). Progesterone replacement decreased both GAD isoenzymes mRNA ratio after acute cocaine in the PFC (P < 0.001) and repeated cocaine treatment reversed this decrease (P < 0.001). These results suggest that cocaine does not immediately affect GAD mRNA expression, while repeated cocaine decreases both GAD65 and GAD67 mRNA in the dSTR of female rats, independently of their hormonal conditions. In the PFC, repeated cocaine increases the expression of GAD isoenzymes, which were decreased due to progesterone replacement.
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Cocaine is a widely used drug and its abuse is associated with physical, psychiatric and social problems. Abnormalities in newborns have been demonstrated to be due to the toxic effects of cocaine during fetal development. The mechanism by which cocaine causes neurological damage is complex and involves interactions of the drug with several neurotransmitter systems, such as the increase of extracellular levels of dopamine and free radicals, and modulation of transcription factors. The aim of this review was to evaluate the importance of the dopaminergic system and the participation of inflammatory signaling in cocaine neurotoxicity. Our study showed that cocaine activates the transcription factors NF-κB and CREB, which regulate genes involved in cellular death. GBR 12909 (an inhibitor of dopamine reuptake), lidocaine (a local anesthetic), and dopamine did not activate NF-κB in the same way as cocaine. However, the attenuation of NF-κB activity after the pretreatment of the cells with SCH 23390, a D1 receptor antagonist, suggests that the activation of NF-κB by cocaine is, at least partially, due to activation of D1 receptors. NF-κB seems to have a protective role in these cells because its inhibition increased cellular death caused by cocaine. The increase in BDNF (brain-derived neurotrophic factor) mRNA can also be related to the protective role of both CREB and NF-κB transcription factors. An understanding of the mechanisms by which cocaine induces cell death in the brain will contribute to the development of new therapies for drug abusers, which can help to slow down the progress of degenerative processes.
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Cocaine sensitization is a marker for some facets of addiction, is greater in female rats, and may be influenced by their sex hormones. We compared the modulatory effects of endogenous or exogenous estradiol and progesterone on cocaine-induced behavioral sensitization in 106 female rats. Ovariectomized female rats received progesterone (0.5 mg/mL), estradiol (0.05 mg/mL), progesterone plus estradiol, or the oil vehicle. Sham-operated control females received oil. Control and acute subgroups received injections of saline, while the repeated group received cocaine (15 mg/kg, ip) for 8 days. After 10 days, the acute and repeated groups received a challenge dose of cocaine, after which locomotion and stereotypy were monitored. The estrous cycle phase was evaluated and blood was collected to verify hormone levels. Repeated cocaine treatment induced overall behavioral sensitization in female rats, with increased locomotion and stereotypies. In detailed analysis, ovariectomized rats showed no locomotor sensitization; however, the sensitization of stereotypies was maintained. Only females with endogenous estradiol and progesterone demonstrated increased locomotor activity after cocaine challenge. Estradiol replacement enhanced stereotyped behaviors after repeated cocaine administration. Cocaine sensitization of stereotyped behaviors in female rats was reduced after progesterone replacement, either alone or concomitant with estradiol. The behavioral responses (locomotion and stereotypy) to cocaine were affected differently, depending on whether the female hormones were of an endogenous or exogenous origin. Therefore, hormonal cycling appears to be an important factor in the sensitization of females. Although estradiol increases the risk of cocaine sensitization, progesterone warrants further study as a pharmacological treatment in the prevention of psychostimulant abuse.