NOVEL NEUROREGULATION OF CRACK DEPENDENCE

该提案的目标是迅速但明确地调查 新的神经化学途径可以帮助对抗 对可卡因的依赖 我们提出了一个有前途的推定的疗效调查 兴奋剂滥用药物治疗，卡托普利，作为戒断促进剂 和预防复发的治疗。 本研究将采用安慰剂对照、双盲、随机 分配，双细胞平行组设计，将评估80名受试者 在24周的实验治疗期间，有3次随访。 我们假设服用活性卡托普利而不是安慰剂的受试者， 证据：1. 快克可卡因滥用严重程度降低，投入运作 在尿液中的定量GCMS和 自我报告的数量和使用频率，因为对 可卡因的渴望，随着禁欲持续时间的增加， 药物治疗中的保留。 2. 增加利用正式和 12-对快克可卡因滥用的分阶段治疗服务投入运作 使用自然史治疗暴露清单。 3.降低 多维度损伤操作为非药物性 成瘾严重程度指数的维度。

The goal of this proposal is to rapidly but definitively investigate a new neurochemical avenue to help combat the decimation created by dependence on crack cocaine smoking. We propose an investigation of the efficacy of a promising putative stimulant abuse pharmacotherapy, captopril, as abstinence facilitation and relapse prevention treatment for crack cocaine dependence. The investigation will employ a placebo controlled, double-blind, random assignment, two cell parallel group design that will assess 80 subjects during 24 weeks of experimental treatment, with 3 follow-ups. We hypothesize that subjects on active captopril, but not placebo, will evidence: 1. Decreased crack cocaine abuse severity, operationalized as a decrease in crack cocaine use on quantitative GCMS in urine and on self-reported amounts and frequency of use, as increased control over crack cocaine craving, and as increased durations of abstinence and retention in drug treatment. 2. Increased utilization of formal and 12-step treatment services for crack cocaine abuse, operationalized using Natural History treatment exposure inventories. 3. Decreased multidimensional impairment operationalized as decreases of the non-drug dimensions of the Addiction Severity Index.