酒精是最常用的精神药物,通常与阿片类药物一起服用。由于酒精和阿片类药物均可诱发中枢神经系统抑制,因此通常认为酒精会增强阿片类药物已知的缺氧作用。为了解决这个假设,我们使用氧传感器来检查酒精对清醒、自由活动大鼠静脉注射海洛因诱导的脑氧合和缺氧反应的影响。为了消除酒精在口服或腹腔内给药后的强烈感官影响,通过长期植入的胃内导管以人体相关剂量将酒精直接注入胃中。以 0.5 g/kg 剂量递送的酒精不会影响脑氧水平,除了在药物递送过程中短暂的微弱增加。这种阶段性氧气增加在 2 时更强。0 g/kg 酒精剂量和随后较弱的补品增加。由于与腹腔内或静脉内注射相比,胃内给药的酒精吸收速度要慢得多且时间更长,因此脑氧水平的快速上升表明,在药物通过循环物理到达脑组织之前,酒精对胃中的感觉传入神经有直接作用。尽管脑氧含量缓慢增加,但 2.0 g/kg 剂量的酒精会强烈增强海洛因诱导的氧反应,增加氧减少的幅度和持续时间。因此,在酒精的影响下,使用阿片类药物变得更加危险,增加大脑缺氧并增加严重健康并发症的可能性,包括昏迷和死亡。由于与腹腔内或静脉内注射相比,胃内给药的酒精吸收速度要慢得多且时间更长,因此脑氧水平的快速上升表明,在药物通过循环物理到达脑组织之前,酒精对胃中的感觉传入神经有直接作用。尽管脑氧含量缓慢增加,但 2.0 g/kg 剂量的酒精会强烈增强海洛因诱导的氧反应,增加氧减少的幅度和持续时间。因此,在酒精的影响下,使用阿片类药物变得更加危险,增加大脑缺氧并增加严重健康并发症的可能性,包括昏迷和死亡。由于与腹腔内或静脉内注射相比,胃内给药的酒精吸收速度要慢得多且时间更长,因此脑氧水平的快速上升表明,在药物通过循环物理到达脑组织之前,酒精对胃中的感觉传入神经有直接作用。尽管脑氧含量缓慢增加,但 2.0 g/kg 剂量的酒精会强烈增强海洛因诱导的氧反应,增加氧减少的幅度和持续时间。因此,在酒精的影响下,使用阿片类药物变得更加危险,增加大脑缺氧并增加严重健康并发症的可能性,包括昏迷和死亡。脑氧水平的快速上升表明,在药物通过循环到达脑组织之前,酒精对胃中的感觉传入神经有直接作用。尽管脑氧含量缓慢增加,但 2.0 g/kg 剂量的酒精会强烈增强海洛因诱导的氧反应,增加氧减少的幅度和持续时间。因此,在酒精的影响下,使用阿片类药物变得更加危险,增加大脑缺氧并增加严重健康并发症的可能性,包括昏迷和死亡。脑氧水平的快速上升表明,在药物通过循环到达脑组织之前,酒精对胃中的感觉传入神经有直接作用。尽管脑氧含量缓慢增加,但 2.0 g/kg 剂量的酒精会强烈增强海洛因诱导的氧反应,增加氧减少的幅度和持续时间。因此,在酒精的影响下,使用阿片类药物变得更加危险,增加大脑缺氧并增加严重健康并发症的可能性,包括昏迷和死亡。0 g/kg 剂量强烈增强海洛因诱导的氧气反应,增加氧气减少的幅度和持续时间。因此,在酒精的影响下,使用阿片类药物变得更加危险,增加大脑缺氧并增加严重健康并发症的可能性,包括昏迷和死亡。0 g/kg 剂量强烈增强海洛因诱导的氧气反应,增加氧气减少的幅度和持续时间。因此,在酒精的影响下,使用阿片类药物变得更加危险,增加大脑缺氧并增加严重健康并发症的可能性,包括昏迷和死亡。
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Effects of alcohol on brain oxygenation and brain hypoxia induced by intravenous heroin
Alcohol is the most commonly used psychoactive drug, often taken in conjunction with opioid drugs. Since both alcohol and opioids can induce CNS depression, it is often assumed that alcohol potentiates the known hypoxic effects of opioid drugs. To address this supposition, we used oxygen sensors to examine the effects of alcohol on brain oxygenation and hypoxic responses induced by intravenous heroin in awake, freely moving rats. To eliminate robust sensory effects of alcohol following its oral or intraperitoneal delivery, alcohol was administered directly into the stomach via chronically implanted intragastric catheters at human relevant doses. Alcohol delivered at a 0.5 g/kg dose did not affect brain oxygen levels, except for a weak transient increase during drug delivery. This phasic oxygen increase was stronger at a 2.0 g/kg alcohol dose and followed by a weaker tonic increase. Since alcohol absorption from intragastric delivery is much slower and more prolonged than with intraperitoneal or intravenous injections, the rapid rise of brain oxygen levels suggests that alcohol has a direct action on sensory afferents in the stomach well before the drug physically reaches brain tissue via circulation. Despite slow tonic increases in brain oxygen, alcohol at the 2.0 g/kg dose strongly potentiates heroin-induced oxygen responses, increasing both the magnitude and duration of oxygen decrease. Therefore, under the influence of alcohol, the use of opioid drugs becomes much more dangerous, increasing brain hypoxia and enhancing the probability of serious health complications, including coma and death.