Behavioral Neuroscience Branch, National Institute on Drug Abuse - Intramural Research Program, National Institutes of Health, DHHS, 333 Cassell Drive, Baltimore, MD, 21224, USA.
Behavioral Neuroscience Branch, National Institute on Drug Abuse - Intramural Research Program, National Institutes of Health, DHHS, 333 Cassell Drive, Baltimore, MD, 21224, USA.
Neuropharmacology. 2019 Nov 1;158:107677. doi: 10.1016/j.neuropharm.2019.107677. Epub 2019 Jun 19.
Benzodiazepines are important therapeutic drugs, but they are often abused and co-abused with opioids. Clinical evidence suggests that benzodiazepines can inhibit respiration, and when combined with the respiratory-depressive effects of opioids, may increase likelihood of death. In this study we used oxygen sensors coupled with high-speed amperometry and multi-site thermorecording to examine how intravenous (iv) midazolam, a potent benzodiazepine, modulates the brain hypoxic and temperature effects of iv heroin in freely-moving rats. Oxygen levels and brain temperature were assessed with high temporal resolution in the nucleus accumbens (NAc), an important structure in the motivational-reinforcement circuit. When administered alone, midazolam (2 mg/kg) modestly decreased NAc temperature but had no evident effects on oxygen levels in this structure. In contrast, heroin (0.4 mg/kg) induced a strong decrease in NAc oxygen that was followed by a weaker, rebound-like oxygen increase. Midazolam pretreatment did not affect heroin-induced brain hypoxia but potentiated the initial hypothermia induced by heroin. However, co-administration of these drugs potentiated the heroin-induced oxygen decrease and enhanced heroin-induced brain hypothermia. Co-administration of heroin and midazolam also resulted in enhanced locomotor inhibition and loss of motor control. This effect caused some rats to collapse, resulting in nose and mouth occlusion, which caused a secondary hypoxic phase. These results could have important implications for human drug users, as the combined use of benzodiazepines with potent opioids not only results in sustained brain hypoxia but creates conditions of loss of motor control which could result in asphyxia and death. This article is part of the Special Issue entitled 'New Vistas in Opioid Pharmacology'.
苯二氮䓬类药物是重要的治疗药物,但它们经常被滥用,并与阿片类药物共同滥用。临床证据表明,苯二氮䓬类药物可抑制呼吸,与阿片类药物的呼吸抑制作用结合时,可能会增加死亡的可能性。在这项研究中,我们使用氧传感器结合高速安培法和多点热敏记录来检查静脉注射(iv)咪达唑仑(一种强效苯二氮䓬类药物)如何调节静脉注射海洛因对自由活动大鼠大脑缺氧和温度的影响。在伏隔核(NAc)中,以高时间分辨率评估氧水平和大脑温度,这是动机强化回路中的一个重要结构。单独给予咪达唑仑(2mg/kg)时,NAc 温度略有降低,但对该结构中的氧水平没有明显影响。相比之下,海洛因(0.4mg/kg)引起 NAc 氧的强烈下降,随后是较弱的反弹样氧增加。咪达唑仑预处理不影响海洛因引起的大脑缺氧,但增强了海洛因引起的初始体温过低。然而,这些药物的联合给药增强了海洛因引起的氧减少,并增强了海洛因引起的大脑低温。海洛因和咪达唑仑的联合给药还导致运动抑制增强和运动控制丧失。这种作用导致一些大鼠跌倒,导致口鼻阻塞,导致继发性缺氧期。这些结果可能对人类药物使用者具有重要意义,因为苯二氮䓬类药物与强效阿片类药物的联合使用不仅会导致持续的大脑缺氧,而且会导致运动控制丧失,从而导致窒息和死亡。本文是特刊“阿片类药物药理学的新视角”的一部分。