Gilbert J C, Valtier D, Huguet R, Hulin C, Aquino J P, Meyer P
Departement of Pharmacology, Hopital Necker-Enfants Malades, Paris, France.
Eur J Clin Pharmacol. 1988;34(3):303-6. doi: 10.1007/BF00540960.
Peripheral-type benzodiazepine binding sites on intact platelets from untreated chronic insomniac patients and those chronically treated with benzodiazepine hypnotics were investigated to evaluate their putative involvement in sleep pathology and the influence of treatment. There were 34 elderly subjects in the study, 14 controls (80.7 years) and 20 insomniac patients, of whom 7 were untreated (61.1 years) and 13 were treated (84.4 years). There was an equivalent number of peripheral-type benzodiazepine 3H-PK 11195 binding sites on platelets from untreated (7.61 pmol/mg protein) and treated insomniacs (6.39 pmol/mg protein) and on platelets from the controls (6.21 pmol/mg protein). However, there was a twofold reduction in the affinity of these sites in untreated (Kd = 8.02 nM) and treated (Kd = 7.40 nM) insomniacs compared to controls (3.79 nM). This difference raises the possibility that peripheral-type benzodiazepine sites are involved in abnormal sleep.
对未经治疗的慢性失眠患者以及长期接受苯二氮䓬类催眠药治疗的患者的完整血小板上的外周型苯二氮䓬结合位点进行了研究,以评估它们在睡眠病理中的可能作用以及治疗的影响。该研究中有34名老年受试者,14名对照组(80.7岁)和20名失眠患者,其中7名未接受治疗(61.1岁),13名接受了治疗(84.4岁)。未经治疗的失眠患者(7.61 pmol/mg蛋白)、接受治疗的失眠患者(6.39 pmol/mg蛋白)以及对照组患者(6.21 pmol/mg蛋白)的血小板上外周型苯二氮䓬3H-PK 11195结合位点数量相当。然而,与对照组(3.79 nM)相比,未经治疗的失眠患者(Kd = 8.02 nM)和接受治疗的失眠患者(Kd = 7.40 nM)这些位点的亲和力降低了两倍。这种差异增加了外周型苯二氮䓬位点参与异常睡眠的可能性。