Billingsley M, Suria A, Williams J
Arch Int Pharmacodyn Ther. 1979 Nov;242(1):95-103.
Intravenous administration of chlordiazepoxide (CDP) caused respiratory depression in both rats and cats. The maximally tolerated dose of CDP was found to be 165 +/- 15 mg/kg, i.v., in rats. Pretreatment with picrotoxin (1.5 mg/kg) or naloxone (20 mg/kg, i.v.) significantly increased the maximally tolerated dose of CDP to 330 +/- 40 mg/kg, i.v., and 270 +/- 35 mg/kg, i.v., respectively. The protective effects of both naloxone and picrotoxin were absent in bilaterally vagotomized rats. Naloxone pretreatment (25 mg/kg, i.v.) was also found to block the respiratory depressant effects of CDP in anesthetized cats, but had no effect on the cardiovascular actions of CDP. It is possible that the respiratory effects of CDP are due to its actions on GABA receptors, and that peripheral GABA receptors may mediate the protective actions of picrotoxin and naloxone.
静脉注射氯氮䓬（CDP）可导致大鼠和猫出现呼吸抑制。在大鼠中，CDP的最大耐受剂量为静脉注射165±15毫克/千克。用印防己毒素（1.5毫克/千克）或纳洛酮（20毫克/千克，静脉注射）预处理可使CDP的最大耐受剂量分别显著增加至静脉注射330±40毫克/千克和270±35毫克/千克。双侧迷走神经切断的大鼠中，纳洛酮和印防己毒素均无保护作用。还发现纳洛酮预处理（25毫克/千克，静脉注射）可阻断麻醉猫中CDP的呼吸抑制作用，但对CDP的心血管作用无影响。CDP的呼吸作用可能归因于其对GABA受体的作用，并且外周GABA受体可能介导印防己毒素和纳洛酮的保护作用。
