Kubota K, Sun F Y, Sugaya K, Sunagane N
J Pharmacobiodyn. 1986 Apr;9(4):428-31. doi: 10.1248/bpb1978.9.428.
Benzodiazepines, chlordiazepoxide and diazepam reversed the antinociceptive action of caerulein in mice. Benzodiazepines (1-5 mg/kg) were administered intraperitoneally and 100 ng of caerulein was injected intracisternally to mice. Benzodiazepines did not change the basal pain threshold of mice but significantly antagonized the antinociceptive effect of caerulein. Proglumide (200 mg/kg, i.p.), which has been claimed to be a specific cholecystokinin receptor antagonist, could also antagonize the antinociceptive effects of caerulein. Naloxone (5 mg/kg) partially but significantly antagonized the antinociceptive effect of caerulein, suggesting that one of the mechanisms of antinociceptive action of caerulein is related to endogenous opioid peptides since benzodiazepines do not act on opioid receptors. Benzodiazepines may decrease the antinociceptive effect of caerulein through acting on cholecystokinin receptors in the central nervous system.
苯二氮䓬类药物、氯氮䓬和地西泮可逆转蛙皮素在小鼠中的抗伤害感受作用。将苯二氮䓬类药物（1 - 5毫克/千克）腹腔注射给小鼠，并向小鼠脑池内注射100纳克蛙皮素。苯二氮䓬类药物并未改变小鼠的基础痛阈，但显著拮抗了蛙皮素的抗伤害感受作用。已被宣称是一种特异性胆囊收缩素受体拮抗剂的丙谷胺（200毫克/千克，腹腔注射），也能拮抗蛙皮素的抗伤害感受作用。纳洛酮（5毫克/千克）部分但显著地拮抗了蛙皮素的抗伤害感受作用，这表明蛙皮素抗伤害感受作用的机制之一与内源性阿片肽有关，因为苯二氮䓬类药物并不作用于阿片受体。苯二氮䓬类药物可能通过作用于中枢神经系统中的胆囊收缩素受体来降低蛙皮素的抗伤害感受作用。
