Paakkari I, Karppanen H
Neuropharmacology. 1982 Feb;21(2):171-8. doi: 10.1016/0028-3908(82)90158-7.
Intracerebroventricularly administered dimaprit decreased the depth of urethane anaesthesia. Ventilatory stimulation, positive corneal reflex and increased susceptibility to pain were observed. Furthermore, dimaprit decreased the lethal effect of large doses of urethane. The analeptic property of dimaprit was not shared by the potent H2-receptor agonist, impromidine, Histamine increased ventilatory tidal volume but no other stimulatory effects were observed. These findings suggest that the analeptic effects of dimaprit were not mediated by H2-receptors. Among the analeptic effects of dimaprit, only the protection against urethane toxicity was antagonized by metiamide. However, this phenomenon appeared to be due to the nonspecific interaction between the three bradypnoeic drugs metiamide, dimaprit and urethane. The histamine-induced increase in ventilatory tidal volume was not antagonized by diphenhydramine or metiamide, suggesting the existence of a novel histaminergic mechanism in the central nervous system.
脑室内注射地马普明可降低氨基甲酸乙酯麻醉的深度。观察到通气刺激、角膜反射阳性以及对疼痛的敏感性增加。此外，地马普明降低了大剂量氨基甲酸乙酯的致死作用。强效H2受体激动剂英普咪定不具有地马普明的兴奋作用。组胺增加了通气潮气量，但未观察到其他刺激作用。这些发现表明，地马普明的兴奋作用不是由H2受体介导的。在地马普明的兴奋作用中，只有对氨基甲酸乙酯毒性的保护作用被甲硫米特拮抗。然而，这种现象似乎是由于三种呼吸抑制药物甲硫米特、地马普明和氨基甲酸乙酯之间的非特异性相互作用所致。组胺引起的通气潮气量增加未被苯海拉明或甲硫米特拮抗，提示中枢神经系统中存在一种新的组胺能机制。
