Laorden M L, Miralles F S, Puig M M
Department of Pharmacology, Murcia University School of Medicine, Espinardo, Spain.
J Pharm Pharmacol. 1988 Mar;40(3):223-4. doi: 10.1111/j.2042-7158.1988.tb05229.x.
The effects of the non-specific opiate antagonist L-naloxone and the inactive isomer D-naloxone, as well as the specific mu receptor antagonist beta-funaltrexamine, have been examined on hyperthermia-induced seizures in unrestrained 15 days old rats. Saline-injected animals exposed to an ambient temperature of 40 degrees C showed a gradual increase in body temperature reaching a maximum of 42 +/- 0.1 degrees C at 50 min exposure. At this time all the pups had seizures and died. Similar results were obtained when the animals were pretreated with different doses of D-naloxone and beta-funaltrexamine. Rats pretreated with L-naloxone also showed an increase in rectal temperature; but the temperature was lower than in saline-injected animals. Only high doses of L-naloxone prevented seizures and deaths. These data indicate that endogenous opioid peptides may play a role in seizures induced by hyperthermia and that receptors other than mu receptors could be involved in hyperthermia-induced seizures.
已对非特异性阿片拮抗剂L-纳洛酮和无活性异构体D-纳洛酮以及特异性μ受体拮抗剂β-芬太尼胺对15日龄未束缚大鼠热诱导惊厥的影响进行了研究。暴露于40摄氏度环境温度下注射生理盐水的动物体温逐渐升高,在暴露50分钟时达到最高值42±0.1摄氏度。此时所有幼崽均发生惊厥并死亡。当动物用不同剂量的D-纳洛酮和β-芬太尼胺预处理时,也得到了类似结果。用L-纳洛酮预处理的大鼠直肠温度也有所升高;但该温度低于注射生理盐水的动物。只有高剂量的L-纳洛酮可预防惊厥和死亡。这些数据表明内源性阿片肽可能在热诱导的惊厥中起作用,并且除μ受体外的其他受体可能参与热诱导的惊厥。