Feldman D S, Buccafusco J J
Department of Veterans Affairs Medical Center, Medical Research Service, Augusta, GA 30910.
Eur J Pharmacol. 1993 Dec 21;250(3):483-7. doi: 10.1016/0014-2999(93)90039-k.
Recent studies in this laboratory have demonstrated the ability of acetylcholine receptor agonists to produce systemic arterial pressor responses through stimulation of spinal muscarinic receptors. In urethane-anesthetized rats a new surgical procedure was employed to permit microinjection of drugs into the cerebrospinal fluid surrounding the medulla without significant redistribution to spinal sites and vice versa. Pretreatment with intracisternal (medullary level) injection of 10 micrograms of atropine significantly inhibited the expression of the pressor response produced by intrathecal injection of 5 micrograms of carbachol. This inhibition was due at least partly to the interruption of a medullary component of a spinobulbar pathway involving medullary muscarinic receptors. It was not due to redistribution of atropine from medullary to spinal sites since significant levels of atropine were not detected in the spinal cord after intracisternal injection of the drug. The remainder of the pressor response to intrathecal carbachol after medullary muscarinic receptor blockade was most likely due to interactions within the spinal cord itself.
本实验室最近的研究表明,乙酰胆碱受体激动剂能够通过刺激脊髓毒蕈碱受体产生全身性动脉升压反应。在氨基甲酸乙酯麻醉的大鼠中,采用了一种新的手术方法,以便在不显著重新分布到脊髓部位的情况下,将药物微量注射到延髓周围的脑脊液中,反之亦然。脑池内(延髓水平)注射10微克阿托品预处理可显著抑制鞘内注射5微克卡巴胆碱所产生的升压反应的表达。这种抑制至少部分是由于涉及延髓毒蕈碱受体的脊髓-延髓通路的延髓成分被阻断。这并非是由于阿托品从延髓部位重新分布到脊髓部位,因为在脑池内注射该药物后,脊髓中未检测到显著水平的阿托品。在延髓毒蕈碱受体被阻断后,对鞘内注射卡巴胆碱的其余升压反应很可能是由于脊髓自身内部的相互作用。