Kendig J J, Kodde A, Gibbs L M, Ionescu P, Eger E I
Department of Anesthesia, Stanford University School of Medicine, CA 94305-5117.
Eur J Pharmacol. 1994 Nov 3;264(3):427-36. doi: 10.1016/0014-2999(94)00499-4.
Two halogenated cyclobutanes, one anesthetic and one not, were compared on receptor-specific pathways in isolated neonatal rat spinal cord. The anesthetic 1-chloro-1,2,2-trifluorocyclobutane depressed the monosynaptic reflex (glutamate non-NMDA receptors) and abolished a slow ventral root potential (glutamate NMDA, non-NMDA and tachykinin receptors). This compound slightly enhanced the muscimol-evoked dorsal root potential (GABAA) but reversibly depressed the dorsal root potential elicited by dorsal root stimulation. The non-anesthetic 1,2-dichlorohexafluorocyclobutane increased monosynaptic reflex, depressed slow ventral root potential approximately 50%, had little effect on muscimol-evoked dorsal root potential, and irreversibly depressed dorsal root-evoked dorsal root potential. Hypoxia accounts for slow ventral root potential depression, but not monosynaptic reflex enhancement. In this preparation and for this pair of compounds, anesthetic properties are related to blockade of transmission at glutamate synapses, with a small component of GABAA enhancement. Monosynaptic reflex increase may be related to the non-anesthetic cyclobutane's convulsant and anti-anesthetic properties.
在新生大鼠离体脊髓的受体特异性途径上,对两种卤代环丁烷进行了比较,其中一种是麻醉剂,另一种不是。麻醉剂1-氯-1,2,2-三氟环丁烷抑制单突触反射(谷氨酸非NMDA受体)并消除慢腹根电位(谷氨酸NMDA、非NMDA和速激肽受体)。该化合物略微增强了蝇蕈醇诱发的背根电位(GABAA),但可逆地抑制了背根刺激诱发的背根电位。非麻醉剂1,2-二氯六氟环丁烷增加单突触反射,使慢腹根电位降低约50%,对蝇蕈醇诱发的背根电位影响很小,并不可逆地抑制背根诱发的背根电位。缺氧是慢腹根电位降低的原因,但不是单突触反射增强的原因。在此制备过程中以及对于这一对化合物,麻醉特性与谷氨酸突触处传递的阻断有关,伴有少量GABAA增强成分。单突触反射增加可能与非麻醉性环丁烷的惊厥和抗麻醉特性有关。