Bosnjak Z J, Dujic Z, Roerig D L, Kampine J P
Department of Anesthesiology, Medical College of Wisconsin, Milwaukee.
Anesthesiology. 1988 Oct;69(4):500-6. doi: 10.1097/00000542-198810000-00009.
Depression of synaptic transmission is one of the actions common to many general anesthetics. They appear to act primarily on the chemical transmission process itself without affecting the conduction of impulses in nerve axons. The objective of the present study was to directly examine the effects of halothane on the release of acetylcholine and overall ganglionic transmission. The effects of halothane on ganglionic transmission were studied in the stellate ganglion of the cat in vitro. The preganglionic nerves of the stellate ganglion were stimulated electrically to generate threshold and suprathreshold evoked potentials in the postganglionic nerves. The picomole levels of released acetylcholine in the superfusate were determined with a radioenzymatic method using 32P-ATP following a 5-min preganglionic stimulation before and after the addition of 0.28 and 0.59 mM halothane (vaporizer settings of 1% and 2%, respectively). Halothane at both concentrations: 1) depressed sympathetic ganglionic transmission induced by either threshold or suprathreshold stimulation of the preganglionic nerves; and 2) caused a dose-dependent decrease in acetylcholine release during threshold stimulation with no change in neurotransmitter release during suprathreshold stimulation. In summary, the interruption of synaptic transmission by halothane involves at least two mechanisms: 1) decrease in acetylcholine release during low level of synaptic transmission; and 2) postsynaptic decrease in sensitivity to acetylcholine during low and high levels of synaptic transmission.
突触传递抑制是许多全身麻醉药共有的作用之一。它们似乎主要作用于化学传递过程本身，而不影响神经轴突中冲动的传导。本研究的目的是直接检测氟烷对乙酰胆碱释放和整体神经节传递的影响。在体外猫的星状神经节中研究了氟烷对神经节传递的影响。电刺激星状神经节的节前神经，以在节后神经中产生阈电位和阈上诱发电位。在添加0.28和0.59 mM氟烷（分别为1%和2%的蒸发器设置）之前和之后，在5分钟的节前刺激后，使用32P-ATP通过放射酶法测定超滤液中释放的乙酰胆碱的皮摩尔水平。两种浓度的氟烷：1）抑制节前神经阈刺激或阈上刺激诱导的交感神经节传递；2）在阈刺激期间导致乙酰胆碱释放呈剂量依赖性减少，而在阈上刺激期间神经递质释放无变化。总之，氟烷对突触传递的阻断至少涉及两种机制：1）在低水平突触传递期间乙酰胆碱释放减少；2）在低水平和高水平突触传递期间对乙酰胆碱的突触后敏感性降低。
