Gothert M, Wendt J
Anesthesiology. 1977 Jun;46(6):400-3.
The effects of enflurane anesthesia on adrenal medullary catecholamine secretion and on the pressor effect of splanchnic-nerve stimulation were studied in cats given pentobarbital for basal anesthesia. Inhalation of enflurane, 1.2 and 2.2 per cent, caused dose-related inhibition of both spontaneous catecholamine release and secretion evoked by splanchnic-nerve stimulation. During inhalation of 2.2 per cent enflurane spontaneous release of epinephrine was decreased to 19 and 25 per cent, respectively, of the initial values, and the stimulated release was decreased to 30 and 15 per cent, respectively. Enflurane also inhibited the pressor effect of splanchnic-nerve stimulation, whereas that of norepinephrine was not changed significantly. These results are similar to those previously obtained with halothane and methoxyflurane. It is concluded that the decrease in catecholamine secretion caused by enflurane is in part due to a direct effect on the chromaffin cell, namely to an inhibition of the secretion-stimulating effect of acetylcholine released from splanchnic nerves.
在给予戊巴比妥进行基础麻醉的猫中,研究了恩氟烷麻醉对肾上腺髓质儿茶酚胺分泌以及对内脏神经刺激的升压作用的影响。吸入1.2%和2.2%的恩氟烷会引起与剂量相关的对自发儿茶酚胺释放以及内脏神经刺激诱发的分泌的抑制。在吸入2.2%恩氟烷期间,肾上腺素的自发释放分别降至初始值的19%和25%,刺激释放分别降至30%和15%。恩氟烷还抑制内脏神经刺激的升压作用,而去甲肾上腺素的升压作用没有显著变化。这些结果与先前用氟烷和甲氧氟烷获得的结果相似。得出的结论是,恩氟烷引起的儿茶酚胺分泌减少部分是由于对嗜铬细胞的直接作用,即抑制从内脏神经释放的乙酰胆碱的分泌刺激作用。