Anesthesiology
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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. ⋯ 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.
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Comparative Study
Mucociliary flow in the trachea during anesthesia with enflurane, ether, nitrous oxide, and morphine.
Tracheal mucociliary flow rates in dogs were measured with a radioactive droplet technique during thiopental anesthesia, and subsequently during enflurane, either, and nitrous oxide-morphine anesthesia on different occasions. Enflurane, at 0.6, 1.2, 1.8 MAC, produced a dose-dependent, reversible depression of mucociliary flow equal to that previously reported for halothane. Nitrous oxide-halothane and nitrous oxide-morphine depressed mucociliary flow to the same extent as halothane at equivalent MAC levels. Ether did not depress mucociliary flow significantly from the thiopental control at any MAC level.