Fentanyl in the Fourth Cerebral Ventricle Causes Respiratory Depression in the Anesthetized but Not in the Awake Dog

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Abstract
Specific binding sites for opiate-induced bradycardia, hypotension and EEG-synchronization are located in areas bordering the 4th cerebral ventricle in the dog. To see if the clinically observed opiate-induced respiratory depression is mediated selectively from ponto-bulbar respiratory neurons, increasing concentrations of fentanyl (2.5-5-10-20 .mu.g/ml) were perfused through the 4th cerebral ventricle in canines. Contrary to the awake state, fentanyl-perfusion during halothane-anesthesia (0.75 vol%/O2) induced a dose-related increase in arterial P[partial pressure]CO2. This effect was served by subsequent naloxone-perfusion (20 .mu.g/ml). The administration of halothane alone over the same period of time did not affect PCO2 in a similar manner. Higher cortical centers which are involved in sensory awareness may modulate respiratory neurons in the medulla, as the depression of the higher centers by halothane caused opiate-induced respiratory impairment. An additive effect of fentanyl- and halothane-induced release of opiate-like peptides (enkephalins) on respiration should be considered.