Abstract

ObjectivesTo evaluate the effect of a prolonged constant rate infusion (CRI) of fentanyl on the minimum alveolar concentration (MAC) of isoflurane (ISOMAC) and to establish whether concurrent atropine administration influences ISOMAC in dogs. Study designProspective, crossover study. AnimalsSix healthy dogs weighing 13.0 ± 4.1 kg. MethodsDogs were anesthetized with isoflurane under conditions of normocapnia and normothermia. Arterial blood pressure was monitored invasively. Each dog was administered two treatments, on different occasions, in a crossover design. The dogs were administered intravenously (IV) an atropine bolus 0.02 mg kg−1 and CRI at 0.04 mg kg−1 hour−1 (fentanyl–atropine treatment) or no atropine (fentanyl treatment). For each dog, baseline ISOMAC was measured in duplicate using a tail clamp technique. Subsequently, all dogs were administered a fentanyl bolus (5 μg kg−1) and CRI (9 μg kg−1 hour−1) IV, and ISOMAC was re-determined at 120 and 300 minutes after initiation of the fentanyl CRI. ResultsBaseline ISOMAC values in the fentanyl and fentanyl–atropine treatments were 1.38 ± 0.16% and 1.39 ± 0.14%, respectively. Fentanyl significantly decreased the ISOMAC by 50 ± 9% and 47 ± 13% after 120 minutes and by 51 ± 14% and 50 ± 9% after 300 minutes (p < 0.001) in the fentanyl and fentanyl–atropine treatments, respectively. Compared with baseline, heart rate decreased significantly in the fentanyl treatment by 35% and 43% at 120 and 300 minutes, respectively. In the fentanyl–atropine treatment, heart rate did not change significantly over time. In both treatments, systolic arterial pressure increased from baseline after fentanyl. Conclusions and clinical relevanceIn this study, fentanyl reduced the ISOMAC by approximately 50%. The ISOMAC remained stable throughout the 300 minute CRI of fentanyl, suggesting no cumulative effect of the opioid. Atropine did not influence ISOMAC in dogs.

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