Nicotinamide Adenine Dinucleotide Does Not Improve Anesthetic Recovery in Rodents.

Nicotinamide Adenine Dinucleotide (NAD) is implicated in bioenergetics, DNA repair, and senescence. Depletion of NAD is associated with aging and neurodegenerative disease, prompting a growing interest in NAD supplementation. With rising over-the-counter use of NAD, understanding their impact on perioperative recovery becomes essential. This study investigates the effect of NADH, a common NAD precursor, on anesthesia in rodents. Baseline and post-anesthesia (1.5% isoflurane) open field and Y-maze activity were recorded in adult male and female C57/BL6 mice (n = 8-10/group). NADH (150 mg/kg, intraperitoneal) or vehicle (0.9% normal saline) were given at baseline or during anesthesia. The NADH-treated group exhibited a significant decrease in open-field activity relative to vehicle-treated. This diminished activity was reflected in reduced distance travelled and average velocity after emergence from anesthesia in the NADH-treated group. NADH treatment did not improve Y-maze performance after anesthesia as the number of visits to the novel arm was significantly decreased. This study demonstrates a potentially adverse impact of NADH on recovery from anesthesia. We revealed a depression in open-field activity and Y-maze performance with NADH supplementation, an indicator of cognitive recovery in rodents. The broad implications of NAD in aging are likely to shape supplementation trends, highlighting the importance of understanding the potential influence of administering NAD on anesthetic sensitivity and recovery.