Abstract SNACC-42

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Dexmedetomidine Attenuates Gestational Propofol Anesthesia-Induced Spatial Memory Impairment in Offspring Rats

Li J, Xiong M, Nadavaluru P, Ye J, Puri S, Patel A, Bekker A
Rutgers-New Jersey Medical School, Newark, NJ, U.s.a.

Background: Maternal exposure to commonly used anesthetics, including propofol, causes neuronal injury in the fetal brains, which may be associated with long-term neurobehavioral disturbances in the offspring. Recent evidence suggests that dexmedetomidine (Dex) is neuroprotective in isoflurane-induced brain injury [1]. The authors set out to assess whether administration of Dex ameliorates the neurocognitive deficits in offspring exposed to propofol in utero.
Methods: With IACUC approval, pregnant rats (gestational day 20) were assigned to receive control condition or propofol anesthesia for 1 h with saline or Dex. Propofol was administered to pregnant rats by continuous infusion via a tail vein catheter. Control pregnant rats had catheter placed in tail vein, but no infusion. For Dex study, Dex (5.0 ug/kg, i.p.) or saline were administered 10 minutes before the 1-h propofol anesthesia. Pregnant rats were allowed to deliver their pups in their respective cages. Beginning at 4 weeks (postnatal day 28) of age, the offspring rats were evaluated for spontaneous locomotor activity and spatial working memory in 8-arm radial maze (ARM).
Results: The maternal vital signs and blood gas analysis indicated that the dams under propofol general anesthesia with or without Dex were hemodynamically and metabolically stable. Juvenile rats exposed to propofol in utero were not different than controls on spontaneous locomotor activity. However, they require significantly longer time to complete the radial arm maze on the first (control 74.9 ± 8.9 s vs. propofol 122.7 ± 13.2 s), second (control 56.2 ± 4.9 s vs. propofol 89.9 ± 7.8 s) and third (control 48.7 ± 5.8 s vs. propofol 130.2± 23 s) day and made more errors on the first (control 3.0 ± 0.6 s vs. propofol 5.1 ± 0.5 s) and third day (control 1.1 ± 0.5 vs. propofol 4.2 ± 0.3) across 5-day test in ARM. These neurocognitive deficits were prevented by administration of Dex. The juvenile rats exposed to propofol with Dex in utero took shorter time on the first (propofol+ Dex 79.9 ± 8.9 s vs. propofol + saline 113.4 ± 10.7 s), second (propofol + Dex 66.8 ± 3.5 s vs. propofol + saline 85.7 ± 6.2 s) and third (propofol+ Dex 57.4 ± 2.0 s vs. propofol + saline 114.1 ± 18.7 s) day and made less errors on the first (propofol+ Dex 3.2 ± 0.6 vs. propofol + saline 4.5 ± 0.5) and third (propofol+ Dex 1.7 ± 0.3 vs. propofol + saline 4.0 ± 0.7) day across 5-day test in ARM than that the juvenile pups exposed to propofol with saline in utero. There were no differences on spontaneous locomotor activity between juvenile rats exposed to propofol with saline in utero and rats exposed to propofol with Dex in utero.

Conclusion: Offspring rats exposed to propofol in utero show neurocognitive deficits measured by pup’s performance in ARM. It appears that co-administration of Dex attenuates this effect.

1. Sander, R.D., et al. Anesthesiology, 2009. 110(5):1077-85

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