Postoperative cognitive dysfunction may be associated with neuroinflammation, and sevoflurane suppresses surgery-induced inflammation. We hypothesized that low concentrations of sevoflurane would result in more impaired postoperative cognitive function compared to high concentrations.
Aged male Sprague–Dawley rats (n = 21, 17–22 months) were randomly assigned to 1 of 3 groups: control (C), sevoflurane 2% (S2), and sevoflurane 4% (S4). Rats in the S2 and S4 groups underwent open femoral fracture and intramedullary fixation of the left hind limb under 2 hours of sevoflurane anesthesia. Neurological outcomes were evaluated using the Morris water maze (MWM) test, and histopathological outcomes were assessed 28 days after surgery.
The S2 group showed prolonged swimming latency compared to S4 on day 7 (difference of means, 34.4; 95% confidence interval [CI], 2.57–66.3; P = .031) and compared to the C group on day 9 (difference of means, –33.4; 95% CI, –65.3 to –1.55; P = .037). The intact CA1 cells in the S2 group were significantly less than those in the C and S4 groups (H statistic, 10.87; P = .006 versus C; P = .033 versus S4).
We found that low concentrations of sevoflurane prolonged the swimming latency of the MWM compared to high concentrations and reduced intact CA1 hippocampal neurons in aged rats. These results suggest that low-concentration sevoflurane anesthesia may be more detrimental than high concentration for spatial cognitive function and postoperative impairment of hippocampal CA1 cells in aged rats.