Sevoflurane Affects Neurogenesis After Forebrain Ischemia in Rats

Abstract

The present data suggest that high concentrations of sevoflurane stimulate neurogenesis in the dentate gyrus after cerebral ischemia.

Assessment of Postischemic Neurogenesis in Rats with Cerebral Ischemia and Propofol Anesthesia

“…The absent effect of propofol on neurogenesis in shamoperated animals agrees with a recent study where neurogenesis remained unaffected in sham-operated rats 28 days after 100 min of sevoflurane administration compared with the natural rate of neurogenesis in naive animals. 10 To exclude the possibility that the propofol administration was too short or the dosage was too low, a further group receiving high-dose propofol for 6 h (Prop6h) was performed. The applied propofol infusion protocol (90 -30 mg · kg Ϫ1 · h…”

“…10 In brief, sections for immunohistochemistry staining were incubated with the primary mouse anti-BrdU antibody (monoclonal mouse immunoglobulin G [IgG], 1:500; Roche Diagnostics Corp., Indianapolis, IN) followed by an incubation with the biotinylated secondary donkey anti-mouse antibody (Biotin-SP-conjugated donkey antimouse IgG, 1:500; Jackson ImmunoResearch Laboratories Inc., West Grove, PA).…”

“…Sevoflurane anesthesia in two different concentrations has demonstrated an increase in postischemic neurogenesis with higher sevoflurane concentrations in the same ischemia model as used in this study. 10 However, the 80% decrement time of sevoflurane is less than 8 min and does not increase significantly with the duration of anesthesia. 35 Therefore, it can be assumed that, following an equilibration period of 30 min after the end of sevoflurane administration, sevoflurane is almost completely eliminated, and an effect on postischemic neurogenesis is unlikely.…”

“…Recent experiments in rats show that the amount of newly generated neurons in the hippocampus is dose-dependently affected by sevoflurane 28 days after forebrain ischemia. 10 The intravenous anesthetic propofol is popular for operations with a risk of cerebral ischemia, such as neurosurgery, cardiac surgery, and vascular surgery. It decreases intracranial pressure, maintains cerebrovascular autoregulation, and possesses a short context-sensitive half-life, which enables rapid recovery from anesthesia to control for surgical complications.…”

“…10 In rodents, the proliferation peak induced by ischemia is after 7-11 days. 18,19 Therefore, proliferation of neuronal stem cells was assessed 9 days after cerebral ischemia in the current study.…”