“…This is in consistent with previous findings that prolonged exposure to sevoflurane leads to cognitive deficiency and disproportion of excitatory/inhibitory synapses during brain development. 22 , 23 Figure 2 GO analysis of hippocampal tissues in the Sevo group compared with the Con group. …”
Purpose
Postoperative cognitive dysfunction (POCD) is a central nervous system complication that occurs after anesthesia, particularly among the elderly. However, the neurological pathogenesis of postoperative cognitive dysfunction remains unclear. The aim of this study was to evaluate the effects of sevoflurane exposure on serum metabolites and hippocampal gene expression in elderly patients and aging mice by metabolomics and transcriptomic analysis and to explore the pathogenesis of sevoflurane induced POCD.
Patients and Methods
Human serum samples from five patients over 60 years old were collected before sevoflurane anesthesia and 1 hour after anesthesia. Besides, mice aged at 12 months (n=6 per group) were anesthetized with sevoflurane for 2 hours or with sham procedure. Subsequently, serum and hippocampal tissues were harvested for analysis. Further investigation into the relationship between isatin and neuroinflammation was conducted using BV2 microglial cells.
Results
Sevoflurane anesthesia led to the activation of inflammatory pathways, an increased presence of hippocampal astrocytes and microglia, and elevated expression of neuroinflammatory cytokines. Comparative analysis identified 12 differential metabolites that exhibited changes in both human and mouse serum post-sevoflurane anesthesia. Notably, isatin levels were significantly decreased after anesthesia. Notably, isatin levels significantly decreased after anesthesia, a factor known to stimulate proliferation and proinflammatory gene expression in microglia—the pivotal cell type in inflammatory responses.
Conclusion
Sevoflurane-induced alterations in serum metabolites in both elderly patients and aging mice, subsequently contributing to increased inflammation in the hippocampus.
“…This is in consistent with previous findings that prolonged exposure to sevoflurane leads to cognitive deficiency and disproportion of excitatory/inhibitory synapses during brain development. 22 , 23 Figure 2 GO analysis of hippocampal tissues in the Sevo group compared with the Con group. …”
Purpose
Postoperative cognitive dysfunction (POCD) is a central nervous system complication that occurs after anesthesia, particularly among the elderly. However, the neurological pathogenesis of postoperative cognitive dysfunction remains unclear. The aim of this study was to evaluate the effects of sevoflurane exposure on serum metabolites and hippocampal gene expression in elderly patients and aging mice by metabolomics and transcriptomic analysis and to explore the pathogenesis of sevoflurane induced POCD.
Patients and Methods
Human serum samples from five patients over 60 years old were collected before sevoflurane anesthesia and 1 hour after anesthesia. Besides, mice aged at 12 months (n=6 per group) were anesthetized with sevoflurane for 2 hours or with sham procedure. Subsequently, serum and hippocampal tissues were harvested for analysis. Further investigation into the relationship between isatin and neuroinflammation was conducted using BV2 microglial cells.
Results
Sevoflurane anesthesia led to the activation of inflammatory pathways, an increased presence of hippocampal astrocytes and microglia, and elevated expression of neuroinflammatory cytokines. Comparative analysis identified 12 differential metabolites that exhibited changes in both human and mouse serum post-sevoflurane anesthesia. Notably, isatin levels were significantly decreased after anesthesia. Notably, isatin levels significantly decreased after anesthesia, a factor known to stimulate proliferation and proinflammatory gene expression in microglia—the pivotal cell type in inflammatory responses.
Conclusion
Sevoflurane-induced alterations in serum metabolites in both elderly patients and aging mice, subsequently contributing to increased inflammation in the hippocampus.
“…Regarding the effects on synaptogenesis, a previous study found that P6 mice treated with 3% sevoflurane 2 h daily for 3 consecutive days had significantly decreased synaptogenesis in the hippocampus ( 23 ). Furthermore, another study found that P7 rats receiving a single exposure to 2.5% sevoflurane for 6 h showed not only a decrease in synaptogenesis but also an increase in the proportion of symmetric synapses in the hippocampus at P30 ( 24 ). That study demonstrated that the effects of neonatal exposure to sevoflurane were not limited to decreased synaptogenesis in the process of growth ( 24 ); in particular, this agent could promote synaptogenesis to some extent, leading to a shift in the excitatory/inhibitory synapse balance ( 24 ).…”
Section: Discussionmentioning
confidence: 99%
“…Furthermore, another study found that P7 rats receiving a single exposure to 2.5% sevoflurane for 6 h showed not only a decrease in synaptogenesis but also an increase in the proportion of symmetric synapses in the hippocampus at P30 ( 24 ). That study demonstrated that the effects of neonatal exposure to sevoflurane were not limited to decreased synaptogenesis in the process of growth ( 24 ); in particular, this agent could promote synaptogenesis to some extent, leading to a shift in the excitatory/inhibitory synapse balance ( 24 ). In the same study, cognitive function tested by the MWM on P23-25 in the 6 h sevoflurane-treated group was not much lower than that in the control group ( 24 ).…”
Section: Discussionmentioning
confidence: 99%
“…That study demonstrated that the effects of neonatal exposure to sevoflurane were not limited to decreased synaptogenesis in the process of growth ( 24 ); in particular, this agent could promote synaptogenesis to some extent, leading to a shift in the excitatory/inhibitory synapse balance ( 24 ). In the same study, cognitive function tested by the MWM on P23-25 in the 6 h sevoflurane-treated group was not much lower than that in the control group ( 24 ). In the results shown above, we found that cognitive function was most damaged in the 2 h sevoflurane-treated group, while the extension of sevoflurane exposure time reduced the adverse effect on cognitive function.…”
Clinical studies have found that neonatal sevoflurane exposure can increase the risk of cognitive dysfunction. However, recent studies have found that it can exhibit neuroprotective effects in some situations. In this study, we aimed to explore the effects of sevoflurane neonatal exposure in rats. A total of 144 rat pups (72 males and 72 females) were assigned to six groups and separately according to sevoflurane exposure of different times on the seventh day after birth. Blood gas analysis and western blot detection in the hippocampus were conducted after exposure. The Morris water maze test was conducted on the 32nd to 38th days after birth. The expression of PSD95 and synaptophysin in the hippocampus was detected after the Morris water maze test. We found that neonatal exposure to sevoflurane promoted apoptosis in the hippocampus, and Bax and caspase-3 were increased in a dose-dependent manner. The 2-h exposure had the greatest effects on cognitive dysfunction. However, with the extension of exposure time to 6 h, the effects on cognitive function were partly compensated. In addition, sevoflurane exposure decreased synaptogenesis in the hippocampus. However, as the exposure time was extended, the suppression of synaptogenesis was attenuated. In conclusion, neonatal sevoflurane exposure exhibited duration-dependent effects on cognitive function via Bax-caspase-3-dependent apoptosis and bidirectional effects on synaptogenesis in rats.
“…Studies have found that many anesthetics cause nerve damage and learning and memory impairment. [1][2][3][4] Therefore, more attention has been paid to the safety of anesthetics.…”
With the advancement of medical technology, there are increasing opportunities for new-borns, infants, and pregnant women to be exposed to general anaesthesia. Propofol is commonly used for the induction of anaesthesia, maintenance of general intravenous anaesthesia and sedation of intensive-care children. Many previous studies have found that propofol has organ-protective effects, but growing evidence suggests that propofol interferes with brain development, affecting learning and cognitive function. The purpose of this review is to summarize the latest progress in understanding the neurotoxicity of propofol. Evidence from case studies and clinical studies suggests that propofol has neurotoxicity on the developing brain. We classify the findings on propofol-induced neurotoxicity based on its damage mechanism. We end by summarizing the current protective strategies against propofol neurotoxicity. Fully understanding the neurotoxic mechanisms of propofol can help us use it at a reasonable dosage, reduce its side effects, and increase patient safety.
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