Background: Sevoflurane and isoflurane had been reported to improve ischemia/reperfusion injury (I/R) through amelioration of the inflammatory response. We aimed to explore and compare the molecular mechanisms involved in sevoflurane and isoflurane anesthesia in liver ischemia-reperfusion of rat model.
Methods: Forty male Wistar rats were randomly divided into 4 groups: sham group, I/R group, sevoflurane group, and isoflurane group. The liver I/R injury model was established to investigate the effect of sevoflurane and isoflurane anesthesia on liver ischemia/reperfusion. The inflammatory markers and complement C3, C5a, and C6 were detected by enzyme-linked immunosorbent assay. Oxidative stress was detected by measuring the levels of malondialdehyde (MDA), superoxide dismutase (SOD), and nitric oxide (NO).
Results: Our results showed that sevoflurane anesthesia significantly decreased alanine transaminase, aspartate transaminase, and lactate dehydrogenase levels compared with isoflurane and controls. Sevoflurane inhibited I/R injury induced production of tumor necrosis factor α, interleukin 1, interleukin 6, and intercellular cell adhesion molecule-1 and promoted interleukin 10 production more significantly compared with isoflurane. Reduced MDA and NO and elevated SOD release suggested that oxidative stress was attenuated by sevoflurane and isoflurane anesthesia. Both sevoflurane and isoflurane anesthesia significantly decreased plasma C3 levels compared with the I/R injury group without differences.
Conclusion: Sevoflurane anesthesia produced a more significant inhibitive effect on inflammatory cytokines and oxidative stress in liver I/R injury model than isoflurane, suggesting that sevoflurane is more suitable in surgery.
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