Sevoflurane anesthesia alters cognitive function by activating inflammation and cell death in rats

Cui,Rong-Sheng; Wang,Kai; Wang,Zhong-Li

doi:10.3892/etm.2018.5976

Sevoflurane anesthesia alters cognitive function by activating inflammation and cell death in rats

Authors:
- Rong-Sheng Cui
- Kai Wang
- Zhong-Li Wang
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Affiliations: Department of Anesthesia, People's Hospital of Rizhao, Rizhao, Shandong 276800, P.R. China
Published online on: March 20, 2018 https://doi.org/10.3892/etm.2018.5976
Pages: 4127-4130
Copyright: © Cui et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

The present study was designed to investigate the effects of sevoflurane inhalation anesthesia on the cognitive function of rats and to investigate the molecular mechanisms mediating this effect. A total of 100 healthy male Sprague‑Dawley rats were divided into four groups: i) Control (air inhalation), ii) low‑dose (1.5% sevoflurane inhalation for 2 h), iii) high‑dose (3% sevoflurane inhalation for 2 h), and iv) nimodipine group (3% sevoflurane inhalation for 2 h + nimodipine). Sevoflurane inhalation anesthesia resulted in cognitive dysfunction in a dose-dependent manner. Sevoflurane also upregulated the expression of tumour necrosis factor-α (TNF-α), interleukin (IL) -6, -8, and Caspase-3 in the hippocampus. The intervention with nimodipine partially recovered the cognitive function and the abnormal expression of TNF-α, IL-6, IL-8, and Caspase-3 induced by sevoflurane. The results showed that the cognitive dysfunction caused by sevoflurane inhalation in rats may be related to the activation of inflammatory and apoptotic pathways. The neuroprotective effect of nimodipine suggests that abnormal calcium transport is partially responsible for the sevoflurane toxicity.

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