2％七氟烷反复吸入会导致青年大鼠神经毒性和认知功能障碍
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Repeated 2% sevoflurane administration in 7‑ and 60-day-old rats : Neurotoxicity and neurocognitive dysfunction
背景与目的
七氟醚是儿科麻醉中使用最广泛的吸入麻醉药之一。大量研究表明，在新生儿期七氟醚高浓度麻醉或持续时间较长的反复治疗可诱发神经细胞凋亡和长期学习障碍。在临床实践中，我们观察到一部分患者在七氟醚麻醉下从出生到青春期不止一次进行了小手术。因此，本研究旨在探讨七氟醚浓度为2％（七氟烷临床相关用量）持续1 h（持续时间短）在新生儿期是否可诱导接受七氟醚（2％，1 h）的青春期大鼠神经细胞凋亡和神经认知功能障碍。
方 法
第一组：出生后第7天的新生大鼠（PND-7）在受控条件下用氧气处理，然后升至PND-60。第二组：PND-7大鼠用2％七氟烷处理1小时，然后饲养至PND-60。第三组：PND-60大鼠用2％七氟醚处理1小时，第四组PND-7大鼠用2％七氟醚处理1小时，然后再用2％七氟醚在PND-60再麻醉1小时。 Western blot检测海马齿状回（DG）中caspase-3，Bax和Bcl-2的表达。用NeuN / caspase-3双免疫荧光染色评估海马DG中的神经凋亡。空间参考记忆由Morris水迷宫测试测试。
结 果
七氟醚（2％，1 h）对PND-7大鼠和PND-60大鼠未引起明显的海马神经细胞凋亡;它们在海马依赖的空间记忆中的表现没有显着受损;然而，第四组大鼠在Morris水迷宫实验中表现不佳，第四组神经细胞凋亡显着增加。
结 论
我们的研究结果表明，七氟醚可以诱导产后期反复七氟醚（2％，1 h）的青春期大鼠的神经细胞凋亡和认知功能障碍。这些研究结果将促进进一步的研究，以调查重复七氟烷暴露对中枢神经系统的发展和学习和记忆功能，以及体内和体外的潜在机制的影响。
原始文献摘要
Huang H, Liu C M, Sun J, et al. Repeated 2% sevoflurane administration in 7‑ and 60-day-old rats : Neurotoxicity and neurocognitive dysfunction[J]. Anaesthesist, 2017, 66(11):850.
BACKGROUND:Sevoflurane is one of the most widely used inhalation anesthetics in pediatric anesthesia. A large number of studies have demonstrated that repeated treatment with high concentrations or long durations of sevoflurane anesthesia during the neonatal period can induce neuroapoptosis and long-term learning disability. In clinical practice, we observed that a subset of patients underwent minor surgery under sevoflurane anesthesia more than once from birth to adolescence. Therefore, this research was conducted to investigate whether a 2% concentration of sevoflurane (clinically relevant usage of sevoflurane) for 1 h (a short duration) can induce neuroapoptosis and neurocognitive dysfunction in adolescent rats that received sevoflurane (2% for 1 h) during the neonatal period.
MATERIAL AND METHODS:Group I: neonatal rats at postnatal day 7 (PND-7) were treated with oxygen under controlled conditions and then raised to PND-60. Group II: PND-7 rats were treated with 2% sevoflurane for 1 h and then raised to PND-60. Group III: the PND-60 rats were treated with 2% sevoflurane for 1 h and in group IV the PND-7 rats were treated with 2% sevoflurane for 1 h and then anesthetized with 2% sevoflurane for 1 h at PND-60 again. The expression of caspase-3, Bax and Bcl-2 in the hippocampal dentate gyrus (DG) were measured by Western blot analysis. Neuroapoptosis in the hippocampal DG was assessed using NeuN/caspase-3 double-immunofluorescence staining. Spatial reference memory was tested by the Morris water maze test.
RESULTS:The present data showed that sevoflurane (2% for 1 h) did not induce obvious hippocampal neuroapoptosis in the PND-7 rats and PND-60 rats; their performance in hippocampal-dependent spatial memory was not significantly impaired; however, the rats in group IV showed poor performance in the Morris water maze test and the neuroapoptosis in group IV was significantly increased.
CONCLUSION:Our findings suggested that sevoflurane can induce neuroapoptosis and cognitive dysfunction in adolescent rats that received repeated sevoflurane (2% for 1 h) during the postnatal period. These findings will promote further studies to investigate the effects of repeated sevoflurane exposure on the development of the central nervous system and function of learning and memory, as well as the underlying mechanisms in vitro and in vivo.
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