Effects of sevoflurane on primary neuronal cultures of embryonic rats

被引:14
作者
Berns, Monika [1 ]
Zacharias, Robert [2 ,3 ]
Seeberg, Lucas [2 ,3 ]
Schmidt, Maren [2 ,3 ]
Kerner, Thoralf [2 ,3 ]
机构
[1] Charite Univ Med Berlin, Klin Neonatol, Ctr Frauen Kinder & Jugendmed Perinatalzentrum &, D-13353 Berlin, Germany
[2] Klin Anasthesiol & Operat Intens Med, Berlin, Germany
[3] Charite Univ Med Berlin, Ctr Anasthesiol OP Management & Intens Med 7, D-13353 Berlin, Germany
关键词
anaesthesia general; apoptosis; embryonic culture; necrosis; neurons; sevoflurane; APOPTOTIC NEURODEGENERATION; CELL-DEATH; IN-VITRO; ANESTHETIC AGENTS; DEVELOPING BRAIN; GABAERGIC NEURONS; CORTICAL-NEURONS; NITROUS-OXIDE; MOUSE-BRAIN; KETAMINE;
D O I
10.1097/EJA.0b013e32832a0c61
中图分类号
R614 [麻醉学];
学科分类号
100217 ;
摘要
Background and objective Commonly used anaesthetics can cause neurodegeneration in the developing brain. Sevoflurane, a widely used substance in paediatric anaesthesia, has not been analysed thus far. This study was carried out to investigate the effects of sevoflurane on neuronal cell viability. Methods Primary cortical neuronal cultures were prepared from Wistar rat embryos (E18), kept in 100 mu l Gibco-Neurobasal-A medium and exposed to 4 and 8 Vol.% sevoflurane for up to 48 h. Cell viability was assessed using the methyltetrazolium assay and was related to untreated controls. To evaluate the role of gamma-aminobutyric acid type A receptors, untreated cells were preincubated with the receptor antagonists gabazine or picrotoxin and were subsequently exposed to 8 Vol.% sevoflurane and the receptor antagonist. Cell viability was assessed and compared with that of sevoflurane-treated controls. Results Up to 6 (8 Vol.%) and 12 h (4 Vol.%) of exposure to sevoflurane, cell viability was equal when compared with untreated controls. Only longer exposure times led to significantly lowered cell viability. After 12 h of exposure, no significant differences in cell viability were found between these two series. Cell viability of cultures treated with sevoflurane and the receptor antagonists showed no significant differences when compared with sevoflurane-exposed controls. Conclusion These results suggest that sevoflurane does not cause neurodegeneration in primary cortical neurons of the rat following clinically relevant exposure times and concentrations. Eur J Anaesthesiol 26:597-602 (C) 2009 European Society of Anaesthesiology.
引用
收藏
页码:597 / 602
页数:6
相关论文
共 43 条
[21]   Ethanol-induced apoptotic neurodegeneration and fetal alcohol syndrome [J].
Ikonomidou, C ;
Bittigau, P ;
Ishimaru, MJ ;
Wozniak, DF ;
Koch, C ;
Genz, K ;
Price, MT ;
Stefovska, V ;
Hörster, F ;
Tenkova, T ;
Dikranian, K ;
Olney, JW .
SCIENCE, 2000, 287 (5455) :1056-1060
[22]   Ketamine potentiates cerebrocortical damage induced by the common anaesthetic agent nitrous oxide in adult rats [J].
Jevtovic-Todorovic, V ;
Benshoff, N ;
Olney, JW .
BRITISH JOURNAL OF PHARMACOLOGY, 2000, 130 (07) :1692-1698
[23]   Nitrous oxide (laughing gas) is an NMDA antagonist, neuroprotectant and neurotoxin [J].
Jevtovic-Todorovic, V ;
Todorovic, SM ;
Mennerick, S ;
Powell, S ;
Dikranian, K ;
Benshoff, N ;
Zorumski, CF ;
Olney, JW .
NATURE MEDICINE, 1998, 4 (04) :460-463
[24]   Early exposure to common anesthetic agents causes widespread neurodegeneration in the developing rat brain and persistent learning deficits [J].
Jevtovic-Todorovic, V ;
Hartman, RE ;
Izumi, Y ;
Benshoff, ND ;
Dikranian, K ;
Zorumski, CF ;
Olney, JW ;
Wozniak, DF .
JOURNAL OF NEUROSCIENCE, 2003, 23 (03) :876-882
[25]   GABA(A) receptor pharmacology [J].
Johnston, GAR .
PHARMACOLOGY & THERAPEUTICS, 1996, 69 (03) :173-198
[26]   Differential expression of NeuroD in primary cultures of cerebral cortical neurons [J].
Katayama, M ;
Mizuta, I ;
Sakoyama, Y ;
KohyamaKoganeya, A ;
Akagawa, K ;
Uyemura, K ;
Ishii, K .
EXPERIMENTAL CELL RESEARCH, 1997, 236 (02) :412-417
[27]   Caspases: pharmacological manipulation of cell death [J].
Lavrik, IN ;
Golks, A ;
Krammer, PH .
JOURNAL OF CLINICAL INVESTIGATION, 2005, 115 (10) :2665-2672
[28]   Postconditioning with isoflurane reduced ischemia-induced brain injury in rats [J].
Lee, Jeong Jin ;
Li, Liaoliao ;
Jung, Hae-Hyuk ;
Zuo, Zhiyi .
ANESTHESIOLOGY, 2008, 108 (06) :1055-1062
[29]   Inhalational anesthetics [J].
Lerman, J .
PEDIATRIC ANESTHESIA, 2004, 14 (05) :380-383
[30]   Xenon mitigates isoflurane-induced neuronal apoptosis in the developing rodent brain [J].
Ma, Daqing ;
Williamson, Peter ;
Januszewski, Adam ;
Nogaro, Marie-Caroline ;
Hossain, Mahmuda ;
Ong, Lay Ping ;
Shu, Yi ;
Franks, Nicholas P. ;
Maze, Mervyn .
ANESTHESIOLOGY, 2007, 106 (04) :746-753