Desflurane and sevoflurane attenuate oxygen and glucose deprivation-induced neuronal cell death

被引:13
作者
Wise-Faberowski, L
Raizada, MK
Sumners, C
机构
[1] Univ Florida, Coll Med, Dept Anesthesiol, Gainesville, FL USA
[2] Univ Florida, Coll Med, Dept Physiol, Gainesville, FL USA
[3] Univ Florida, Inst Brain, Gainesville, FL USA
关键词
ischemia; neuronal; necrosis; volatile; anesthesia;
D O I
10.1097/00008506-200307000-00006
中图分类号
R614 [麻醉学];
学科分类号
100217 ;
摘要
Neuronal cell death may occur via two pathways: those causing necrosis or those causing apoptosis. Apoptosis can be activated during periods of stress such as oxygen and glucose deprivation. Anesthetic agents such as desflurane or sevoflurane can attenuate early neuronal necrotic death, but their effect on oxygen and glucose deprivation-induced apoptosis has not been investigated. Neuronal cell cultures were prepared from neonatal rat cortex and were used between 10 and 14 days in vitro. The neuronal cell cultures were pretreated 30 minutes prior to oxygen and glucose deprivation with either desflurane or sevoflurane (N = 18). Three concentrations of each anesthetic were evaluated. The cultures were then deprived of oxygen and glucose for 30, 60, or 90 minutes. Treatment with desflurane or sevoflurane was continued during the period of oxygen and glucose deprivation. Forty-eight hours after exposure, the cells were examined for apoptosis using TUNEL and DNA gel electrophoresis. Comparisons were made to neuronal cortical cell cultures exposed to oxygen and glucose deprivation alone (N = 9). This in vitro model of oxygen and glucose deprivation was successful in producing neuronal cell death during the exposure times examined. During 30-, 60-, and 90-minute periods of oxygen and glucose deprivation, both desflurane and sevoflurane significantly (similar to98%) attenuated neuronal cell death regardless of concentration.
引用
收藏
页码:193 / 199
页数:7
相关论文
共 31 条
[1]   EXPRESSION OF C-FOS AND C-JUN FAMILY GENES AFTER FOCAL CEREBRAL-ISCHEMIA [J].
AN, G ;
LIN, TN ;
LIU, JS ;
XUE, JJ ;
HE, YY ;
HSU, CY .
ANNALS OF NEUROLOGY, 1993, 33 (05) :457-464
[2]   Glucose deprivation and hypoxia increase the expression of the GLUT1 glucose transporter via a specific mRNA cis-acting regulatory element [J].
Boado, RJ ;
Pardridge, WM .
JOURNAL OF NEUROCHEMISTRY, 2002, 80 (03) :552-554
[3]   A cautionary note on the use of the TUNEL stain to determine apoptosis [J].
CharriautMarlangue, C ;
BenAri, Y .
NEUROREPORT, 1995, 7 (01) :61-64
[4]   EARLY ENDONUCLEASE ACTIVATION FOLLOWING REVERSIBLE FOCAL ISCHEMIA IN THE RAT-BRAIN [J].
CHARRIAUTMARLANGUE, C ;
MARGAILL, I ;
PLOTKINE, M ;
BENARI, Y .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 1995, 15 (03) :385-388
[5]  
CHOI DW, 1987, J NEUROSCI, V7, P369
[6]   EXCITOTOXIC CELL-DEATH [J].
CHOI, DW .
JOURNAL OF NEUROBIOLOGY, 1992, 23 (09) :1261-1276
[7]   EXPRESSION OF MINERALOCORTICOID TYPE-I AND GLUCOCORTICOID TYPE-II RECEPTORS IN ASTROCYTE GLIA AS A FUNCTION OF TIME IN CULTURE [J].
CHOU, YC ;
LUTTGE, WG ;
SUMNERS, C .
DEVELOPMENTAL BRAIN RESEARCH, 1991, 61 (01) :55-61
[8]   Very delayed infarction after mild focal cerebral ischemia: A role for apoptosis? [J].
Du, C ;
Hu, R ;
Csernansky, CA ;
Hsu, CY ;
Choi, DW .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 1996, 16 (02) :195-201
[9]   Desflurane and isoflurane improve neurological outcome after incomplete cerebral ischaemia in rats [J].
Engelhard, K ;
Werner, C ;
Reeker, W ;
Lu, H ;
Möllenberg, O ;
Mielke, L ;
Kochs, E .
BRITISH JOURNAL OF ANAESTHESIA, 1999, 83 (03) :415-421
[10]   SECOBARBITAL ATTENUATES EXCITOTOXICITY BUT POTENTIATES OXYGEN-GLUCOSE DEPRIVATION NEURONAL INJURY IN CORTICAL CELL-CULTURE [J].
GIFFARD, RG ;
WEISS, JH ;
SWANSON, RA ;
CHOI, DW .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 1993, 13 (05) :803-810