Neuroprotective effect of volatile anesthetic agents: molecular mechanisms

被引:64
作者
Matchett, Gerald A. [2 ]
Allard, Martin W. [2 ]
Martin, Robert D. [2 ]
Zhang, John H. [1 ,2 ,3 ]
机构
[1] Loma Linda Univ, Sch Med, Dept Physiol & Pharmacol, Loma Linda, CA 92350 USA
[2] Loma Linda Univ, Sch Med, Dept Anesthesiol, Loma Linda, CA 92350 USA
[3] Loma Linda Univ, Sch Med, Div Neurosurg, Loma Linda, CA 92350 USA
关键词
Isoflurane; sevoflurane; desflurane; halothane; enflurane; cerebral ischemia; FOCAL CEREBRAL-ISCHEMIA; PRECONDITIONING INDUCES NEUROPROTECTION; COMPLETE FOREBRAIN ISCHEMIA; OXYGEN-GLUCOSE DEPRIVATION; NITROUS OXIDE ANESTHESIA; ARTERY STUMP PRESSURE; TOXICITY IN-VIVO; BLOOD-FLOW; CAROTID-ENDARTERECTOMY; INTRACELLULAR CA2+;
D O I
10.1179/174313209X393546
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Introduction: Intra-operative cerebral ischemia can be catastrophic, and volatile anesthetic agents have been recognized for their potential neuroprotective properties since the 1960s. In this review, we examine the neuroprotective effects of five volatile anesthetic agents in current or recent clinical use: isoflurane, sevoflurane, desflurane, halothane and enflurane. Methods: A review of publications in the National Library of Medicine and National Institutes of Health database from 1970 to 2007 was conducted. Results: Volatile anesthetic agents have been shown to be neuroprotective in multiple animal works of ischemic brain injury. Short-term neuroprotection (<1 week post-ischemia) in experimental cerebral ischemia has been reported in multiple works, although long-term neuroprotection (>= 1 week post-ischemia) remains controversial. Comparison works have not demonstrated superiority of one specific volatile agent over another in experimental models of brain injury. Relatively few human works have examined the protective effects of volatile anesthetic agents and conclusive evidence of a neuroprotective effect has yet to emerge from human works. Conclusion: Proposed mechanisms related to the neuroprotective effect of volatile anesthetic agents include activation of ATP-dependent potassium channels, up-regulation of nitric oxide synthase, reduction of excitotoxic stressors and cerebral metabolic rate, augmentation of peri-ischemic cerebral blood flow and up-regulation of antiapoptotic factors including MAP kinases. [Neurol Res 2009; 31: 128-134]
引用
收藏
页码:128 / 134
页数:7
相关论文
共 103 条
[1]  
[Anonymous], CLIN ANESTHESIA
[2]   Central nervous system complications of cardiac surgery [J].
Arrowsmith, JE ;
Grocott, HP ;
Reves, JG ;
Newman, MF .
BRITISH JOURNAL OF ANAESTHESIA, 2000, 84 (03) :378-393
[3]   Neuronal calcium signaling [J].
Berridge, MJ .
NEURON, 1998, 21 (01) :13-26
[4]   Anesthetic choice of halothane versus propofol - Impact on experimental perioperative stroke [J].
Bhardwaj, A ;
Castro, AF ;
Alkayed, NJ ;
Hurn, PD ;
Kirsch, JR .
STROKE, 2001, 32 (08) :1920-1925
[5]   EFFECTS OF ISOFLURANE AND HYPOTHERMIA ON GLUTAMATE RECEPTOR-MEDIATED CALCIUM INFLUX IN BRAIN-SLICES [J].
BICKLER, PE ;
BUCK, LT ;
HANSEN, BM .
ANESTHESIOLOGY, 1994, 81 (06) :1461-1469
[6]   Isoflurane preconditions hippocampal neurons against oxygen-glucose deprivation -: Role of intracellular Ca2+ and mitogen-activated protein kinase signaling [J].
Bickler, PE ;
Zhan, XH ;
Fahlman, CS .
ANESTHESIOLOGY, 2005, 103 (03) :532-539
[7]   VOLATILE AND INTRAVENOUS ANESTHETICS DECREASE GLUTAMATE RELEASE FROM CORTICAL BRAIN-SLICES DURING ANOXIA [J].
BICKLER, PE ;
BUCK, LT ;
FEINER, JR .
ANESTHESIOLOGY, 1995, 83 (06) :1233-1240
[8]   γ-aminobutyric acid-A receptors contribute to isoflurane neuroprotection in organotypic hippocampal cultures [J].
Bickler, PE ;
Warner, DS ;
Stratmann, G ;
Schuyler, JA .
ANESTHESIA AND ANALGESIA, 2003, 97 (02) :564-571
[9]   The inhaled anesthetic, isoflurane, enhances Ca2+-dependent survival signaling in cortical neurons and modulates MAP kinases, apoptosis proteins and transcription factors during hypoxia [J].
Bickler, Philip E. ;
Fahlman, Christian S. .
ANESTHESIA AND ANALGESIA, 2006, 103 (02) :419-429
[10]   Isoflurane pretreatment ameliorates postischemic neurologic dysfunction and preserves hippocampal Ca2+/calmodulin-dependent protein kinase in a canine cardiac arrest model [J].
Blanck, TJJ ;
Haile, M ;
Xu, F ;
Zhang, J ;
Heerdt, P ;
Veselis, RA ;
Beekman, J ;
Kang, R ;
Adamo, A ;
Hemmings, H .
ANESTHESIOLOGY, 2000, 93 (05) :1285-1293