Abstract
Neurons are strongly dependent on continuous substrate delivery; accordingly physiologic resistance of neuronal tissues against ischemia is very low. Even short periods of cerebral ischemia can, therefore, cause severe neuronal damage. Certain surgical procedures (for example, during cardiovascular- or neuro-surgery) may involve periods of decreased or diminished cerebral perfusion, putting the patient at risk for neuronal damage and subsequent neurological deficit. Physicians caring for these patients will try to prevent or reduce damage using different neuroprotective strategies (aimed mainly at the reduction of cerebral metabolism). In addition to this, a modulation of neuronal ischemic tolerance (‘preconditioning’) prior to respective operative interventions may add substantially to the further improvement in patient outcome.
Keywords
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.
This is a preview of subscription content, log in via an institution.
Buying options
Tax calculation will be finalised at checkout
Purchases are for personal use only
Learn about institutional subscriptionsPreview
Unable to display preview. Download preview PDF.
References
Murry CE, Jennings RB, Reimer KA (1986) Preconditioning with ischemia: a delay of lethal cell injury in ischemic myocardium. Circulation 74: 1124–1136
Kitagawa K, Matsumoto M, Tagaya M (1990) “Ischemic tolerance” phenomenon found in the brain. Brain Res 528:21–24
Perez-Pinzon MA, Xu GP, Dietrich WD, Rosenthal M, Sick TJ (1997) Rapid preconditioning protects rats against ischemic neuronal damage after 3 but not 7 days of reperfusion following global cerebral ischemia. J Cereb Blood Flow Metab 17: 175–182
Stagliano NE, Perez-Pinzon MA, Moskowitz MA, Huang PL (1999) Focal ischemic preconditioning induces rapid tolerance to middle cerebral artery occlusion in mice. J Cereb Blood Flow Metab 19: 757–761
Barone FC, Whigte RF, Spera PA, Ellison J, Currie WX, Feuerstein GZ (1998) Ischemic preconditioning and brain tolerance. Temporal histological and functional outcomes, protein synthesis requirement, and interleukin-1 receptor antagonist and early gene expression. Stroke 29: 1937–1951
Wiegand F, Liao W, Busch C (1999) Respiratory chain inhibition induces tolerance to focal cerebral ischemia. J Cereb Blood Flow Metab 19: 1229–1237
Sugino T, Nozaki K, Takagi Y, Hashimoto N (1999) 3-Nitropropionic acid induces ischemic tolerance in gerbil hippocampus in vivo. Neurosci Lett 259: 9–12
Neurteaux C, Lauritzen I, Widmann C, Lazdunski M (1995) Essential role of adenosine, adenosine Al receptors, and ATP-sensitive K+ chanels in cerebral ischemic preconditioning. Proc Natl Acad Sci USA 92: 4666–4670
Gross GJ, Fryer RM (1999) Sarcolemmal versus mitochondrial ATP-sensitive K+-channels and myocardial preconditioning. Circ Res 84: 973–979
Riepe MW, Esclaire F, Kasischke K, et al (1997) Increased hypoxic and ischemic tolerance by chemical inhibition of oxidative phosphorylation: “chemical preconditioning”. J Cereb Blood Flow Metab 17: 257–264
Nandagopal K, Dawson TM, Dawson VL (2001) Critical role for nitric oxide signaling in cardiac and neuronal ischemic preconditioning and tolerance. J Pharmacol Exp Ther 297: 474–478
Schaller B, Graf R (2002) Cerebral ischemic preconditioning: An experimental phenomenon or a clinical important entity of stroke prevention? J Neurol 249: 1503–1511
Andoh T, Chock PB, Chieueh CC (2002) Preconditioning-mediated neuroprotection: role of nitric oxide, cGMP, and new protein expression. Ann NY Acad Sci 962: 1–7
Truettner J, Busto R, Zhao W, Ginsberg MD, Perez-Pinzon MA (2002) Effect of ischemic preconditioning on the expression of putative neuroprotective genes in the rat brain. Brain Res Mol Brain Res 103: 106–115
Honkaniemi J, Massa SM, Breckinridge M, Sharp FR (1996) Global ischemia induces apoptosis-associated genes in hippocampus. Brain Res Mol Brain Res 42: 79–88
Shimazaki K, Ishida A, Kawai N (1994) Increase in Bd-2 oncoprotein and the tolerance to ischemia-induced neuronal death in the gerbil hippocampus. Neurosci Res 20: 95–99
Nakase H, Heimann A, Uranishi R, Riepe MW, Kempski 0 (2000) Early-onset tolerance in rat global cerebral ischemia induced by a mitochondrial inhibitor. Neurosci Lett 290: 105–108
Brambrink AM, Noppens R, Dick WF, Heimann A, Kempski 0 (1998) 3-nitropropionic acid (3-NPA) induces tolerance against global brain ischemia in rats. Abstr Soc Neurosci 24:253 (abst)
Oltvai ZN, Milliman CL, Korsmeyer SJ (1993) Bd-2 heterodimerizes in vivo with a conserved homolog, bax, that accelerates programmed cell death. Cell 74: 609–619
Krajewski S, Mai J, Krajewska M, Sikorska M, Mossakowski M, Reed J (1995) Upregulation of Bax protein levels in neurons following cerebral ischemia. J Neurosci 15: 6364–6376
Martinou J, Dubois-Dauphin M, Staple JK, et al (1994) Overexpression of bd-2 in trans-genic mice protects from naturally occurring cell death and experimental ischemia. Neuron 13: 1017–1030
Niwa M, Hara A, Iwai T (1997) Expression of Bax and Bd-2 protein in the gerbil hippo-campus following transient forebrain ischemia and its modification by phencyclidine. Neurology Res 19: 629–633
Zhu Y, Prehn JHM, Culmsee C, Krieglstein J (1999) The beta2-adrenoceptor agonist clenbuterol modulates Bd-2, Bcl-xl and Bax protein expression following transient forebrain ischemia. Neuroscience 90: 1255–1263
Dubal DB, Shughrue PJ, Wilson ME (1999) Estradiol modulates bd-2 in cerebral ischemia: a potential role for estrogen receptors. J Neurosci 19: 6385–6393
Antonawich FJ, Federoff HJ, Davis JN (1999) Bd-2 transfection, using a herpes simplex virus amplicon, protects hippocampal neurons from transient global ischemia. Exp Neurol 156: 130–137
Abe H, Nowak TS Jr (1996) Gene expression and induced ischemic tolerance following brief insults. Acta Neurobiol Exp (Warsz) 56: 3–8
Kawahara N, Croll SD, Wiegand SJ, Klatzo I (1997) Cortical spreading depression induces long-term alteration of BDNF levels in cortex and hippocampus distinct form lesion effects: implications for ischemic tolerance. Neurosci Res 29: 37–47
Ide T, Takada K, Qiu JH, et al (1999) Ubiquitin stress response in postischemic hippocampal neurons under nontolerant and tolerant conditions. J Cereb Blood Flow Metab 19: 750756
Yamaguchi K, Yamaguchi F, Miyamoto O, Hatase O, Tokuda M (1999) The reversible change of GluR2-RNA editing in gerbil hippocampus in course of ischemic tolerance. J Cereb Blood Flow Metab 19: 370–375
Kato H, Liu Y, Araki T (1991) Temporal profile of the effects of pretreatment with brief cerebral ischemia on the neuronal damage following secondary ischemic insult in the gerbil: cumulative damage and protective effects. Brain Res 553: 238–242
Garcia-Ruiz C, Colell A, Morales A, Koplowitz N, Fernandez-Checa JC (1995) Role of oxidative stress generated from the mitochondrian electron transport chain and mitochondrial glutathion status in loss of mitochondrial function and activation of transcription factor-kappa B: studies with isolated mitochondria and rat hepatocytes. Mol Pharmacol 48: 825–834
Hockenberry DM, Oltvai ZN, Yin XM, Milliman CL, Korsmeyer SJ (1993) Bd-2 functions in an antioxidant pathway to prevent apoptosis. Cell 75: 241–251
Ellerby HM, Martin SJ, Ellerby LM, et al (1997) Establishment of a cell-free system of neuronal apoptosis: comparison of premitochondrial, mitochondrial, and postmitochondrial phases. J Neurosci 17: 6165–6178
Zamzami N, Brenner C, Marzo I, Susin SA, Kroemer G (1998) Subcellular and submitochondrial mode of action of bd-2 like oncoproteins. Oncogene 16: 2265–2282
Jürgensmeier JM, Xie Z, Deferaux Q, Ellerby L, Bredesen D, Reed JC (1998) Bax directly induces release of cytochrome c from isolated mitochondria. Proc Natl Acad Sci USA 95: 4997–5002
Paschen W, Doutheil J (1999) Disturbances of the functioning of endoplasmatic reticulum: a key mechanism underlying neuronal cell injury? J Cereb Blood Flow Metab 19: 1–18
Zha J, Harada H, Yang E, Jockel J, Korsmeyer SJ (1996) Serine phosphorylation of death agonist BAD in response to survival factor results in binding to 14–3–3 not BCL–X(L). Cell 87: 619 – 628
Chen J, Graham SH, Nakayama M, et al (1997) Apoptosis repressor genes bd-2 and bd-xlong are expressed in the rat brain following global ischemia. J Cereb Blood Flow Metab 17: 2–10
Shamloo M, Wieloch T (1999) Changes in protein tyrosine phosphorylation in the rat brain after cerebral ischemia in a model of ischemic tolerance. J Cereb Blood Flow Metab 19: 173–183
Perez-Pinzon MA, Mumford PL, Carranza V (1998) Calcium influx from the extracellular space promotes NADH hyperoxidation and electrical dysfunction after anoxia in hippocampal slices. J Cereb Blood Flow Metab 18: 215–221
Carriedo SG, Sensi SL, Yin HZ, Weiss JH (2000) AMPA exposures induce mitochondrial Cat+ overload and ROS generation in spinal motor neurons in vitro. J Neurosci 20: 240–250
Ohtsuki T, Matsumoto M, Kuwabara K, et al (1992) Influence of oxidative stress on induced tolerance to ischemia in gerbil hippocampal neurons. Brain Res 599: 246–252
Wang X, Li X, Erhardt JA, Barone FC, Feuerstein GZ (2000) Detection of tumor necrosis factor-a mRNA induction in ischemic brain tolerance by means of real time polymerase chain reaction. J Cereb Blood Flow Metabol 20: 15–20
Brambrink AM, Diehl K, Heimann A, Riepe MW, Kempski O (2000) Erythromycin induces tolerance against cerebral ischemia in rats. Abstr Soc Neurosci 26: 266 (abst)
Korner IP, Kempski O, Brambrink AM (2002) Pharmacological preconditioning: effects of erythromycin pretreatment on expression of bd-2 mRNA in rat brain. Anesthesiology 97: A803 (abst)
Brambrink AM, Schneider A, Noga H, et al (2000) Tolerance-inducing dose of 3-nitropropionic acid modulates bd-2 and bax balance in the rat brain: a potential mechanism of chemical preconditioning. J Cereb Blood Flow Metab 20: 1425–1436
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 2003 Springer-Verlag Berlin Heidelberg
About this paper
Cite this paper
Brambrink, A.M., Körner, I.P. (2003). Induction of Ischemic Tolerance in the Brain: A Novel Neuroprotective Strategy?. In: Vincent, JL. (eds) Intensive Care Medicine. Springer, New York, NY. https://doi.org/10.1007/978-1-4757-5548-0_67
Download citation
DOI: https://doi.org/10.1007/978-1-4757-5548-0_67
Publisher Name: Springer, New York, NY
Print ISBN: 978-1-4757-5550-3
Online ISBN: 978-1-4757-5548-0
eBook Packages: Springer Book Archive