[Cerebral ischemia tolerance].
Ischemic tolerance means a rapid adaptative cerebral reaction to one or more cycles of short ischemia and reperfusion, improving the tolerance to a subsequent longer ischemia. The basic molecular mechanisms of ischemic tolerance are largely unknown. The pathophysiological course can be divided in induction, transduction and tolerance. During induction NMDA- and adenosin receptors, free radicals and conservation of energy metabolism are required. Protein kinases, transcription factors, and immediate early genes play a role in transduction. Tolerance can be observed in different time windows. The early phase lasts for several hours after the preconditioning stimulus and can be related to adenosine receptors and ATP-dependent potassium channels. A delayed phase, after 1-7 days, is explained by genetic remodeling. Clinically, there is evidence for a protective effect of transient ischemic attacks occurring before stroke.
Schaller
B
B
Max-Planck-Institut für Neurologische Forschung, Köln. Bernhard.Schaller@pet.mpin-koeln.mpg.de
Graf
R
R
D002544:Cerebral Infarction / Q000235:genetics / Q000503:physiopathology*; D004734:Energy Metabolism / Q000235:genetics / Q000502:physiology; D005609:Free Radicals; D015870:Gene Expression / Q000502:physiology; D006706:Homeostasis / Q000235:genetics / Q000502:physiology; D006801:Humans; D002546:Ischemic Attack, Transient / Q000235:genetics / Q000503:physiopathology*; D019194:Ischemic Preconditioning; D015221:Potassium Channels / Q000235:genetics / Q000502:physiology; D016194:Receptors, N-Methyl-D-Aspartate / Q000235:genetics / Q000502:physiology; D018047:Receptors, Purinergic P1 / Q000235:genetics / Q000502:physiology; D014161:Transduction, Genetic
D005609:Free Radicals; D015221:Potassium Channels; D016194:Receptors, N-Methyl-D-Aspartate; D018047:Receptors, Purinergic P1