[Ischemic preconditioning in the brain].
Stroke-related death is the third most common cause of mortality in Hungary after cardiovascular diseases and cancer. In addition to the unfavourable mortality figures, the consequent development of neurological and psychiatric disorders in stroke patients imposes an enormous burden on the health care system and on the families. Numerous studies are being conducted world wide on the prevention of stroke and other cerebrovascular disorders like chronic hypoperfusion, as well as on acute stroke management and patient rehabilitation issues. As a result, our understanding of the mechanism of hypoxic brain damage steadily increased over the past years and decades which brought along promising achievements both in the field of stroke prevention and therapy. However, these broad-spectrum approaches also made clear that preventing neuronal death and thus reducing neurological damage are complex tasks that cannot be successfully resolved by targeting single mechanisms. Therefore, the development of alternative new drugs and clinically applicable complex neuroprotective strategies is warranted. One of the most promising approaches is to create ischemic tolerance in the brain by using pharmacological preconditioning paradigms. These drugs trigger similar events to those initiated by brief ischemic insults that later can make the cerebral tissue resistant to subsequent otherwise lethal stress (ischemic preconditioning).
Nagy
Krisztina
K
Szegedi Tudományegyetem, Elettani Intézet, Szeged.
Domoki
Ferenc
F
Bari
Ferenc
F
D000818:Animals; D000992:Antitoxins / Q000378:metabolism; D017209:Apoptosis; D001921:Brain / Q000187:drug effects* / Q000378:metabolism / Q000503:physiopathology; D002545:Brain Ischemia / Q000139:chemically induced* / Q000378:metabolism / Q000503:physiopathology; D002560:Cerebrovascular Circulation; D006360:Heat-Shock Proteins / Q000378:metabolism; D006801:Humans; D006814:Hungary / Q000453:epidemiology; D002534:Hypoxia, Brain / Q000139:chemically induced* / Q000378:metabolism / Q000503:physiopathology; D018836:Inflammation Mediators / Q000378:metabolism; D019194:Ischemic Preconditioning / Q000379:methods*; D020521:Stroke / Q000401:mortality / Q000503:physiopathology / Q000517:prevention & control*
D000992:Antitoxins; D006360:Heat-Shock Proteins; D018836:Inflammation Mediators