| Literature DB >> 18219260 |
Abstract
Ischemic brain damage can be prevented or at least significantly reduced when there is a preceding brief ischemic period that does not exceed the threshold for tissue damage--a phenomenon termed "ischemic preconditioning" (ischemic PC). Experimental PC in rodents is now considered to be a model for transient ischemic attacks in humans, and there is increasing hope for translating the knowledge of underlying mechanisms in the animal models into the clinic to enhance endogenous neuroprotective mechanisms in patients with stroke. However, although PC was originally defined as a subtoxic stimulus without any morphologic damage, there is a growing body of evidence from studies using sensitive techniques that postischemic structural alterations of brain tissue manifest not only after ischemia with prior PC but also after the PC stimulus itself. Furthermore, it has become evident over time that the primary shortcomings of many experimental studies on PC are the short observation intervals. The few studies with extended postischemic survival periods done to date provide clear evidence of considerable structural changes and even cell death, which may only be postponed by PC. Therefore, further studies are needed to elucidate structural long-term changes after PC and to validate the persistence of the neuroprotective effects.Entities:
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Year: 2008 PMID: 18219260 DOI: 10.1097/nen.0b013e3181630ba6
Source DB: PubMed Journal: J Neuropathol Exp Neurol ISSN: 0022-3069 Impact factor: 3.685