Abstract
Normal compensatory mechanisms protect the central nervous system (CNS) from moderate hypoxia and ischemia; however, after more severe ischemia progressive brain hypoperfusion ensues and irreversible damage occurs. Ischemic brain injury remains greatly significant clinically and elucidating the determinants of ischemic neuronal injury and death continues to challenge researchers. Although altered perfusion and decreased energy charge may contribute to the production of irreversible damage, the distribution of lesions seen after insult does not correspond with the degree of ischemic blood flow impairment, nor can neuronal energy deprivation explain the cell damage. Other factors, such as derangements in astrocyte function, calcium homeostasis, free radical metabolism, acid-base regulation and excitatory neurotransmitters also probably mediate ischemic neuronal death. Continued investigation to establish the cellular pathophysiology of cerebral ischemia can guide rational research and therapeutic strategies.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 149-169 |
| Number of pages | 21 |
| Journal | Resuscitation |
| Volume | 15 |
| Issue number | 3 |
| DOIs | |
| State | Published - Sep 1987 |
Bibliographical note
Funding Information:*This paper was supported in part by an ACEP research scholar grant awarded by the Emergency Medicine Foundation. **To whom reprint requests should be sent at: Department of Emergency Medicine, University of Cincinnati Medical Center, Cincinnati, OH 45267-0769, U.S.A.
Keywords
- Calcium overload
- Cerebral ischemia
- Excitotoxins
- Free radical generation
- Ischemic cell damage
- Lactic acidosis