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Evolving Concepts About the Role of Acidosis in Ischemic Neuropathology
Abstract
Abstract: Cerebral ischemia is one of the most common neurological insults. Many pathological events are undoubtedly triggered by ischemia, but only recently has it become accepted that ischemic cell injury arises from a complex interaction between multiple biochemical cascades. Tissue acidosis is a well established feature of ischemic brain tissue, but its role in ischemic neuropathology is still not fully understood. Within the last few years, new evidence has challenged the historically negative view of acidosis and suggests that it may play more of a beneficial role than previously thought. This review reintroduces the concept of acidosis to ischemic brain injury and presents some new perspectives on its neuroprotective potential.
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Citations
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Kauer, J. A., Malenka, R. C., & Nicoll, R. A. (1988) · Nature · doi:10.1038/334250a0 · Cited by 423
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Ischemic Cell Death in Brain Neurons
Lipton, P. (1999) · Physiological Reviews · doi:10.1152/physrev.1999.79.4.1431 · Cited by 3,043
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Kristián, T., & Siesjö, B. K. (1998) · Stroke · doi:10.1161/01.str.29.3.705 · Cited by 825
Stress, Glucocorticoids, and Damage to the Nervous System: The Current State of Confusion
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Metadata
- Authors
- Tombaugh, G. C., & Sapolsky, R. M.
- Venue
- Journal of Neurochemistry
- Publisher
- Wiley
- Published
- 1993-09
- Volume
- 61
- Issue
- 3
- Pages
- 793-803
- ISSN
- 0022-3042 (ISSN-L)
- 1471-4159
- OpenAlex
- W2089229290
- Cited by
- 188
- References
- 1
- FWCI
- 4.74
- Type
- journal article
- Language
- en
- Open access
- closed
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- Tombaugh, G. C., & Sapolsky, R. M. (1993). Evolving Concepts About the Role of Acidosis in Ischemic Neuropathology. Journal of Neurochemistry. https://doi.org/10.1111/j.1471-4159.1993.tb03589.x
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.