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Ion Homeostasis in Rat Brain in vivo: Intra- and Extracellular [Ca2+] and [H+] in the Hippocampus during Recovery from Short-Term, Transient Ischemia
Abstract
Changes in intra- and extracellular [Ca 2+] and [H+], together with alterations in tissue Po 2 and local blood flow, were measured in areas CA 1 and CA 3 of the hippocampus during recovery (up to 8 h) after an 8-min period of low-flow ischemia. Restoration of blood supply was followed by an immediate rise in flow and tissue Po 2 above normal, with large fluctuations in both persisting for up to 4 h. In area CA 1, [Ca 2+]i decreased rapidly from an ischemic mean value of 30 μ M to a control mean level of 73.1 n M in 20–30 min, whereas normalization of [Ca 2+]e took ∼1 h. Recovery of [Ca 2+]i was accelerated by preischemic administration of a calcium antagonist, nifedipine, and a free radical scavenger, N-tert-butyl-α-phenylnitrone (PBN), but not by MK-801, a blocker of N-methyl-d-aspartate receptors. There was a secondary rise in [Ca 2+]i in many cells beginning ∼2 h after reperfusion. This was attenuated somewhat by PBN but not clearly influenced by either nifedipine or MK-801. Changes of [Ca 2+]i in area CA 3 were much smaller and slightly slower than in area CA 1 and were not affected by the drugs mentioned above. In both areas CA 1 and CA 3, pH e and pH i fell during ischemia to an average value of 6.2, from which there was a rapid initial recovery in the first 5–10 min when blood flow was restored. Thereafter tissue pH rose slowly and did not reach control levels for ∼1 h, and in some microareas not at all. It is concluded that (a) effective mechanisms for restoring normal [Ca 2+]i remain intact after 8 min of low-flow ischemia; (b) in neurons of area CA 1, some insidious change in the homeostasis of calcium triggers a secondary rise in its free cytosolic concentration, which may be causally related to activation of irreversible cell damage; and (c) the changes in [Ca 2+]i and [Ca 2+]e during and following 8 min of ischemia can be adequately accounted for by movements of a fixed pool of Ca between intra- and extracellular compartments, and possible mechanisms are discussed.
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Tissue oxygen tension and brain sensitivity to hypoxia
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Self-citation
Metadata
- Authors
- Silver, I. A., & Erecińska, M.
- Venue
- Journal of Cerebral Blood Flow & Metabolism
- Publisher
- SAGE Publications
- Published
- 1992-09
- Volume
- 12
- Issue
- 5
- Pages
- 759-772
- ISSN
- 0271-678X (ISSN-L)
- 1559-7016
- OpenAlex
- W1969778094
- Cited by
- 233
- References
- 1
- FWCI
- 7.24
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- journals.sagepub.com/page/policies/text-and-data-mining-license (tdm)
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