| pubmed-article:3082219 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:3082219 | lifeskim:mentions | umls-concept:C0007027 | lld:lifeskim |
| pubmed-article:3082219 | lifeskim:mentions | umls-concept:C0007786 | lld:lifeskim |
| pubmed-article:3082219 | lifeskim:mentions | umls-concept:C0392747 | lld:lifeskim |
| pubmed-article:3082219 | lifeskim:mentions | umls-concept:C0006353 | lld:lifeskim |
| pubmed-article:3082219 | lifeskim:mentions | umls-concept:C0205197 | lld:lifeskim |
| pubmed-article:3082219 | pubmed:issue | 3 Pt 2 | lld:pubmed |
| pubmed-article:3082219 | pubmed:dateCreated | 1986-4-18 | lld:pubmed |
| pubmed-article:3082219 | pubmed:abstractText | Simultaneous measurements of tissue PCO2 (PtCO2), interstitial H+ concentration ([H+]o), and tissue lactate content were used to examine changes in interstitial HCO3- concentration ([HCO3-]o) during complete ischemia. In normoglycemic rats (blood glucose of 6-8 mM; neocortical ischemic-induced lactate content 8-12 mmol/kg) [H+]o increased from 7.22 +/- 0.02 to 6.79 +/- 0.02 pH (n = 3). By contrast, in hyperglycemic rats (blood glucose 18-75 mM; ischemic-induced lactate content 19-31 mmol/kg) [H+]o rose by a significantly larger amount to 6.19 +/- 0.02 pH (n = 7). Given that HCO3- is the predominant interstitial H+ buffer, changes in peak PtCO2 show why peak [H+]o were bimodally distributed compared with lactate content. Between 8 and 12 mmol/kg lactate, when peak PtCO2 rose from 99 to 186 Torr but [H+]o was constant at 6.79 pH, calculated [HCO3-]o increased from 11.9 to 21.9 mM. Then after transitional changes, peak PtCO2 and [H+]o remained constant at 389 +/- 9 Torr (n = 7) and 6.19 pH despite the fact that tissue lactate ranged from 19 to 31 mmol/kg lactate, respectively; [HCO3-]o must have remained constant at 12.3 +/- 0.7 mM (n = 7). Since ischemic brain continued to produce another 12 more mmol/kg of lactic acid above 19 mmol/kg lactate without further changes in PtCO2 or [H+]o, H+ and HCO3- must have been heterogeneously compartmented. The continued lactic acid production occurred in a compartment that occupied 36% of neocortical space. This compartment is likely to represent glial cells. | lld:pubmed |
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| pubmed-article:3082219 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:3082219 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:3082219 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:3082219 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:3082219 | pubmed:issn | 0002-9513 | lld:pubmed |
| pubmed-article:3082219 | pubmed:author | pubmed-author:PulsinelliW... | lld:pubmed |
| pubmed-article:3082219 | pubmed:author | pubmed-author:PlumFF | lld:pubmed |
| pubmed-article:3082219 | pubmed:author | pubmed-author:KraigR PRP | lld:pubmed |
| pubmed-article:3082219 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:3082219 | pubmed:volume | 250 | lld:pubmed |
| pubmed-article:3082219 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:3082219 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:3082219 | pubmed:pagination | R348-57 | lld:pubmed |
| pubmed-article:3082219 | pubmed:dateRevised | 2011-8-1 | lld:pubmed |
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| pubmed-article:3082219 | pubmed:year | 1986 | lld:pubmed |
| pubmed-article:3082219 | pubmed:articleTitle | Carbonic acid buffer changes during complete brain ischemia. | lld:pubmed |
| pubmed-article:3082219 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:3082219 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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