Carbonic acid buffer changes during complete brain ischemia
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 lact...
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ftpubmed:oai:pubmedcentral.nih.gov:2806331 2023-05-15T15:52:51+02:00 Carbonic acid buffer changes during complete brain ischemia KRAIG, RICHARD P. PULSINELLI, WILLIAM A. PLUM, FRED 1986-03 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2806331 http://www.ncbi.nlm.nih.gov/pubmed/3082219 en eng http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2806331 http://www.ncbi.nlm.nih.gov/pubmed/3082219 Article Text 1986 ftpubmed 2013-09-02T20:35:03Z 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. Text Carbonic acid PubMed Central (PMC) |
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Article KRAIG, RICHARD P. PULSINELLI, WILLIAM A. PLUM, FRED Carbonic acid buffer changes during complete brain ischemia |
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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. |
format |
Text |
author |
KRAIG, RICHARD P. PULSINELLI, WILLIAM A. PLUM, FRED |
author_facet |
KRAIG, RICHARD P. PULSINELLI, WILLIAM A. PLUM, FRED |
author_sort |
KRAIG, RICHARD P. |
title |
Carbonic acid buffer changes during complete brain ischemia |
title_short |
Carbonic acid buffer changes during complete brain ischemia |
title_full |
Carbonic acid buffer changes during complete brain ischemia |
title_fullStr |
Carbonic acid buffer changes during complete brain ischemia |
title_full_unstemmed |
Carbonic acid buffer changes during complete brain ischemia |
title_sort |
carbonic acid buffer changes during complete brain ischemia |
publishDate |
1986 |
url |
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2806331 http://www.ncbi.nlm.nih.gov/pubmed/3082219 |
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Carbonic acid |
genre_facet |
Carbonic acid |
op_relation |
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2806331 http://www.ncbi.nlm.nih.gov/pubmed/3082219 |
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1766387955990003712 |