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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Experimental brain research 2 (1966), S. 176-190 
    ISSN: 1432-1106
    Keywords: Brain ; CSF ; Bicarbonate ; Acidosis ; Alkalosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Changes in the bicarbonate and the chloride concentrations in the brain, as well as in the bicarbonate concentration of the cisternal cerebrospinal fluid (CSF), were measured in rats made acidotic or alkalotic for a period of 6 hours by means of intraperitoneal injections of acid and basic solutions. The difference in the plasma chloride concentrations between the acidotic and the alkalotic groups was 8.6 mEq/l, while the corresponding difference in the tissue concentrations was 4.5 mEq/kg of wet tissue. These results demonstrate that the chloride ion equilibrated between the plasma and the “chloride space” of the brain tissue under the conditions of the experiments. However, although the marked difference in the plasma bicarbonate concentrations between the same groups (17.4 mEq/l) was accompanied by a difference in the CSF bicarbonate concentrations of 7.6 mEq/kg, there were no significant differences in the actual tissue bicarbonate concentrations, attributable to the extracellular bicarbonate changes. Provided that CSF is representative of the extracellular fluid (ECF), these results can either be interpreted to show that the bicarbonate of the ECF is distributed in a very small tissue compartment (probably less than 5 per cent of the tissue volume), or that nonrespiratory acid-base changes are not accompanied by net fluxes of bicarbonate ions between the plasma and the extracellular space of the brain tissue but rather by redistributions of bicarbonate ions between extra-and intracellular fluids.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Experimental brain research 104 (1995), S. 462-466 
    ISSN: 1432-1106
    Keywords: Transient ischemia ; Extracellular calcium ; Acidosis ; Brain ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The object of the study was to find out how preischemic hyperglycemia (in normocapnic animals) or excessive hypercapnia (in normoglycemic animals) affect the calcium transient during ischemia, as this can be assessed by measurements of the extracellular calcium concentration ([Ca2+]e). To that extent, normocapnic-normoglycemic control animals were compared with animals with induced hyperglycemia or hypercapnia, all being subjected to 10 min of forebrain ischemia, the [Ca2+]e and d.c. potential being measured with ion-sensitive glass microelectrodes. Hyperglycemia and hypercapnia delayed the loss of ion homeostasis following induction of ischemia. Furthermore, both hyperglycemia and hypercapnia reduced the delay of Ca2+ extrusion upon recirculation. As a result, both hyperglycemia and hypercapnia significantly reduced the ischemic calcium transient, as this was assessed by calculating the duration of maximal calcium load of cells. The results make it less likely that aggravation of brain damage by hyperglycemia or excessive hypercapnia is related to a further derangement of cell calcium homeostasis.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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