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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The interconnections between EEG, intermediary and energy metabolism of the brain cortex and CSF potassium level are studied during severe hypercapnia in anaesthetized, artificially ventilated cats. Hypercapnic animals were ventilated with 40 to 50% to CO2 in oxygen. During severe hypercapnia the EEG becomes isoelectric. The CSF potassium concentration is raised and the changes in metabolism suggest an acidosis-induced inhibition of phosphofructokinase and, probably, of hexokinase. The energy charge potential remains unchanged whereas the cortical ATP concentration increases slightly. It is assumed that the changes in P-creatine and creatine levels are related to the pH-dependency of creatine phosphokinase. Recovery animals were ventilated with 40% CO2 in O2 and subsequently with room air. After termination of CO2 inhalation the EEG reappears, the CSF potassium concentration normalizes, and the inhibition of the glycolytic enzymes disappears. The energy charge potential shows a small decrease. It is not possible to trace back the disappearance of the EEG to only one of the recorded parameters. Cortical P-creatine levels, CSF potassium concentration, changes in membrane permeability and cortical amino acid concentrations are considered in this context.
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PMID:Influence of severe hypercapnia upon cerebral cortical metabolism, CSF electrolyte concentrations and EEG in the cat. 13 59

The physiological application of amperometric adenosine triphosphate (ATP) microbiosensors for characterizing the stimulus-response at rat carotid bodies superfused with high potassium concentrations, during normoxic hypercapnia, and during hypoxia is demonstrated using the peripheral arterial chemoreceptors in the carotid body of rats as a model system. Amperometric microbiosensors based on glucose oxidase (GOD) and hexokinase (HEX) immobilized within a polymer matrix at the surface of Pt disk microelectrodes (diameter: 25 microm) are positioned at a distance of approximately 100 microm above the carotid body surface for detecting extracellular ATP. A linear calibration function of ATP microbiosensors in the physiologically relevant concentration range of 0-40 microM ATP enables quantitative detection of ATP released at the carotid body surface in response to physiological stimuli. It is shown that these stimuli induce extracellular ATP release from the carotid body at levels of 4-10 microM. Other electroactive neurotransmitters such as, e.g., catecholamines are coreleased by the carotid body at hypercapnic, hypoxic and high-potassium stimulus, are simultaneously detected utilizing a dual-electrode assembly with an ATP microbiosensor and a second bare channel providing a colocalized reference measurement for ATP quantification.
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PMID:Amperometric ATP microbiosensors for the analysis of chemosensitivity at rat carotid bodies. 1845 10