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Effects of profound hypothermia and circulatory arrest on cerebral oxygen metabolism and cerebrospinal fluid electrolyte composition in dogs
53
Citations
22
References
1974
Year
Electrolyte DisorderOxygen MetabolismCerebral Vascular RegulationAnesthesiaHyperthermiaCerebrospinal FluidElectrolyte DisturbanceIntracranial PressureBrain InjuryNeurologyMetabolismHealth SciencesAnimal PhysiologyCerebral Blood FlowNervous SystemPotassium HomeostasisProfound HypothermiaNeurophysiologyPhysiologyTissue OxygenationElectrophysiologyNeuroscienceCentral Nervous SystemCerebral Oxygen MetabolismMedicineCirculatory Arrest
✓ Cerebral oxygen metabolism was studied in the dog at brain temperatures ranging from 37° to 8°C. As brain temperature decreased, the cerebral oxygen metabolism (CMRO 2 ) decreased following the Arrhenius equation. The natural logarithm of the CMRO 2 was a linear function of the reciprocal of the absolute (K) brain temperature. Oxygen metabolism, although much decreased, continued at very low brain temperatures. The CSF composition was unchanged after 1 hour at brain temperatures down to 10°C. Circulatory arrest for tolerable periods and longer caused changes only in the CSF potassium concentration. The interval between the onset of circulatory arrest and the beginning of the CSF K concentration increased with decreasing temperature and the rate of CSF K increase was increasingly slower at lower temperatures. At all temperatures the rate of CSF K changed gradually increased with time. The interval before the CSF K started to increase was dependent upon the amount of O 2 available in the brain and the length of this interval was inversely proportional to the CMRO 2 . The amount of CSF K concentration was not clearly related to the tolerable periods of circulatory arrest, but at normal temperatures an obviously increased CSF K following a period of acute cerebral anoxia without CSF hemorrhage may indicate brain damage.
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