Summary
This study has demonstrated a linear relationship between cerebral blood flow and arterial oxygen saturation (Sa02) in the cerebral biood flow response in the hypoxic range of Pa02 values, which we believe is documented for the first time. The cerebral blood flow increased 1.02 per cent for each percentage decrease in Sa02 in hypoxia induced with nitrogen. Hypoxia induced with nitrous oxide increased cerebral blood flow at the rate of 2.09 per cent for each one per cent decrease in Sa02 which was dramatically more than the increase associated with hypoxia induced with nitrogen. Increased survival rates at lower Sa02 levels suggested that nitrous oxide also exerts a protective effect on dog myocardium.
The mechanism by which hypoxia increases cerebral blood flow is unclear but the prevalent theory is one of neurogenic control which causes cerebral blood flow to increase as the intracellular hydrogen ion ([H+]I) increases in the progressive lactacidosis of hypoxia. The demonstration of a linear relationship between cerebral blood flow and Sa02 will provide the statistician, the researcher and the clinician with a useful tool for the neurophysiological assessment of cerebral blood flow.
Résumé
Cette étude démontre la relation linéaire qui existe entre le débit sanguin cérébral et la saturation artérielle oxyhémoglobinée (Sa02) lorsque le cerveau est perfusé par du sang hypoxémique. Le débit sanguin cérébral augmente de 1.02 pour cent pour chaque degré de diminution de 1 pour cent de la saturation dans ľhypoxie provoquée par ľazote, Lorsque ľhypoxie est provoquée par le protoxyde ďazote, ľaugmentation du débit cérébral a été beaucoup plus dramatique et s’est produite au rythme de 2.09 pour cent pour chaque point de baisse de la saturation. Ľaugmentation du taux de survie pour des saturations plus basses laisse croire que le protoxyde ďazote peut protéger le myocarde du chien contre ľhypoxie.
Le mécanisme qui cause ľaugmentation du débit sanguin cérébral pendant ľhypoxie est mal connu, la théorie la plus répandue étant celle du contrôle neurogène. Ce contrôle intervient sous ľeffet de ľaccumulation intracellulaire ďions hydrogène causée par ľacidose lactique de ľhypoxie. Cette démonstration de la relation linéaire existante entre le débit sanguin cérébral et la saturation oxyhémoglobinée fournira au statisticien, au chercheur et au clinicien un outil précieux pour ľévaluation neurophysiologique du débit sanguin cérébral.
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Stoyka, W.W., Frankel, D.Z.N. & Kay, J.C. The linear relation of cerebral blood flow to arterial oxygen saturation in hypoxic hypoxia induced with nitrous oxide or nitrogen. Canad. Anaesth. Soc. J. 25, 474–478 (1978). https://doi.org/10.1007/BF03007409
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DOI: https://doi.org/10.1007/BF03007409