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(Stroke. 1971;2:251.)
© 1971 American Heart Association, Inc.

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The Relation Between Cerebral Oxygen Consumption and Cerebral Vascular Reactivity to Carbon Dioxide

MASATOSHI FUJISHIMA M.D.¹; PERITZ SCHEINBERG M.D.²; RAUL BUSTO B.S.²; OSCAR M. REINMUTH M.D.²

¹ Department of Neurology, University of Miami School of Medicine, Miami, Florida, 33152; Second Department of Internal Medicine, Kyushu University School of Medicine, Fukuoka, Japan
² Department of Neurology, University of Miami School of Medicine, Miami, Florida, 33152

The mechanisms whereby CO₂ affects cerebral vessels are not as simple as once thought,^{1, 2} and are probably both directly on cerebral vascular walls^{3, 4} and indirectly by action on brain stem neurones.⁵ Furthermore, cerebral vascular reactivity to CO₂ has been reported to be altered by a number of physiological and pathological circumstances. The capacity to dilate to increased Pa_COCO2 is decreased in cerebral vascular lesions,^6-8 and is affected by changes in cerebral perfusion pressure.⁹ Cervical sympathectomy is said to increase CBF response to Pa_COCO2 changes, whereas sympathetic nerve stimulation abolishes reactivity to CO₂.¹⁰ Deep anesthesia, hypothermia, or trauma to brain reduces reactivity to cerebral vessels to CO₂, the one common denominator for these states being reduced cerebral metabolism. This report demonstrates that the capacity of cerebral vessels to dilate or constrict in response to changes in Pa_COCO2 is influenced by cerebral oxygen consumption.

Key Words: brain stem neurones • autonomic pathways • cerebral anaerobic metabolism • I¹⁸¹ iodo-antipyrine • senile dementia • cerebral seizures

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