The Relation Between Cerebral Oxygen Consumption and Cerebral Vascular Reactivity to Carbon Dioxide
The mechanisms whereby CO2 affects cerebral vessels are not as simple as once thought,1, 2 and are probably both directly on cerebral vascular walls3, 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 PaCOCO2 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 PaCOCO2 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 PaCOCO2 is influenced by cerebral oxygen consumption.
- brain stem neurones
- autonomic pathways
- cerebral anaerobic metabolism
- I181 iodo-antipyrine
- senile dementia
- cerebral seizures
- © 1971 American Heart Association, Inc.