Effect of PaCOCO2 on Blood Flow and Microvasculature of Ischemic and Nonischemic Cerebral Cortex
The right middle cerebral artery (MCA) was occluded in cats; after subsequent craniectomy cortical blood flow (CBF) was measured bilaterally with 85Kr, and photographs of the superficial microvasculature were made. Ventilation was controlled, and PaCOCO2 was altered by changing the concentration of CO2 in the inspired air. In nonischemic cortex CBF varied as an exponential function of PaCOCO2, and the caliber of superficial arterial vessels (50 to 200µ in diameter) increased with increasing PaCOCO2. In ischemic cortex, changes of PaCOCO2 produced no change of CBF in six of ten animals studied within one day of occlusion; in four of these six, there was no change in the caliber of arterial vessels. In the four other animals of this group, there was a paradoxical response (an increase of PaCOCO2 produced a decrease of CBF of ischemic cortex), and in two of these four animals, there also was a paradoxical response of the caliber of arterial vessels. In eight animals allowed to survive 5 to 12 days after MCA occlusion, the arterial vessels of ischemic cortex regained some reactivity: a normal response of CBF to changes of PaCOCO2 was found in four, and appropriate changes of vessel caliber were found in all eight. The ischemia-induced impairment of the reactivity of cortical vessels to changes of PaCOCO2 casts doubt on the usefulness of CO2 inhalation for the treatment of strokes of humans.
- carbon dioxide inhalation
- cerebral circulation
- cerebral ischemia and infarction
- cerebral metabolites
- diffusible indicator methods
- experimental stroke
- isotope clearance methods
- regional cerebral blood flow
- Copyright © 1970 by the American Heart Association, Inc.