Weiss H R, Buchweitz E, Sinha A K
Microvasc Res. 1983 Mar;25(2):194-204. doi: 10.1016/0026-2862(83)90015-8.
The effect of hypoxic-hypocapnia (PaO2, 35 mm Hg, PaCO2, 22 mm Hg) on regional cerebral O2 consumption and supply was determined in 18 alpha-chloralose-anesthetized open-chest adult cats. Regional arterial and venous O2 saturation measurements determined by a microspectrophotometric technique were combined with regional flow measurements by the radioactive microsphere method to calculate cerebral regional O2 consumption. In a control group, after blood flow was determined with 15 +/- 3-microns-diameter microspheres, the heads were quick-frozen and measurements of flow and arterial-venous O2 differences were obtained from nine brain regions. In the experimental group, similar measurements were obtained after the induction of hypoxic-hypocapnia. Cerebral blood flow was significantly lower than the control group during hypocapnia. Cerebral blood flow increased with the induction of hypoxia. Arterial and venous O2 saturation decreased uniformly and to the same extent in the nine examined brain regions. This maintained the arterial-venous O2 saturation difference. O2 extraction and consumption were unaffected. The brain O2 supply/consumption ratio was maintained during hypoxic-hypocapnia indicating adequate and uniform protection in this condition throughout the brain.
