Artru, Alan A.

There are conflicting reports regarding the effects of hypoxemia on the cerebral metabolic rate for oxygen (CMRO 2 ). Accordingly, we examined the changes in CMRO 2 during normoxia, progressive hypoxia (P a O 2 of 37, 27, and 23 mm Hg), and normoxic recovery from hypoxia, Measurements were made in dogs anesthetized with nitrous oxide (60–70%) and halothane (<0.1%) in oxygen. Arterial-cerebral venous blood oxygen content differences and cerebral blood flow (CBF) were measured simultaneously, the latter by a technique (collection of sagittal sinus outflow) previously validated for conditions of near-maximal CBF, The duration of each of the three hypoxic exposures was approximately 10 min. CMRO 2 was significantly decreased (14%) only when the arterial blood oxygen tension was reduced to 23 mm Hg. CBF increased progressively to a maximum of 153% of control. Posthypoxemic brain biopsy values for cerebral metabolites obtained 40 min after normoxemia had been restored were normal. These results, in conjunction with an unchanged CMRO 2 at 40 min normoxic recovery, suggest that no gross irreversible brain cell damage occurred. We conclude that with progressive hypoxemia. CMRO 2 remains stable until oxygen demand exceeds oxygen delivery, resulting there after in a progressive reduction in CMRO 2 .