Canine cerebral metabolism and blood flow during hypoxemia and normoxic recovery from hypoxemia.

There are conflicting reports regarding the effects of hypoxemia on the cerebral metabolic rate for oxygen (CMRO2). Accordingly, we examined the changes in CMRO2 during normoxia, progressive hypoxia (PaO2 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 (less than 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. CMRO2 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 CMRO2 at 40 min normoxic recovery, suggest that no gross irreversible brain cell damage occurred. We conclude that with progressive hypoxemia, CMRO2 remains stable until oxygen demand exceeds oxygen delivery, resulting thereafter in a progressive reduction in CMRO2.