Canine Cerebral Metabolism and Blood Flow during Hypoxemia and Normoxic Recovery from Hypoxemia

Abstract

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 (P_aO₂ 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 (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 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 there after in a progressive reduction in CMRO₂.