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Differential near infrared spectrophotometry was used to monitor sequential in vivo alterations in cerebral hemoglobin saturation, blood volume, and cytochrome c oxidase reduction/oxidation responses during and after a period of incomplete transient ischemia (acute, reversible common carotid artery occlusion). In this study the rat brain was monitored non-invasively in the intact skull by transillumination. The data show that an increase in cerebral deoxygenation of hemoglobin, which occurs simultaneously with a decrease in blood volume subsequent to carotid ligation, acts as a compensatory mechanism to assist in maintaining aerobic energy metabolism. The observations also demonstrate that in this species the effects of bilateral carotid occlusion on the cerebrovascular parameters are not necessarily irrevocable. The intramitochondrial metabolic alterations, as evaluated by cytochrome c oxidase redox transitions, are reversible as long as the systemic arterial blood pressure does not fall below a value of approximately 40 mm Hg. These data suggest that possibility of being able to use a critical reduction level of cytochrome c oxidase as an early indication of ischemia-induced cerebral metabolic dysfunction prior to major changes in high energy stores.

Incomplete transient ischemia: a non-destructive evaluation of in vivo cerebral metabolism and hemodynamics in rat brain.