Oxygen tension, oxygen metabolism, and microcirculation in vasogenic brain edema.

In cold brain injury edema, cerebral pO2, oxygen metabolism, and local CBF were investigated. In randomized groups of 10 rats each, pO2 was measured by polarography using a balanced multiwire surface electrode on the parietal cortex after trepanation. lCMRO2 was approximated by oxygen disappearance rate after sudden complete cerebral circulatory arrest (cervical cuff inflation). Using integrated platinum electrodes, the local CBF was measured by H2 clearance. All data were evaluated on-line by computer. In normal animals we found a regular, normally distributed pO2 histogram in barbiturate and in ketamine anesthesia. Oxygen consumption and local CBF, however, are significantly higher in ketamine narcosis. The local CBF is thereby coupled with metabolic requirements: The more oxygen consumed, the higher the local pO2. In animals 24 hr after cold brain injury, this metabolic coupling is disturbed: In the perifocal edema the pO2 histogram is flat and broad with different mean and median, but with a shifting toward higher oxygen values. Oxygen consumption is reduced; the local CBF, however, is significantly increased with large variations. Also over the contralateral, noninjured hemisphere a decrease in CMRO2 and an increase in pO2 are observed (diachisis). These disturbances with a maximum at 24 hr after injury show a recovery after 72 hr. After infusion of the calcium entry blocker nimodipine a normalization in pO2 distribution was found, combined with an increase in CMRO2. We assume a primary disturbance of oxidative glucose metabolism with uncoupling of metabolic flow control; local CBF and O2 availability are not primarily impaired. Ca2+ may be a main factor in this pathophysiology.