The effects of hypoxic hypoxia on cerebral hemodynamics and somatosensory evoked potential (SEP) were studied in 10 pentobarbital anestheteized dogs. Cerebral blood flow (CBF) was measured using the venous outflow technique and cerebral oxygen consumption (CMRO2) was calculated from the arterio‐cerebro‐venous oxygen difference times CBF. SEP was evaluated by percutaneous stimulation of an upper extremity nerve and was recorded over the contralateral somatosensory cortex. The latencies of the initial negative wave (Nl), second positive wave (P2) and the amplitude of the primary complex (P1N1) were measured. Animals were breathed sequentially with oxygen concentrations of 21,10, 6, 5, and 4.5% for five minutes each. Animals were returned to room air breathing when the amplitude of the SEP decreased to < 20% of control and were observed for 30 minutes following reoxygenation. Severe hypoxia (4.5% O2) increased CBF to 200% of control, decreased CMRO2to 45% of control, decreased amplitude and increased latency of SEP. Following reoxygenation, as CMRO2increased toward control, latency of SEP decreased and amplitude increased and CBF returned to baseline within 30 min. During hypoxia and reoxygenation, the latencies of Nl and P2and the amplitude of P1N1 were correlated with CMR02in individual animals. We conclude that changes in SEP amplitude and latency reflect changes in CMRO2despite high CBF during rapidly progressive hypoxic hypoxia and following reoxygenation.