Although somatosensory evoked potentials are being used in the evaluation of spinal cord injury and the monitoring of cord function during surgical procedures, their limitations in the face of fluctuations in blood pressure await further clarification. To study the effect of hypotension upon spinal cord blood flow (SCBF) and spinal evoked potentials (SEPs), we subjected five anesthetized lambs to graded hypotension to a mean arterial pressure (MAP) of 80, 60, 40, and less than or equal to 30 mm Hg. Five animals served as controls. Maximal hypotension was associated with a significant decrease in renal and sciatic nerve blood flow of 83% and 77%, respectively. SCBF, on the other hand, showed no decrease with hypotension down to a MAP of 40 mm Hg. As hypotension progressed, a gradual but significant slowing in nerve conduction velocity was noted without alteration in the cord conduction velocity from L7 to L1. Control animals demonstrated a decline in sciatic nerve blood flow of 48%, without any change in latency or amplitude of nerve action potentials. These findings suggest that, in hypotension, the peripheral nerve (lacking autoregulation) becomes ischemic, resulting in slowing of nerve conduction velocity with an increase in latency and decrease in amplitude of SEPs. Cord conduction velocity, on the other hand, remains unchanged. Caution is advised in relying upon SEPs generated by peripheral nerve stimulation to monitor cord function in situations where profound hypotension is anticipated. Variations in SEPs may reflect alterations in the peripheral nerve and not the spinal cord.