&NA;The utility of evoked potentials in monitoring spinal cord and cerebral function in various neurosurgical and orthopedic operations has now been established. To study the effects of graded hypotension upon spinal and cortical somatosensory evoked potentials (SEPs), and spinal motor evoked potentials (SMEPs), 12 anesthetized cats were subjected to graded hypotension ranging from a mean arterial blood pressure of 100 mmHg to 30 mmHg or less. Hypotension causes a progressive increase in onset latency and a decrease in amplitude and conduction velocity of SEPs and SMEPs. Cortical SEPs and SMEPs were sensitive to profound hypotension (MAP < 30 mmHg). Spinal SEPs showed more resistance and disappeared at lower levels of hypotension. Immediate blood transfusion caused resumption of cortical SEPs and SMEPs within 30 minutes after infusion; however, the latency and amplitude of responses did not reach the baseline values within 1 hour after transfusion. The sequential recovery of evoked responses was dependent upon the length of hypotension. When 15 minutes elapsed between loss of responses and transfusion, cortical SEPs and SMEPs did not resume within 1 hour after infusion. No return of signals occurred if 30 minutes elapsed between the loss of evoked responses and blood reperfusion. These findings suggest that ischemia associated with profound systemic hypotension can alter or obliterate evoked responses. (Neurosurgery24:246‐252, 1989)