BACKGROUND Paraplegia is a known complication after surgery on the descending thoracic aorta. Thoracic aortic cross-clamping causes an increase in proximal aortic and cerebrospinal fluid pressures. Sodium nitroprusside, though effectively decreasing proximal aortic pressure, has been implicated in worsening the incidence of paraplegia by further increasing cerebrospinal fluid pressure and decreasing distal blood pressure, thereby reducing spinal cord perfusion pressure. Intravenous administration of magnesium sulfate has been shown to offer some spinal cord protection when used with mild hypothermia. This study investigated the effect of intrathecal magnesium on the prevention of paraplegia when sodium nitroprusside is used to control proximal hypertension during thoracic aortic cross-clamping in a dog model of spinal cord ischemia. METHODS Two groups of eight dogs underwent thoracic aortic cross-clamping via a small thoracotomy incision for 45 min. Proximal, distal, and central venous pressures and cerebrospinal fluid pressures were monitored. Temperature was maintained at 36 degrees C. Sodium nitroprusside was used to control proximal hypertension. The control group received no magnesium sulfate, and a second group received 3 mg/kg intrathecal magnesium sulfate before thoracic aortic cross-clamping. The dogs were neurologically evaluated 24 h later by an observer blinded to the dogs' group. Spinal cord segments were obtained for histologic examination. RESULTS Proximal mean arterial pressure, cerebrospinal fluid pressure, spinal cord perfusion pressure, and central venous pressure were not statistically different between the two groups. Neurologic outcome, however, was statistically different between the groups. None of the eight dogs in the magnesium group had any measurable neurologic injury, in contrast to the control group, in which seven of the eight dogs had severe neurologic injury (P < 0.005). Post mortem histologic data supported these findings. CONCLUSIONS Intrathecal magnesium can prevent spinal cord injury despite markedly negative spinal cord perfusion pressure during thoracic aortic cross-clamping in a canine model of spinal cord ischemia.