The neuroprotective effect of epidural cooling before and during spinal cord ischemia on the neurological, neurophysiological, and histopathological outcome was evaluated after 40 min of proximal and distal thoracic aorta crossclamping in dogs. In the normothermic group (n = 12), no attempt was made to change the spinal cord temperature. Four of eight animals showed complete paraplegia and four had partial recovery. The N3 component of spinal somatosensory-evoked potentials recovered to only 11.7 +/- 1.4% after 2 hr of recirculation and to 45% of control value after 2 days of survival. In the transverse sections taken from L1-L7 segments, apparent interneuronal damage in the intermediate zone was found after 2 hr of reperfusion followed by a heavy loss of interneurons after 2 days of survival and functionally defined as fully developed paraplegia. In the hypothermic group (n = 12), the spinal cord temperature was lowered 3 min before aortic crossclamping with a bolus of epidurally administered 0.9 N saline solution (8 ml/kg at 5 degrees C) to 28.5 +/- 1.3 degrees C and was maintained throughout the crossclamping time with the additional infusion of the same solution (20 ml/kg/40 min) using a peristaltic pump. Seven of eight animals had no neurological deficit and one animal showed partial recovery, which was significantly better than the motor score for the normothermic group (P < 0.05). The SSEP revealed 55% of postsynaptic (N3) wave recovery after 2 hr of recirculation and 92% recovery after 2 days survival, which was significantly higher than those for the normothermic animals (P < 0.05). Histological analysis showed almost full protection of interneurons and A-motoneurons verified after 2 hr and 2 days, respectively. We conclude that spinal cord epidural cooling has a highly protective effect against ischemic spinal cord damage under experimental conditions of high thoracic aorta crossclamping in dogs.