Mild
hypothermia and the 21-aminosteroids have both been neuroprotective in several models of
cerebral ischemia. In this study we compared the effects of mild
hypothermia and the 21-aminosteroid
U-74389G, alone and in combination on neurologic and histopathologic outcome after temporary
spinal cord ischemia. Forty male anesthetized New Zealand white rabbits were randomized to four groups (n = 10): (a) normothermia (control); (b)
U-74389G (3 mg/kg intravenously [i.v.] before aortic occlusion, 1.5 mg/kg i.v. and 10 mg/kg intraperitoneally after occlusion); (c) mild
hypothermia (4 degrees C epidural temperature decrease); and (d) mild
hypothermia combined with
U-74389G.
Spinal cord ischemia was produced by 40 min of infrarenal aortic balloon occlusion. Forty-eight hours after the procedure, the neurologic status of the animals was assessed (Tarlov score) and the animals were killed for histologic evaluation. In the normothermic control group, eight of 10 animals became paraplegic. There was a significant reduction of the incidence of
paraplegia and overall
neurologic deficits and a significant improved Tarlov score in the mild hypothermic group (one animal paraplegic) and in the group with both mild
hypothermia and
U-74389G (two animals with a mild
paraparesis). The histopathologic scores showed significantly less damage in both hypothermic groups. In group 2,
U-74389G administration did not improve neurologic or histopathologic outcomes. The results of the current study demonstrate that a slight decrease of intraischemic spinal cord temperature significantly improved neurologic and histopathologic outcomes after
experimental spinal cord ischemia. Protection by the 21-aminosteroid at normothermic conditions, or additional protection when
U-74389G was added to mild
hypothermia, could not be demonstrated.