BACKGROUND: In recent studies, we demonstrated that neuraxial morphine after noninjurious spinal cord ischemia in the rat could induce spastic paraplegia and degeneration of selective spinal ventral neurons. Our objective was to investigate the impact of dexmedetomidine infusion on the degeneration of spinal ventral neurons induced by intrathecal (IT) morphine after spinal cord ischemia. METHODS: Male Sprague-Dawley rats were given repetitive doses of IT morphine (40 microg x 2) at 1 and 5 h after a noninjurious interval (6 min) of spinal cord ischemia. The animals were assigned to one of the following four groups after the first IT injection (n = 8/group): Group S, IV infusion of saline (mL/h); Group Dex 0.1, dexmedetomidine (0.1 microg . kg(-1) x h(-1)); Group Dex 1, dexmedetomidine (1 microg x kg(-1) x h(-1)); Group Dex 3, dexmedetomidine (3 microg x kg(-1) x h(-1)). Follow-up evaluation included a sedation scale, the Motor Deficit Index to determine neurological dysfunction and histopathology of the spinal cord at 72 h of reperfusion. RESULTS: IV dexmedetomidine produced a dose-dependent increase in the sedation index. Repetitive IT morphine injection induced paraplegia and degeneration of the spinal ventral neurons. IV dexmedetomidine at a sedative dose in comparison with saline significantly attenuated neurological dysfunction and histopathological consequences. CONCLUSION: These data show that repetitive administration of IT morphine can induce paraplegia with degeneration of spinal ventral neurons, which can be attenuated by IV dexmedetomidine at a sedative dose. The use of dexmedetomidine may provide beneficial effects on neurological outcome after IT morphine after spinal cord ischemia in rats.
BACKGROUND: In recent studies, we demonstrated that neuraxial morphine after noninjurious spinal cord ischemia in the rat could induce spastic paraplegia and degeneration of selective spinal ventral neurons. Our objective was to investigate the impact of dexmedetomidine infusion on the degeneration of spinal ventral neurons induced by intrathecal (IT) morphine after spinal cord ischemia. METHODS: Male Sprague-Dawley rats were given repetitive doses of IT morphine (40 microg x 2) at 1 and 5 h after a noninjurious interval (6 min) of spinal cord ischemia. The animals were assigned to one of the following four groups after the first IT injection (n = 8/group): Group S, IV infusion of saline (mL/h); Group Dex 0.1, dexmedetomidine (0.1 microg . kg(-1) x h(-1)); Group Dex 1, dexmedetomidine (1 microg x kg(-1) x h(-1)); Group Dex 3, dexmedetomidine (3 microg x kg(-1) x h(-1)). Follow-up evaluation included a sedation scale, the Motor Deficit Index to determine neurological dysfunction and histopathology of the spinal cord at 72 h of reperfusion. RESULTS: IV dexmedetomidine produced a dose-dependent increase in the sedation index. Repetitive IT morphine injection induced paraplegia and degeneration of the spinal ventral neurons. IV dexmedetomidine at a sedative dose in comparison with saline significantly attenuated neurological dysfunction and histopathological consequences. CONCLUSION: These data show that repetitive administration of IT morphine can induce paraplegia with degeneration of spinal ventral neurons, which can be attenuated by IV dexmedetomidine at a sedative dose. The use of dexmedetomidine may provide beneficial effects on neurological outcome after IT morphine after spinal cord ischemia in rats.