| It is a complicated pathological process on spinal cord ischemia/ reperfusion (SCI/R) injury. The exact molecular and cellular mechanism is not understood. It is suggested at present that it is parallel with these changes, excessive excitatory amino acid release, intracellular Ca2+ accumulation, generation of oxygen free radicals, disorder of Na+ -K+-ATP balance, inflammation reaction, apoptosis et al. A series of measures were taken to these changes, including hypothermia, ischemia preconditioning, drainage of cerebrospinal fluid, various of bypass, pharmacological interventions et al, but there is no a sole valid measure. Hypothermia, especially moderate hypothermia, was paid attention to for its protective effects of neurotic system through experiment and clinic. There is no literature in tissue levels of I1-8 in the ischemia/reperfusion spinal cord on protection of hypothermia. So we did it.In the current study, New Zealand white rabbits were randomly assigned to one of the three groups: a sham control group (S: n=6), a normothermia control group (N: n=35), a hypothermia group(H: n=35). The rabbits were then subjected to 40 min of spinal cord ischemia produced byocclusion of the lumbar arteries.1 The effect of hypothermia to the levels of spinal D-8 after SCI/R in rabbitsTo detect the protective effects of hypothermia to spinal cord after SCI/R in rabbits through determining the levels of spinal I1-8, and to inquire into the mechanism of protection. The spinal cords were taken and put in the -80 "C refrigerator at different time after reperfusion. Then the spinal I1-8 levels were determined in Sandwich ELISA. Our results suggest that the levels of spinal I1-8 at 1h after reperfusion are no significant differences among three groups, and their levels are low. In N group, the levels of IL-8 in spinal cord increase at 6h after reperfusion, reach their peak at 12h after reperfusion, decrease at 24h, and recover normal levels at 48h after reperfusion. The tendency of change in tissue levels of EL-8 in the spinal cord in H group is similar with that in the N group, but their levels decrease and are significantly different from that of the N group (p<0.01). It shows that the ischemic spinal cords are protected by hypothermia in rabbits.2 To observe the pathologic change and apoptosis of spinal cord suffered from ischemia/reperfusion before and after the protection of hypothermia.In the current study, the spinal cords were taken and put in the 10% buffered formalin. They were embedded in paraffin and cut for hematoxylinand eosin (HE) staining and specific staining (terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end-labeling [TUNEL] staining method) of DNA fragmentation with the use of a molecular biological-histochemical system. Our results suggest that the pathologic change of N group is significantly more serious than that of H group. Apoptotic neurons can be seen in spinal cord at 6h after reperfusion, reaching a peak at 24h, decreasing at 48h. The number of apoptotic neurons of H group is significantly less than that of N group (p<0.05). This shows that apoptosis can be inhibited by hypothermia. 3 To assess the neurologic function by Tarlov scoreThe hind limb motor function of rabbits was assessed by Tarlov score before death. Our results show that the score of H group is significantly higher than that of N group (p<0.01).
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