The effects of graded hyperthermic (32, 20 ℃) on spinal cord protection during ischemia-reperfusion in rat

Abstract

Objective To study the neuroprotective effects of moderate hypothermia (32 ℃) and profound hypothermia (20 ℃) on spinal cord ischemia-reperfusion in rats. Methods A subcutaneous heat exchanger is used to produce a low temperature of the spinal cord. The balloon blocked the thoracic aorta to induce spinal cord ischemia for 10 minutes. 42 SD rats were randomly divided into 4 groups, group Ⅰ. Non-blocking group (37 ℃, 6); Ⅱ. Normal temperature ischemia group (37 ℃, 12); Ⅲ. moderate hypothermia group (32 ℃, 12); Ⅳ. Profound Hyperthermia group (20℃, 12). Six rats in groups Ⅱ, Ⅲ and Ⅳ were given ischemia for 10 minutes and the lumbar spinal cord was taken. The other 6 rats in each group were given reperfusion, and the neurological function was evaluated at 1, 2, 4, and 8 hours. All the samples from all three rats were examined by histological examination and analyzed. The release of neurotransmitter amino acids was observed by high pressure liquid chromatography, and N-Methyl-D-Aspartate R1 (NMDAR1) mRNA was detected by in situ hybridization. The test results were analyzed by t test. Results Hard palate and neuron necrosis occurred in the normal temperature ischemia-reperfusion group. In terms of histopathological findings, the Moderate Hyperthermia (32 ℃) group and the profound hypothermia (20 ℃) group were significantly better than normal temperature ischemia after reperfusion. After 10 minutes of spinal cord ischemia, The glutamate concentration and NMDAR1 mRNA expression in the profound hypothermia in the Moderate Hyperthermia (32 ℃) group and (20 ℃) group were significantly lower than those in the normal temperature ischemia group. After 8 hours of reperfusion, the concentrations of glutamate and NMDAR1 mRNA in the Moderate Hyperthermia (32 ℃) group and the profound hypothermia (20 ℃) group were significantly higher than those in the normal temperature control group. Spinal cord ischemia was 10 min. The glutamate concentration in the medium-low temperature (32 ℃) group was 10.88±1.17 (t=27.292, P 0.05), and that in the low temperature (20 ℃) group was (12.57±2.59) cells (t=4.154, P<0.01), which was significantly lower than that in the normal temperature ischemia group [(17.36±2.56) cells]. After reperfusion for 8 hours, the glutamate concentration in the medium-low temperature (32 ℃) group was 49.38±13.26 (t=-8.407, P<0.01), and the deep hypothermia (20 ℃) group was 44.95±2.12 (t=-23.933, P<0.01), which was significantly higher than the normal temperature ischemia group (14.08±3.70); the number of NMDAR1 mRNA positive cells in the low temperature (32 ℃) group was (22.47±5.40) cells (t=-5.437, P<0.01), and that in the deep hypothermia (20 ℃) group was (18.89±3.98) cells (t=-4.042, P<0.01), which was significantly higher than that in the normal temperature ischemia group [(12.06±3.45) cells]. Conclusion Mode moderate hyperthermia (32 ℃) and profound hypothermia (20 ℃) have protective effects on histopathology of spinal ischemia-reperfusion cord. The results of spinal ischemia-reperfusion after 8 hours indicate that spinal cord protection are still needed during reperfusion. Key words: Spinal cord ischemia-reperfusion; Moderate hyperthermia; Profound hyperthermia; Glutamate