The primary damage produced by spinal cord trauma is often Limited but there may be progression to extensive tissue damage because of pathophysiological mechanisms that are activated following the original injury. Although the mechanisms involved are not fully understood, It is now wildly thought that the main secondary injury processes are post- traumatic ischemia, neuronal electrolyte shifts, elaboration of oxygen free radicals and peroxidation, apoptosis, glutamate excitotoxicity and inflammation. Each of these mechanisms has been the subject of extensive experimentation, and therapeutic trials of methods to counteract various aspects of these autodestructive events have been performed. Indeed, there has been considerable success in improving the neurological recovery of experimental animals subjected to mild to moderate injuries. But neurologic function recovery after SCI has shown poor results. Recently , with the beneficial application of mild to moderate hypothennia(MIII) in preventing tissue damage following ischemia and traumatic brain injury. Some experiments are designed to find out whether MH can reduce the secondary lesions in spinal cord injury. Up to now, several study have demonstrated that MI-I can provide beneficial effects on spinal cord ischemia, but the role of MI-I in spinal cord traumatic remains disputation. Moreover, there is not enough extensive study to discover the mechanisms of neuroprotection by MH. Thus, we investigated the effect of MH following spinal cord traumatic in rats and provided evidences. In this study, all rats were randomly divided into three groups: Group äºšä½Žæ¸©æ²»ç–—å¤§é¼ è„Šé«“æŸä¼¤çš„å®žéªŒç ”ç©¶ 摘è¦ï¼Ž Arats received normothermlc ireå’–eè¡€(rectaltemper咖比 37℃)ï¼›Oã€‚å© Brecelved MHMHtfeå’–mt(rectaltemperå’–re30ï¼32℃);阶。呷C(coè¡€of gfoå‘·,onlyåˆ Inectomp).he SCI animal models were m刎e by using an improved Alien's weightdrop device(509.cm).he preseè¡€ stud includes the following four aspects. Partï¼Effects of MH onä»°'"h after traumatic iå¼ury of rat spinal cord. Ras were sç ’rificed ailk,2k,4h,shr,12hr aèƒ suå§ery the calclm l创el of llljured Spinal cord was respectively me。ed by calcium hlstochemlcal stain and Confocal laserï¼sc。ng microscopes(CLSM. In roup A,the lourescene Intensity of Intracellular ree C扩"showed a mè¡€ed Increase ail hr that Pe冰ed at 8比 then maintained a r讪er high level.Calcium hlstochemlcal stain Indicated a laå§e ARS(+)area. Althoughthe louresecene Intensltyoflè¡€racellular ree Ca'"also Increased at Zhr In MH animals(gfoup B).It was obvious that he lourescene Intensity was lowerthanthose In normothermlc animals,No pC冰[C&'"lappCgrCd,C8lClllffihlS to ChCm1C81 Stuff ShOæd SCå¨CfCd ARS(+)area. Part 11 Effects ofMHMH on extracellular amlno acids a地r traumanc iå¼uå®of rat spinal cord We evaluated In rats,the effect of MH on extracellular levels of amlno acids,with spedal emphasis on the excltatory amlno acids(EAAS) gin and asp a丘er spinal cordtrå·žmatlc lqW.(三y3 TauTau and GGABABA were slSO ffiCSSllfCd t thC S8fllC tl*C.A LBllllllCCtoffiy Of'flZ Ws i**C,8 PfobC was Inserted Inthe græ—¶ m甜er andmlcrodllysls was performed for 90 mln before and 180 mln狈er spinal cordtrçš¿matlc lmum Dealysate samples were collected tiè¡€ervals of 10 mln and analyzed by hlghperformance llqlll4chomå’–gfapåµ In grollp A...
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