| Part one: Effects of intraperitoneal injection of Dexmedetomidine inRat Model of Focal Cerebral Ischemia and Reperfusion InjuryOcclusion on Neurological Deficit ScoreObjective To find out the effect of intraperitoneal injection of Dexmedetomidine ina rat model of focal cerebral ischemia and reperfusion injury occlusion on neurologicaldeficit scoreMethods Thirty-two male Sprague-Dawley (SD) rats whose weight were280~320g,were randomly divided into4groups(n=8):(1)SHAM group (SHAM),(2)Ischemia/reperfusion group (I/R),(3)Normal saline (NS) treatment group (I/R+NS),(4)Dexmedetomidine treatment group (I/R+DEX). Based on the thread approach,occluded the middle cerebral artery in rats for2hours then pulled out the thread andreperfused to cause transient focal cerebral ischemia. In the group of I/R+DEX,Dexmedetomidine of40ug/kg was instantly intraperitoneally injected after reperfusion; Inthe group of I/R+NS, Normal saline of the same volume was instantly intraperitoneallyinjected as soon as having finished reperfusion. Twenty-four hours after reperfusion,graded the neurological deficit score.Results As compared with the SHAM group, the neurological score in I/R、I/R+NSand I/R+DEX group were higher, the results were statistically significant different fromSHAM group(P<0.01). Compared with the groups of I/R and I/R+NS, the neurologicalscore in I/R+DEX group was statistically significant lower.(P<0.05).Conclusion The results suggest that inject Dexmedetomidine intraperitoneally rightaway after reperfusion in rat model of focal cerebral ischemia and reperfusion injuryocclusion could couse the reduce of neurological score. Part two: Effects of intraperitoneal injection of Dexmedetomidine inRat Model of Focal Cerebral Ischemia and Reperfusion InjuryOcclusion on Infarct Volume and Levels of PhosphorylatedAktObjective To observe the effect of intraperitoneal injection of Dexmedetomidine ina rat model of focal cerebral ischemia and reperfusion injury occlusion on infarct volumeand levels of phosphorylated AktMethods Thirty-two male Sprague-Dawley (SD) rats whose weight were280~320g,were randomly divided into4groups(n=8):(1)SHAM group (SHAM),(2)Ischemia/reperfusion group (I/R),(3)Normal saline (NS) treatment group (I/R+NS),(4)Dexmedetomidine treatment group (I/R+DEX). Based on the thread approach,occluded the middle cerebral artery in rats for2hours then pulled out the thread andreperfused to cause transient focal cerebral ischemia. In the group of I/R+DEX,Dexmedetomidine of40ug/kg was instantly intraperitoneally injected after reperfusion; Inthe group of I/R+NS, Normal saline of the same volume was instantly intraperitoneallyinjected after reperfusion.2,3,5-triphenyl tetrazolium chloride(TTC) staining were used todetermine the infarct volume24hours after reperfusion and western-blotting were used toshow the levels of phosphorylated Akt.Results As compared with the SHAM group, the infarct volume in I/R、I/R+NS andI/R+DEX group were statistically significant higher (P<0.01), as well as the expression ofphosphorylatedAkt in I/R group were significantly lower (P<0.05).In addtion, the infarct volume in I/R+DEX group were significantly lower than I/R andI/R+NS group (P<0.05), and the expression of phosphorylated Akt in I/R+DEX group werehigher than I/R and I/R+NS group(P<0.05).Conclusion The results suggest that inject Dexmedetomidine intraperitoneally rightaway after reperfusion in rat model of focal cerebral ischemia and reperfusion injuryocclusion could reduce the infarct volume and increase the levels of phosphorylated Akt. |
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