Experimental Study on the Protection of Brain Function by Cerebral Ischemic Preconditioning
Li Rong
Abstract
Li Rong
Abstract
ObjectivesTo explore the protection of brain function by cerebral ischemic preconditioning and the mechanisms involved in ischemic tolerance.MethodsSeventy four adult Wistar rats were randomly divided into six group:①Group A (blank control); Group B (experiment control); Group C (lethal ischemia); Group D (ischemic preconditioning);Group E (N 6 cyclopentyladenosine,CPA preconditioning); Group F(8 cyclopenty 1,3 dipropylxcenthine,DPCPX preconditioning). Brain ischemia model was induced by 4 vessel occlusion method as described by Pulsinelli et al.Both common carotid arteries of rats in Groups A,B,C,D were occluded or released with miniature aneurysm clips in order to control the time of brain ischemia or reperfusion; In Group E and F, two drugs? CPA and DPCPX preconditionings were carried out i.p. respectively in different duration before ischemia. was established .The brain tissues in each group were resected following reperfusion for 3 or 7 days after the special ischemic phases ,and neurons from the CA Ⅰ region of hippocampus were studied by morphological and immunohistochemical techniques of heat shock protein(HSP) respectively.ResultsThe CA Ⅰ region neurons of hippocampus in Group D (ischemic preconditioning) and Group E(CPA preconditioning) were protected fairly well, and results of their neuronal density were significantly higher than those of Group C (lethal ischemia)(P0.01), but expressions of HSP were visible within CA Ⅰ region of hippocampus in all three groups. The CA Ⅰ region neurons of hippocampus in Group F (DPCPX preconditioning) were destroyed severely, with negative immunoreaction for HSP 70; and their neuronal density was the lowest as compared with that in Groups A,D and E (P0.01).ConclusionCerebral ischemic preconditioning or prophylactic application with adenosine receptor A 1 agonist can produce obvious protective effects on brain function.
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ObjectivesTo explore the protection of brain function by cerebral ischemic preconditioning and the mechanisms involved in ischemic tolerance.MethodsSeventy four adult Wistar rats were randomly divided into six group:①Group A (blank control); Group B (experiment control); Group C (lethal ischemia); Group D (ischemic preconditioning);Group E (N 6 cyclopentyladenosine,CPA preconditioning); Group F(8 cyclopenty 1,3 dipropylxcenthine,DPCPX preconditioning). Brain ischemia model was induced by 4 vessel occlusion method as described by Pulsinelli et al.Both common carotid arteries of rats in Groups A,B,C,D were occluded or released with miniature aneurysm clips in order to control the time of brain ischemia or reperfusion; In Group E and F, two drugs? CPA and DPCPX preconditionings were carried out i.p. respectively in different duration before ischemia. was established .The brain tissues in each group were resected following reperfusion for 3 or 7 days after the special ischemic phases ,and neurons from the CA Ⅰ region of hippocampus were studied by morphological and immunohistochemical techniques of heat shock protein(HSP) respectively.ResultsThe CA Ⅰ region neurons of hippocampus in Group D (ischemic preconditioning) and Group E(CPA preconditioning) were protected fairly well, and results of their neuronal density were significantly higher than those of Group C (lethal ischemia)(P0.01), but expressions of HSP were visible within CA Ⅰ region of hippocampus in all three groups. The CA Ⅰ region neurons of hippocampus in Group F (DPCPX preconditioning) were destroyed severely, with negative immunoreaction for HSP 70; and their neuronal density was the lowest as compared with that in Groups A,D and E (P0.01).ConclusionCerebral ischemic preconditioning or prophylactic application with adenosine receptor A 1 agonist can produce obvious protective effects on brain function.
Key concepts: Ischemic preconditioning, Ischemia, Hippocampus, Medicine, Anesthesia, Internal medicine, Occlusion, Hsp70