| In recent years,many studies have showed that the role of nitric oxide(NO) might induce "dual effects" during focal cerebral ischemic injurynamely neuroprotective and neurotoxic effects. NO donor and nitric oxide sythase(NOS) inhibitors have been becoming a new subject in clinic and basic researches for the protection of focal cerebral ischemic injury. Our experiment consisted of three sections. In each section the rat model of focal cerebral ischemia was established with middle cerebral artery occlusion(MCAO) by inserting a piece of nylon thread.The following experiments were carried out: 〆ffects of nitric oxide synthase inhibitors on in the focal cerebral ischemic injury in rats; 〆ffects of NO donor (L-arginine) on the focal cerebral ischemic injury in rats; 〆ffects of L-arginine and aminoguanidine on the experimental cerebral ischemic injury.1. Sprague-Dawley(SD) rats,male,weighting 250 to 300g, were randomly devided into 4 groups:Group 1-sham operation control; Group 2-ischemic; Group 3-selective inducible NOS inhibitor aminoguanidine(AG) treatment; Group 4-nonselect- ive NOS inhibitor N G-nitro-L-arginine(L-NA) treatment2. SD rats were also randomly devided into 4 groups: Group 1-sham operation control; Group2-ischemic; Group3- low dose L-arginine treatment; Group 4- high dose L-arginine treatment.3. SD rats were randomly devided into 5 groups:Group 1-sham operation control; Group 2-ischemic; Group 3-AG treatment; Group 4-high dose L-arginine treatment; Group 5-AG and L-arginine combined(AG+L-arg) treatment.In sham operation control group,common carotid artery (CCA), external carotid artery(ECA) and internal carotid artery(lCA) were exposed,but nylon thread was not inserted. AG(100mg/kg,ip), L-NA(500mg/kg,ip)and L-arginine (300 mg/kg,500mg/kg,ip)were respectively administrated intrape- ritoneally.In AG+L-arg group, AG(50mg/kg,ip) and L-argi- nine (250mg/kg,ip) were administrated intraperitoneally at the same time.Normal saline(capacity equal to the other) was injected in ischemic group. Each group was further divided into 3subgroup:drug was administrated at Ih after MCAO and the rats were killed at 2h after administration (lh+2h); drug was administrated at 3h after MCAO and the rats were killed at 3h after administration (3h+3h); drug was administrated at 6h after MCAO and the rats were killed at 3h after administration (6h+3h).Rats were killed at set time,and the brains were taken out at once.The infarct volume of cerebral /volme of whole brain(TV%) was calculated with staining of 2,3,5-triphenyl tetra-zolium chloride(TTC);The NOJvIDA content and NOS,SOD activity in the brain tissue were measured with colorimetric method;Pathological changes were observed with light microscope.Results of the first section showed :when AG was administrated at In-, 31"K 6h after MCAO, the infract volume of cerebral/volume of whole brain(IV%) was much lower in AG group than that of ischemicgroup(/J<0.01/><0.05,P<0.01). IV% was lower in L-NA group than that of ischemic group,when L-NA was administrated at 1 ru 6h after MCAO(P<0.01),but IV% was not significantly different from ischemic at 3h after MCAO^O.OS).At 3h after MCAO (normal saline was administrated at Ih after MCAO and rats were killed 2h after administration, lh+2h in ischemic), NO content in the focal ischemic brain tissues were much higher in ischemic group than those of sham control(P<0.01).At 6h(3h+3h in ischemic ) and 9h(6h+3h in ischemic), NO content were not significantly different from sham control^ 0.05). At lh+2h, NO content were much lower in AG and L-NA group than those of ischemic(/J<0.05/'<0.01).NOS activity in the focal ischemic brain tissues of ischemic group at 3h(lh+2h in ischemic) were significantly higher than those of sham control(/)<0.05),but not significantly different at 6h(3h+3h in ischemic) or 9h(6h+3h in ischemic). NOS activity in AG and L-NA group were not significantly different from ischemic(/?>0.05).MDA content in the ischemic brain tissues of ischemic group were significantly higher...
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