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Objective Angiotensin Ⅱ(Ang Ⅱ)contributes to modulating blood pressure by stimulation of Ang Ⅱ AT1 receptors.We devised a rat transient middle cerebral artery occlusion(MCAO)model to assess whether oxidative damage is decreased after pretreatment with Angiotensin Ⅱ AT1 receptor blocker(ARB).Methods After 2 weeks pretreatment with ARB 0.5 and 1mg/kg,the male Wister rats were subjected to 2h middle cerebral artery occlusion(MCAO).At 24h,the lumen diameter of middle cerebral artery,the plasma level of 8-hydroxy-2’-deoxyguanosine(8-OHdG),and HIF-1α levels were recorded and compared.Results After pretreatment with ARB 0.5 and 1mg/kg,blood pressure did not significantly change compared with that of controls.In the group of candesartan at 1mg/(kg·day),the lumen diameter was significantly increased compared to that in control group [(86.0±5.0)μm vs.(69.0±2.1)μm;P<0.01,n=6-8].The plasma 8-OHdG levels of ARB pretreatment groups were decreased.In immunohistochemical findings,8-OHdG-and HIF-1α-containing cells in ARB pretreatment groups were decreased.Conclusion Brain ischemia and oxidative damage can be reversed by AT1 receptor blockade in normotensive rats after transient cerebral artery occlusion.
Objective Angiotensin Ⅱ (Ang Ⅱ) contributes to modulating blood pressure by stimulation of Ang Ⅱ AT1 receptors. We devised a rat transient middle cerebral artery occlusion (MCAO) model to assess whether oxidative damage is decreased after pretreatment with Angiotensin Ⅱ AT1 receptor blocker (ARB ). After 2 weeks pretreatment with ARB 0.5 and 1 mg / kg, the male Wister rats were subjected to 2h middle cerebral artery occlusion (MCAO). At 24h, the lumen diameter of middle cerebral artery, the plasma level of 8-hydroxy- 2’-deoxyguanosine (8-OHdG), and HIF-1α levels were recorded and compared. Results After pretreatment with ARB 0.5 and 1 mg / kg, blood pressure did not significantly change compared with that of controls. In the group of candesartan at 1 mg / (kg · day), the lumen diameter was significantly increased compared to that in control group [(86.0 ± 5.0) μm vs. (69.0 ± 2.1) μm; P <0.01, n = 6-8] OHdG levels of ARB pretreatment groups were decreased. Immunohistochemical findings, 8-OHdG- and HIF-1α-containing cells in ARB pretreatment groups were decreased.Conclusion Brain ischemia and oxidative damage can be reversed by AT1 receptor blockade in normotensive rats after transient cerebral artery occlusion.