目的:评价血管紧张素转换酶抑制剂(ACE I)贝那普利和血管紧张素Ⅱ受体1拮抗剂(ARB)缬沙坦联合应用预防支架内再狭窄的效果。方法:急性冠脉综合征(ACS)患者81例择期行冠脉介入治疗,植入裸金属支架。术后随机分为两组,对照组给予基础治疗...目的:评价血管紧张素转换酶抑制剂(ACE I)贝那普利和血管紧张素Ⅱ受体1拮抗剂(ARB)缬沙坦联合应用预防支架内再狭窄的效果。方法:急性冠脉综合征(ACS)患者81例择期行冠脉介入治疗,植入裸金属支架。术后随机分为两组,对照组给予基础治疗;联合治疗组服用缬沙坦和贝那普利。术后6月复查冠状动脉造影(CAG),计算机定量测定冠脉病变的直径狭窄程度(QCA)。结果:联合治疗组(n=39)参照血管直径与对照组(n=42)比较无明显差异,支架段血管直径差异明显(2.22±0.21mm vs 1.83±0.25mm,P<0.05)。血管直径减少指数联合治疗组与对照组分别为0.50±0.16mm、0.91±0.11mm,P<0.01。联合治疗组再狭窄率(15.4%)及再介入率(7.7%)均明显低于对照组(28.6%、21.4%,P<0.01)。结论:贝那普利与缬沙坦联合干预可降低冠脉介入治疗术后支架内再狭窄的发生率。展开更多
Objective: To investigate the therapy effect of valsartan on oxidative stress and the formation of atherosclerosis of rabbit. Methods: An atherosclerotic rabbit model was established by feeding high cholesterol diet s...Objective: To investigate the therapy effect of valsartan on oxidative stress and the formation of atherosclerosis of rabbit. Methods: An atherosclerotic rabbit model was established by feeding high cholesterol diet supplemented by bovine serum albumin injection bolus. The rabbits were randomly divided into the control, model, and valsartan treated group, six rabbits in each group. Blood samples were collected at the end of 8 weeks for examination of serum lipid levels and MDA levels; the aortas were harvested for histological morphometry analysis, vascular cell adhesion molecule-1 (VCAM-1) immunohistochemical analysis and in situ superoxide detection to reflect the activity of NAD(P)H oxidase. Results: Rabbits fed with high cholesterol diet showed higher serum lipids levels than those fed with normal diet(P<0.01). Treatment with valsartan (10 mg/kg per day) did not alter serum lipids levels. But the serum MDA level and ratio of lesion to intima area reduced significantly compared with model group(P<0.05). The expression of VCAM-1 decreased significantly in the valsartan treated group than in the model group (P<0.05).In addition, in situ superoxide detection also show the markedly reduction of superoxide as a result of valsartan treatment. Conclusion: These results indicate that the valsartan treatment can reduce the atherosclerotic progression, the mechanisms of which may include the inhibiting the NAD(P)H oxidase activity to produce superoxide and the downregulating the expression of redox sensitive genes in the downstream, such as VCAM-1.展开更多
OBJECTIVE: To explore the pathogenic changes of myocardial apoptosis in heart hypertrophy during hypertension and evaluate the anti-apoptosis effect of Valsartan. METHODS: Thirty spontaneously hypertensive rats (SHRs)...OBJECTIVE: To explore the pathogenic changes of myocardial apoptosis in heart hypertrophy during hypertension and evaluate the anti-apoptosis effect of Valsartan. METHODS: Thirty spontaneously hypertensive rats (SHRs) were divided into two groups: 15 treated with Valsartan (20 mg x kg(-1) x d(-1)) (SHR + Valsartan group), the others with placebo (SHR + placebo group), with 15 normal Wistar rats as control. Systolic blood pressure was measured by the tail-cuff method. The observation period was from 8 to 16 weeks of age. Cardiac apoptosis was evaluated by a Terminal Deoxynucleotidyl Transferase-Mediated dUTP-biotin Nick End Labeling (TUNEL) assay. RESULTS: Mean blood pressure values were 127 +/- 2 mm Hg in controls, 163 +/- 6 mm Hg in the SHR + Valsartan group and 193 +/- 7 mm Hg in the SHR + placebo group at 16 weeks of age, whereas the blood pressure in 8-week-old SHR and Wistar rats were 175 +/- 3 mm Hg and 125 +/- 5 mm Hg, respectively. The ratio of the heart weight over body weight declined in Wistar (3.07 +/- 0.03 mg/g) and SHR + Valsartan groups (3.22 +/- 0.19 mg/g) compared with the SHR + placebo group (4.02 +/- 0.31 mg/g) (P展开更多
With the launch of sacubitril/valsartan(ARNI),there are new options for the treatment of heart failure(HF).However,ARNI is currently only used in HF patients with reduced ejection fraction(HFrEF).No evidence shows tha...With the launch of sacubitril/valsartan(ARNI),there are new options for the treatment of heart failure(HF).However,ARNI is currently only used in HF patients with reduced ejection fraction(HFrEF).No evidence shows that no modern treatment can reduce mortality in HF patients with preserved ejection fraction(HFpEF).Therefore,it is urgently necessary clarify whether ARNI can be used in the treatment of HFpEF.In the present study,we summarized the research progress of ARNI in the treatment of HFpEF.展开更多
文摘目的:评价血管紧张素转换酶抑制剂(ACE I)贝那普利和血管紧张素Ⅱ受体1拮抗剂(ARB)缬沙坦联合应用预防支架内再狭窄的效果。方法:急性冠脉综合征(ACS)患者81例择期行冠脉介入治疗,植入裸金属支架。术后随机分为两组,对照组给予基础治疗;联合治疗组服用缬沙坦和贝那普利。术后6月复查冠状动脉造影(CAG),计算机定量测定冠脉病变的直径狭窄程度(QCA)。结果:联合治疗组(n=39)参照血管直径与对照组(n=42)比较无明显差异,支架段血管直径差异明显(2.22±0.21mm vs 1.83±0.25mm,P<0.05)。血管直径减少指数联合治疗组与对照组分别为0.50±0.16mm、0.91±0.11mm,P<0.01。联合治疗组再狭窄率(15.4%)及再介入率(7.7%)均明显低于对照组(28.6%、21.4%,P<0.01)。结论:贝那普利与缬沙坦联合干预可降低冠脉介入治疗术后支架内再狭窄的发生率。
文摘Objective: To investigate the therapy effect of valsartan on oxidative stress and the formation of atherosclerosis of rabbit. Methods: An atherosclerotic rabbit model was established by feeding high cholesterol diet supplemented by bovine serum albumin injection bolus. The rabbits were randomly divided into the control, model, and valsartan treated group, six rabbits in each group. Blood samples were collected at the end of 8 weeks for examination of serum lipid levels and MDA levels; the aortas were harvested for histological morphometry analysis, vascular cell adhesion molecule-1 (VCAM-1) immunohistochemical analysis and in situ superoxide detection to reflect the activity of NAD(P)H oxidase. Results: Rabbits fed with high cholesterol diet showed higher serum lipids levels than those fed with normal diet(P<0.01). Treatment with valsartan (10 mg/kg per day) did not alter serum lipids levels. But the serum MDA level and ratio of lesion to intima area reduced significantly compared with model group(P<0.05). The expression of VCAM-1 decreased significantly in the valsartan treated group than in the model group (P<0.05).In addition, in situ superoxide detection also show the markedly reduction of superoxide as a result of valsartan treatment. Conclusion: These results indicate that the valsartan treatment can reduce the atherosclerotic progression, the mechanisms of which may include the inhibiting the NAD(P)H oxidase activity to produce superoxide and the downregulating the expression of redox sensitive genes in the downstream, such as VCAM-1.
文摘OBJECTIVE: To explore the pathogenic changes of myocardial apoptosis in heart hypertrophy during hypertension and evaluate the anti-apoptosis effect of Valsartan. METHODS: Thirty spontaneously hypertensive rats (SHRs) were divided into two groups: 15 treated with Valsartan (20 mg x kg(-1) x d(-1)) (SHR + Valsartan group), the others with placebo (SHR + placebo group), with 15 normal Wistar rats as control. Systolic blood pressure was measured by the tail-cuff method. The observation period was from 8 to 16 weeks of age. Cardiac apoptosis was evaluated by a Terminal Deoxynucleotidyl Transferase-Mediated dUTP-biotin Nick End Labeling (TUNEL) assay. RESULTS: Mean blood pressure values were 127 +/- 2 mm Hg in controls, 163 +/- 6 mm Hg in the SHR + Valsartan group and 193 +/- 7 mm Hg in the SHR + placebo group at 16 weeks of age, whereas the blood pressure in 8-week-old SHR and Wistar rats were 175 +/- 3 mm Hg and 125 +/- 5 mm Hg, respectively. The ratio of the heart weight over body weight declined in Wistar (3.07 +/- 0.03 mg/g) and SHR + Valsartan groups (3.22 +/- 0.19 mg/g) compared with the SHR + placebo group (4.02 +/- 0.31 mg/g) (P
文摘With the launch of sacubitril/valsartan(ARNI),there are new options for the treatment of heart failure(HF).However,ARNI is currently only used in HF patients with reduced ejection fraction(HFrEF).No evidence shows that no modern treatment can reduce mortality in HF patients with preserved ejection fraction(HFpEF).Therefore,it is urgently necessary clarify whether ARNI can be used in the treatment of HFpEF.In the present study,we summarized the research progress of ARNI in the treatment of HFpEF.
