目的了解超重合并腹型肥胖正常高值血压人群大动脉僵硬度的变化及其影响因素。方法入选体质量指数(BMI)≥24.0 kg/m^2同时腹围增加(男性≥90,女性≥85 cm),收缩压介于120~139 mm Hg或舒张压80~89 mm Hg者为超重腹型肥胖正常高值血压组(n...目的了解超重合并腹型肥胖正常高值血压人群大动脉僵硬度的变化及其影响因素。方法入选体质量指数(BMI)≥24.0 kg/m^2同时腹围增加(男性≥90,女性≥85 cm),收缩压介于120~139 mm Hg或舒张压80~89 mm Hg者为超重腹型肥胖正常高值血压组(n=87),同时入选BMI<24.0 kg/m^2、血压<120/80 mm Hg无疾病者为对照组(n=87)。所有入选者进行颈股动脉脉搏波传导速度(cfPWV)检测;同时留取清晨空腹血清测定血糖、血脂;并应用酶联免疫吸附试验(ELISA)法进行血清细胞间黏附分子-1(ICAM1)、单核细胞趋化蛋白-1(MCP1)、氧化型低密度脂蛋白(oxLDL)、巨噬细胞炎症蛋白2(GROβ)、中性粒细胞激活蛋白3(NAP3)测定。应用SPSS 17.0统计学软件对数据进行统计学分析。结果超重腹型肥胖正常高值血压组与对照组人群平均年龄[(50.6±9.1)比(51.3±10.4)岁],性别比例差异无统计学意义。超重腹型肥胖正常高值血压组BMI[(28.0±3.1)比(22.1±1.6)kg/m^2],腹围[(96.4±8.1)比(80.0±5.5)cm],血压[(132.3±7.3)/(77.4±7.5)比(114.3±6.0)/(71.1±6.5)mm Hg]高于对照组。超重腹型肥胖正常高值血压组cfPWV[(8.79±1.54)比(8.26±1.51)m/s]、低密度脂蛋白胆固醇(LDL-C)[(3.01±0.71)比(2.80±0.64)mmol/L]、三酰甘油[(1.86±1.32)比(1.10±0.63)mmol/L]、空腹血糖[(5.27±0.98)比(4.89±0.94)mmol/L]、oxLDL高于对照组,血高密度脂蛋白胆固醇(HDL-C)低于对照组。相关性分析结果显示,所有入选者中cfPWV与BMI、腹围、收缩压、舒张压呈正相关(r=0.186,0.211,0.185,0.163;均P<0.05),未发现cfPWV与血脂、空腹血糖、炎症指标相关。分组相关性分析结果显示,超重腹型肥胖正常高值血压组中cfPWV与年龄、收缩压呈正相关(r=0.301,0.218;均P<0.05),对照组未发现cfPWV与检测指标具有相关性。多元逐步线性回归分析结果显示,在排除其他因素影响后,腹围和年龄与cfPWV具有相关性(B=0.031,0.024;均P<0.05)。结论本研究发现在超重合并腹型肥胖的正常高值血压者中已存在大动脉僵硬度的改变,该变化发生的相关因素包括腹围、BMI和血压,而腹围是该人群大动脉僵硬度变化的影响因素之一。展开更多
Background Diabetic nephropathy is a major cause of renal failure in diabetes mellitus （DM）. It has been known that renin-angiotensin system （RAS） blockers have a renal protective effect. This study aimed to inves...Background Diabetic nephropathy is a major cause of renal failure in diabetes mellitus （DM）. It has been known that renin-angiotensin system （RAS） blockers have a renal protective effect. This study aimed to investigate whether treatment with angiotensin Ⅱ receptor blocker, olmesartan, could modify renal hemodynamic variables and vascular structural properties, then attenuate renal injury in streptozotocin （STZ）-induced DM rats.Methods DM was induced in male Wistar rats by intraperitoneal administration of STZ. The rats were then randomized to a DM group and an olmesartan treatment （OLM＋DM） group. The normal group （non-DM） were administered only citrate buffer. At the end of the 14th week, blood glucose, kidney weight/body weight and urinary protein-to-creatinine ratio were determined. Further, the flow-pressure and pressure-glomerular filtration rate （GFR） relationships were determined for maximally vasodilated, perfused kidneys. From the relationship, 3 indices of vascular structural properties were estimated： slope of flow-pressure （minimal renal vascular resistance, reflecting overall luminal dimensions of preglomerular and postglomerular vasculature）, slope of pressure-GFR （glomerular filtration capacity against pressure）and threshold pressure for beginning filtration at pressure-GFR （preglomerular to postglomerular vascular resistance ratio）. Kidneys were then perfusion fixed for histological analysis. The renal histopathology was observed by light microscopy.Results The body weight of DM rats was lower than that of non-DM rats. Blood glucose, kidney weight/body weight,urinary protein-to-creatinine ratio were significantly greater in DM rats than in non-DM rats. The parameters such as kidney weight/body weight, urinary protein-to-creatinine ratio in OLM＋DM rats had dramatically decreased compared with those in DM rats. However, the treatment with olmesartan had no effect on blood glucose levels. The slope of flow-pressure relationship was greater in DM rats than that in non-DM rats （P 〈0.05）. But the slope of the pressure-GFR relationship was lower in DM rats than that in non-DM rats （P 〈0.05） with the x-intercept of the line similar between the two groups. The slope of the flow-pressure relationship was decreased in DM rats group treated with olmesartan （P 〈0.05）. Moreover, olmesartan significantly increased the slope of the pressure-GFR relationship in DM rats （P 〈0.05）.The x-intercept of the pressure-GFR relationship reduced following olmesartan in DM rats.Conclusions Treatment with olmesartan reduced urinary protein-to-creatinine ratio independent of blood glucose and increased average renal vessel lumen diameter in the perfused kidneys of STZ-induced DM rats, predominantly in preglomerular vessels, and then improved renal excretory capability. These findings were consistent with remodeling of the preglomerular vasculature in our hisological measurements.展开更多
文摘目的了解超重合并腹型肥胖正常高值血压人群大动脉僵硬度的变化及其影响因素。方法入选体质量指数(BMI)≥24.0 kg/m^2同时腹围增加(男性≥90,女性≥85 cm),收缩压介于120~139 mm Hg或舒张压80~89 mm Hg者为超重腹型肥胖正常高值血压组(n=87),同时入选BMI<24.0 kg/m^2、血压<120/80 mm Hg无疾病者为对照组(n=87)。所有入选者进行颈股动脉脉搏波传导速度(cfPWV)检测;同时留取清晨空腹血清测定血糖、血脂;并应用酶联免疫吸附试验(ELISA)法进行血清细胞间黏附分子-1(ICAM1)、单核细胞趋化蛋白-1(MCP1)、氧化型低密度脂蛋白(oxLDL)、巨噬细胞炎症蛋白2(GROβ)、中性粒细胞激活蛋白3(NAP3)测定。应用SPSS 17.0统计学软件对数据进行统计学分析。结果超重腹型肥胖正常高值血压组与对照组人群平均年龄[(50.6±9.1)比(51.3±10.4)岁],性别比例差异无统计学意义。超重腹型肥胖正常高值血压组BMI[(28.0±3.1)比(22.1±1.6)kg/m^2],腹围[(96.4±8.1)比(80.0±5.5)cm],血压[(132.3±7.3)/(77.4±7.5)比(114.3±6.0)/(71.1±6.5)mm Hg]高于对照组。超重腹型肥胖正常高值血压组cfPWV[(8.79±1.54)比(8.26±1.51)m/s]、低密度脂蛋白胆固醇(LDL-C)[(3.01±0.71)比(2.80±0.64)mmol/L]、三酰甘油[(1.86±1.32)比(1.10±0.63)mmol/L]、空腹血糖[(5.27±0.98)比(4.89±0.94)mmol/L]、oxLDL高于对照组,血高密度脂蛋白胆固醇(HDL-C)低于对照组。相关性分析结果显示,所有入选者中cfPWV与BMI、腹围、收缩压、舒张压呈正相关(r=0.186,0.211,0.185,0.163;均P<0.05),未发现cfPWV与血脂、空腹血糖、炎症指标相关。分组相关性分析结果显示,超重腹型肥胖正常高值血压组中cfPWV与年龄、收缩压呈正相关(r=0.301,0.218;均P<0.05),对照组未发现cfPWV与检测指标具有相关性。多元逐步线性回归分析结果显示,在排除其他因素影响后,腹围和年龄与cfPWV具有相关性(B=0.031,0.024;均P<0.05)。结论本研究发现在超重合并腹型肥胖的正常高值血压者中已存在大动脉僵硬度的改变,该变化发生的相关因素包括腹围、BMI和血压,而腹围是该人群大动脉僵硬度变化的影响因素之一。
文摘目的比较沙库巴曲缬沙坦与其他临床常见的血管紧张素受体阻滞药(ARB)在原发性高血压患者中的降压效果。方法采用网状荟萃分析,计算机检索了PubMed、EMBASE、Cochrane Library、Medline、Medline In-process和中国生物医学文献数据库,检索时间截至2020年10月20日,纳入比较沙库巴曲缬沙坦或其他临床常见的ARB或安慰剂治疗原发性高血压的随机对照试验。观察结局主要包括治疗8周后诊室坐位收缩压和舒张压的变化以及总体血压达标率。结果共纳入39项研究。与安慰剂相比,沙库巴曲缬沙坦治疗8周后对诊室坐位收缩压降压效果显著[-16.24(95%CI-19.03~-13.49) mm Hg]。概率排序图和累积排序曲线下面积(SUCRA)结果显示,对于诊室坐位收缩压和舒张压、总体血压达标率结局,与ARB相比,沙库巴曲缬沙坦的降压效果最佳(SUCRA分别为91.39%,85.06%,91.26%)。结论对于原发性高血压患者,沙库巴曲缬沙坦降压效果优于其他临床常见的ARB。
文摘Background Diabetic nephropathy is a major cause of renal failure in diabetes mellitus （DM）. It has been known that renin-angiotensin system （RAS） blockers have a renal protective effect. This study aimed to investigate whether treatment with angiotensin Ⅱ receptor blocker, olmesartan, could modify renal hemodynamic variables and vascular structural properties, then attenuate renal injury in streptozotocin （STZ）-induced DM rats.Methods DM was induced in male Wistar rats by intraperitoneal administration of STZ. The rats were then randomized to a DM group and an olmesartan treatment （OLM＋DM） group. The normal group （non-DM） were administered only citrate buffer. At the end of the 14th week, blood glucose, kidney weight/body weight and urinary protein-to-creatinine ratio were determined. Further, the flow-pressure and pressure-glomerular filtration rate （GFR） relationships were determined for maximally vasodilated, perfused kidneys. From the relationship, 3 indices of vascular structural properties were estimated： slope of flow-pressure （minimal renal vascular resistance, reflecting overall luminal dimensions of preglomerular and postglomerular vasculature）, slope of pressure-GFR （glomerular filtration capacity against pressure）and threshold pressure for beginning filtration at pressure-GFR （preglomerular to postglomerular vascular resistance ratio）. Kidneys were then perfusion fixed for histological analysis. The renal histopathology was observed by light microscopy.Results The body weight of DM rats was lower than that of non-DM rats. Blood glucose, kidney weight/body weight,urinary protein-to-creatinine ratio were significantly greater in DM rats than in non-DM rats. The parameters such as kidney weight/body weight, urinary protein-to-creatinine ratio in OLM＋DM rats had dramatically decreased compared with those in DM rats. However, the treatment with olmesartan had no effect on blood glucose levels. The slope of flow-pressure relationship was greater in DM rats than that in non-DM rats （P 〈0.05）. But the slope of the pressure-GFR relationship was lower in DM rats than that in non-DM rats （P 〈0.05） with the x-intercept of the line similar between the two groups. The slope of the flow-pressure relationship was decreased in DM rats group treated with olmesartan （P 〈0.05）. Moreover, olmesartan significantly increased the slope of the pressure-GFR relationship in DM rats （P 〈0.05）.The x-intercept of the pressure-GFR relationship reduced following olmesartan in DM rats.Conclusions Treatment with olmesartan reduced urinary protein-to-creatinine ratio independent of blood glucose and increased average renal vessel lumen diameter in the perfused kidneys of STZ-induced DM rats, predominantly in preglomerular vessels, and then improved renal excretory capability. These findings were consistent with remodeling of the preglomerular vasculature in our hisological measurements.
