哈萨克族原发性高血压患者血浆EPCsCD34+水平及其相关性研究

目的:探讨血浆内皮祖细胞(EPCs)CD34+水平与新疆哈萨克族(哈族)原发性高血压病患者血压、血脂、血糖、肥胖等的相关性.方法:选取新疆哈族原发性高血压患者87为观察组,哈族健康对照组79例,测量血压(BP)、身高、体重、腰围(WC)、臀围(HC),抽取空腹静脉血测定血糖(FPG)、总胆固醇(TC)、甘油三酯(TG)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C),计算体重指数(BMI)腰臀比(WHR).结果:①原发性高血压组血浆EPCs CD34+水平明显低于对照组(p<0.01)②原发性高血压组血浆EPCs CD34+水平与收缩压、舒张压、总胆固醇、甘油三酯、低密度脂蛋白胆固醇、血糖、体重指数呈显著负相关.对照组血浆EPCs CD34+水平与收缩压、舒张压、总胆固醇、甘油三酯、体重指数呈负相关.③多元回归分析显示在原发性高血压组中收缩压、甘油三酯是影响血浆EPCs CD34+水平的独立因素,在对照组中总胆固醇、体重指数是影响血浆EPCs CD34+水平水平的独立因素.结论:哈族原发性高血压患者血浆EPCs CD34+水平与血压水平存在一定的相关性.     

哈萨克族原发性高血压患者血浆EPCs CD34^＋水平及其相关性研究

目的：探讨血浆内皮祖细胞（EPCs） CD34＋水平与新疆哈萨克族（哈族）原发性高血压病患者血压、血脂、血糖、肥胖等的相关性。方法：选取新疆哈族原发性高血压患者87为观察组,哈族健康对照组79例,测量血压（BP）、身高、体重、腰围（WC）、臀围（HC）,抽取空腹静脉血测定血糖（FPG）、总胆固醇（TC）、甘油三酯（TG）、高密度脂蛋白胆固醇（HDL-C）、低密度脂蛋白胆固醇（LDL-C）,计算体重指数（BMI）腰臀比（WHR）。结果：①原发性高血压组血浆EPCs CD34^＋水平明显低于对照组（p〈0.01）②原发性高血压组血浆EPCs CD34^＋水平与收缩压、舒张压、总胆固醇、甘油三酯、低密度脂蛋白胆固醇、血糖、体重指数呈显著负相关。对照组血浆EPCsCD34^＋水平与收缩压、舒张压、总胆固醇、甘油三酯、体重指数呈负相关。③多元回归分析显示在原发性高血压组中收缩压、甘油三酯是影响血浆EPCs CD34^＋水平的独立因素,在对照组中总胆固醇、体重指数是影响血浆EPCs CD34^＋水平水平的独立因素。结论：哈族原发性高血压患者血浆EPCs CD34^＋水平与血压水平存在一定的相关性。     

高血压患者颈动脉粥样硬化与血脂、血压和血尿酸水平的相关性分析

目的:探讨高血压患者颈动脉粥样硬化(CAS)与血脂、血压以及血尿酸水平的相关性。方法:选择2017年2月至2018年8月在我院就诊的高血压患者117例作为研究组,另选择同期在我院进行体检的健康志愿者50例作为对照组。采用彩色多普勒超声诊断仪测定所有受试者的颈动脉内中膜厚度(IMT),并根据研究组患者的颈动脉IMT将其分为斑块组(IMT≥1.3 mm,33例)、IMT增厚组(1.0 mm≤IMT1.3 mm,49例)和IMT正常组(IMT1.0 mm,35例)。比较研究组与对照组受试者IMT,同时分别比较研究组与对照组受试者以及不同IMT高血压患者平均收缩压(SBP)、平均舒张压(DBP)、血清总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)以及尿酸水平,并采用Pearson相关性分析法分析高血压患者IMT与各指标的相关性。结果:与对照组比较,研究组IMT、SBP、DBP、TC、TG、LDL-C、血尿酸水平升高,HDL-C水平降低,差异均有统计学意义(P0.05)。斑块组患者SBP、DBP、TC、TG、LDL-C、血尿酸水平高于IMT增厚组和IMT正常组,HDL-C水平低于IMT增厚组和IMT正常组,差异均有统计学意义(P0.05);IMT增厚组患者SBP、DBP、TC、TG、LDL-C、血尿酸水平高于IMT正常组,HDL-C水平低于IMT正常组,差异均有统计学意义(P0.05)。Pearson相关性分析显示,高血压患者的IMT与SBP、DBP、TC、TG、LDL-C、血尿酸均呈正相关,与HDL-C呈负相关(P0.05)。结论:高血压患者IMT与血脂、血压和血尿酸水平均有明显相关性,血压、血脂、血尿酸参与了高血压患者CAS的发生与发展。     

不同剂量阿伐他汀联合阿司匹林治疗原发性高血压并动脉粥样硬化的临床研究

目的:探讨不同剂量阿托伐他汀联合阿司匹林治疗原发性高血压并动脉粥样硬化的临床疗效。方法:选取2015年1月-2016年12月在我院治疗的原发性高血压并动脉粥样硬化患者80例,随机分为对照组和实验组,每组40例。实验组给予口服高剂量阿托伐他汀(40 mg/d)联合阿司匹林肠溶片(100 mg/d)治疗,对照组给予口服高剂量阿托伐他汀(20 mg/d)联合阿司匹林肠溶片(100 mg/d)治疗,疗程均为3个月。观察和比较两组患者治疗前后的总胆固醇(total cholesterol,TC)、高密度脂蛋白胆固醇(high-density lipoproteincholesterol,HDL-C)、甘油三酯(triglyceride,TG)、低密度脂蛋白胆固醇(low-density lipoprotein cholesterol,LDL-C)、收缩压(systolic blood pressure,SBP)、舒张血压(diastolic blood pressure,DBP)以及颈动脉斑块分级。结果:两组治疗后的SBP、DBP、血清TC、TG和LDL-C水平均较治疗前显著降低,血清HDL-C水平较治疗前明显升高,且实验组SBP、DBP、血清TC、TG和LDL-C水平均显著低于对照组(P0.05),血清HDL-C水平明显高于对照组(P0.05)。实验组颈动脉斑块0-Ⅰ级的比例显著高于对照组(P0.05)。结论:口服高剂量阿托伐他汀(40 mg/d)联合阿司匹林肠溶片(100 mg/d)治疗原发性高血压并动脉粥样硬化较低剂量阿托伐他汀(20 mg/d)联合阿司匹林肠溶片(100 mg/d)疗效更好,可以有效降低血压,调节血脂并改善患者预后。     

甲状腺功能异常患者血清同型半胱氨酸及血脂水平检测的临床意义

目的:研究原发性甲状腺功能减退症患者和甲状腺功能亢进患者血清同型半脱氨酸(Hey)、血脂水平与心血管疾病的关系.方法:检测29例原发性甲减者、35例甲亢患者以及30例健康体检者(对照组)的空腹血清游离三碘甲状腺原氨酸(FT3)、游离甲状腺素(FT4)、Hcy、甘油三酯(TG)、总胆固醇(Tch)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)水平,并对其进行相关分析.结果:原发性甲减患者Hcy、TG、Tch、LDL-C水平明显高于对照组(p＜0.01、0.01、0.01、0.01),而HDL-C水平却与对照组相比明显降低(p＜0.01);相关分析表明,甲减患者Hey与FT3、FT4水平间呈显著负相关(r=-0.432、-0.354,p＜0.01、0.01),与TG、Tch水平呈显著正相关(r=0.339、0.452,p＜0.01、0.01);而与HDL-C、LDL-C均无相关性.甲亢组Hcy和Tch水平较正常对照组明显降低(p＜0.01、0.01),Hcy与FT4水平间呈显著负相关(r=-0.408,p＜0.01).结论:血清同型半胱氨酸水平可能对判断甲状腺功能有辅助作用;甲状腺激素水平影响了Hcy及血脂水平的代谢;血清Hcy水平升高是甲减患者易患心血管疾病的危险因素.     

血压、血脂、血糖、同型半胱氨酸及超敏C反应蛋白水平与脑梗死发病危险性的关系

目的:探讨血压、血脂、血糖、糖化血红蛋白、同型半胱氨酸(HCY)和超敏C反应蛋白(hs-CRP)与脑梗死发病危险性的相关性,为及时防止脑梗死的发病及早期诊断脑梗死提供理论依据。方法:采用回顾性病例对照研究,用全自动生化分析仪器检测各项生化指标,并运用SPSS 20.0软件包对256例脑梗死患者和216例健康对照者的血生化指标进行统计分析。同时,将脑梗死组分为三组:单纯脑梗死组、合并高血压组、合并糖尿病组,分别与正常对照组进行血脂水平的分析比较。结果:血压、总胆固醇(TC)、三酰甘油(TG)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇酯(HDL-C)、同型半胱氨酸(HCY)、血糖、hs-CRP水平和总胆固醇/高密度脂蛋白胆固醇(TC/HDL-C)比值在病例组和对照组间有显著性差异(P0.05)。同时,在三组不同的病例组中血脂(TC、TG、LDL-C、TC/HDL-C)水平和HCY水平明显高于正常对照组,而HDL-C水平则明显低于对照组。(P0.05)。结论:高血压、高血糖、HCY、hs-CRP水平增高及血脂异常均与脑梗死发病危险性相关,联合检测上述指标对预防及治疗脑梗死均有重要意义。     

2011~2014 年体检者血压水平与血清尿酸水平的关系

目的：分析2011~2014 年我院体检者血压水平与血清尿酸(UA)水平的关系。方法：选择我院2011~2014 年2150 例体检者为 研究对象,均完成血压（SBP、DBP),心率（HR）、身高、体重指数（BMI）、空腹血糖（FPG）、高密度脂蛋白胆固醇(HDL-C) 、低密度脂 蛋白胆固醇(LDL-C) 、血清总胆固醇(TC) 、甘油三酯(TG)及UA 指标检测,并对检测结果进行分析。结果：2150 例体检人群中,高 血压为860 人,占40.0%,高血压组BMI、FPG、LDL-C、TC、TG 及UA 均明显高于非高血压组,而HDL-C 明显低于非高血压组, 比较差异具有统计学意义（P＜0.05）;多因素Logistic 回归分析显示,上述指标均为高血压的独立危险因素（P＜0.05）。结论：血压 水平的升高与UA水平具有密切联系,早期控制UA水平对预防高血压的发生具有重要意义。     

9758 例健康体检者血糖与血脂的关系分析

目的:探讨健康体检人群血糖与血脂现况及两者之间的相关性。方法:采集我院9758例健康体检者的空腹静脉血,检测其空腹血糖(FPG)、总胆固醇(TC)、甘油三酯(TG)、高密度脂蛋白(HDL-C)和低密度脂蛋白(LDL-C)水平,比较不同FPG水平组间各血脂水平,分析FPG水平与血脂的相关性。结果:各年龄组FPG、TC、TG、HDL-C和LDL-C水平差异均具有统计学意义(P0.05);FPG均与TC、TG和LDL-C水平呈现正相关(r=0.127,0.189,0.141,P0.005),而与HDL-C呈现负相关(r=-0.112,P0.005);根据FPG水平由高到低分为糖尿病(DM)组,血糖调节受损(IFG)组及血糖正常组,其中对TC和LDL-C水平异常率而言,IFG组DM组血糖正常组;对TG、HDL-C水平异常率而言,DM组IFG组血糖正常组。结论:健康人群中血糖和血脂水平呈现一定的相关性,两者的水平异常会增加慢性疾病的发生风险。     

老年原发性高血压患者脉搏波传导速度与心脑血管危险因素关系的研究

目的:探讨老年原发性高血压患者脉搏波传导速度与心脑血管危险因素关系。方法:随机选取2012年5月至2012年8月在我院体检的160例新诊老年原发性高血压患者及120例健康个体,所有个体均未接受治疗,采用动脉硬化检测仪测定患者肱踝脉搏波传导速度(baPWV),同时测量身高、腰围、体重、血压、总胆固醇(TC)、甘油三酯(TG)、空腹血糖(FBS)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)、尿酸(UA)、肌酐(Cr)等指标,探讨老年原发性高血压患者高脂血症、吸烟、肥胖、糖尿病等危险因素与baPWV指标变化的关系。结果:不同血压分级的老年原发性高血压患者之间肱踝脉搏波传导速度值存在显著差异(P0.01)。合并冠心病、肥胖、糖尿病、吸烟、高脂血症等危险因素的高血压患者baPWV值显著高于单纯性原发性高血压患者(P0.01)。多元回归分析表明:吸烟史(P0.01)、冠心病史(P0.01)、糖尿病史(P0.01)、年龄(P0.01)、腰围(P0.01)、血压(P0.01)、HDL-C(P0.01)、TC(P0.01)、FBS(P0.01)、LDL-C(P0.01)、Cr(P0.01)是baPWV升高的独立风险因素。结论:老年原发性高血压患者存在不同程度的的动脉僵硬增高,常见心脑血管风险因素同样影响老年原发性高血压患者僵硬度。     

藏族原发性高血压患者血管内皮功能与糖脂代谢指标和血压变异性的关系

目的:研究藏族原发性高血压患者血管内皮功能与糖脂代谢指标和血压变异性的关系。方法:以2017年2月-2018年2月暨南大学医学院附属广州红十字会医院收治的200例藏族原发性高血压患者为研究对象。将所有患者按照肱动脉血流介导的血管舒张功能(FMD)值分为正常FMD组(FMD≥6%)48例与异常FMD组(FMD6%)152例。分别比较两组患者的基本资料、糖脂代谢指标以及血压变异性指标水平,并分析藏族原发性高血压患者FMD与糖脂代谢和血压变异性的相关性。结果:异常FMD组年龄、空腹血糖水平高于正常FMD组(P0.05),而两组总胆固醇、甘油三酯、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)水平对比差异均无统计学意义(P0.05)。异常FMD组日间收缩压、日间舒张压、夜间收缩压、夜间舒张压、24h收缩压、24h舒张压水平均高于正常FMD组(P0.05)。经Preason相关性分析可得:藏族原发性高血压患者FMD值与空腹血糖、日间收缩压、日间舒张压、夜间收缩压、夜间舒张压、24h收缩压、24h舒张压均呈负相关关系(P0.05)。结论:藏族原发性高血压患者血管内皮功能受损越严重,其空腹血糖、血压就越高,临床工作中可通过联合检查上述指标水平,有助于评估藏族原发性高血压患者血管内皮功能。     

Altered vascular reactivity in arterioles of chronic intermittent hypoxic rats.

Recurrent episodic hypoxia (EH) is a feature of sleep apnea that may be responsible for some chronic cardiovascular sequelae such as systemic hypertension. Chronic EH (8 h/day for 35 days) causes elevation of diurnal resting (unstimulated) mean arterial blood pressure (MAP) in the rat. We used in vivo video microscopy to examine arteriolar reactivity in the cremaster muscle of male Sprague-Dawley rats subjected to 35 days of EH. Cremaster muscles of EH (n = 6) and control (n = 6) rats were exposed to varying doses of norepinephrine (NE) (10(-10) to 10(-5) M), ACh (10(-9) to 10(-5) M), and endothelin-1 (10(-12) to 10(-8) M). In a separate experiment, EH (n = 5) and control (n = 6) rats were given one dose of a nitric oxide synthase (NOS) inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME; 10(-5) M). We also examined endothelial NOS mRNA from the kidneys of EH-stimulated and control (unstimulated) rats. Telemetry-monitored EH rats showed a 16-mmHg increase in MAP over 35 days, whereas control rats showed no change. The response to NE and endothelin-1 were similar for EH and control rats. ACh vasodilatation of arterioles in EH rats was significantly attenuated compared with that of controls. The degree of vasoconstriction in response to blockade of the nitric oxide system by L-NAME was significantly less (83% of baseline diameter with L-NAME) for arterioles of EH rats compared with that for controls (61% of baseline diameter), implying lower basal resting nitric oxide release in the EH rats. Whole kidney mRNA endothelial NOS levels were not different between groups. These data support the hypothesis that chronic elevation of blood pressure associated with EH involves increased peripheral resistance from decreased basal release or production of nitric oxide after 35 days of EH.     

Evidence for physiological coupling of insulin-mediated glucose metabolism and limb blood flow

We hypothesized that the vasodilation observed during insulin stimulation is closely coupled to the rate of glucose metabolism. Lean (L, n = 13), obese nondiabetic (OB, n = 13), and obese type 2 diabetic subjects (Type 2 DM, n = 16) were studied. Leg blood flow (LBF) was examined under conditions of euglycemic hyperinsulinemia (EH) and hyperglycemic hyperinsulinemia (HH), which produced a steady-state whole body glucose disposal rate (GDR) of approximately 2,000 micromol. m(-2). min(-1). At this GDR, under both conditions, subjects across the range of insulin sensitivity exhibited equivalent LBF (l/min EH: L, 0.42 +/- 0.03; OB, 0.43 +/- 0. 03; Type 2 DM, 0.38 +/- 0.07; P = 0.72 by ANOVA. HH: L, 0.44 +/- 0. 04; OB, 0.39 +/- 0.05; Type 2 DM, 0.41 +/- 0.04; P = 0.71). The continuous relationship between LBF and GDR did not differ across subject groups [slope x 10(-5) l/(micromol. m(-2). min(-1)) by ANOVA. EH: L, 8.6; OB, 9.2; Type 2 DM, 7.9; P = 0.91. HH: L, 4.2; OB, 2.5; Type 2 DM, 4.1; P = 0.77], although this relationship did differ between the EH and HH conditions (P = 0.001). These findings support a physiological coupling of LBF and insulin-mediated glucose metabolism. The mechanism(s) linking substrate delivery and metabolism appears to be intact in insulin-resistant states.     

Obesity--a risk factor for diabetic retinopathy in type 2 diabetes?

The aim of the study was to investigate whether obesity, independently or associated with other risk factors, increases the risk for the diabetic retinopathy in type 2 diabetic persons. Data of 156 diabetic persons that have consecutively attended the Outpatient Department in the Vuk Vrhovac Institute in Zagreb during two months period were studied. According to their body mass index (BMI) they were divided into three groups: group 1 (BMI < or = 25; n = 49), group 2 (BMI 26-29.9; n = 52) and group 3 (BMI > or = 30; n = 55). The three groups did not differ in age, duration of diabetes, treatment, cholesterol, HDL-cholesterol and triglycerides. With increase in BMI, we observed a significant deterioration of HbA1c and a significant increase in LDL-cholesterol, systolic and diastolic blood pressure. Statistical analyses shown that the prevalence of retinopathy increased significantly with higher body weight (gr. 1: 40.8%, gr. 2: 63.4%, gr. 3: 63.6%;p < 0.05), but also with correlation to quality of metabolic control (HbA1c) and systolic blood pressure. Therefore, obesity may be, because of its significant correlation to quality of metabolic control (HbA1c) and systolic blood pressure, considered as risk factor for diabetic retinopathy in type 2 diabetic persons.     

检测窦性心率震荡对诊断2型糖尿病患者隐性高血压效果的临床研究

目的:研究窦性心率震荡诊断2型糖尿病合并隐性高血压患者的临床效果。方法:对2009年12月至2013年4月我院心内科收治的2型糖尿病合并高血压患者123例进行回顾性分析,根据诊室内手测血压及24 h动态血压监测结果将患者分为高血压组(EH组)及隐性高血压组(MH)组,另取在我院体检的诊室及24小时动态血压均正常者为NT组,三组研究对象均进行诊室内手测血压,24 h动态血压监测及HRT检测,比较三组检测结果。结果:(1)诊室内手测血压结果显示MH组收缩压及舒张压与NT组差异无统计学意义(P0.05);EH组收缩压及舒张压与NT组比较差异具有统计学意义(P0.05)。(2)24 h动态血压监测结果显示MH组及EH组收缩压与舒张压与NT组比较差异均具有统计学意义(P0.05)。(3)HRT检测结果显示MH组及EH组TO值与TS值与NT组比较差异均具有统计学意义(P0.05)。结论:HRT检测结果可作为诊断2型糖尿病患者隐性高血压的一项可靠指标。     

血浆Apelin-36水平与高血压病的相关性研究

目的：探讨原发性高血压（EH）患者24小时平均血压水平与血浆Apelin-36水平的相关性。方法：选择2009年6月一2010年6月在我院心内二科住院的EH患者146例为观察组,选择144例血压正常者作为对照组。抽取空腹静脉血,采用放射免疫法（RIA）检测所有研究对象的血浆Apelin-36水平。结果：①血压正常组血浆Apelin-36水平24.65±4.10pmol/l;EH组20.81±4.98 pmol/l;两组间比较有显著统计学差异（P〈0.01）。②EH患者者血浆Apelin-36水平与24小时平均收缩压、白天平均收缩压、夜间平均收缩压均呈负相关（P〈0.05）。结论：EH组血浆Apelin-36水平显著低于正常对照组,24小时平均血压越高,血浆Apelin-36水平越低,且血浆Apelin-36水平与24小时平均血压水平呈负相关。     

Plasma cortisol and corticosteroid-binding globulin in essential hypertension

Plasma concentration of cortisol, total CBG-binding capacity, and blood pressure were measured in control subjects (n = 171), patients with essential hypertension (EH; n = 210) and their first-degree normotensive (NR; n = 84) or hypertensive (HR; n = 66) relatives. Mean (+/- SD) plasma cortisol was significantly (p less than 0.001) decreased in EH (10.1 +/- 4.3 g/dl) patients and HR (11.7 +/- 4.1). Plasma cortisol in NR did not differ from control values (14.3 +/- 4.5) but the distribution of individual values covered the entire control-EH (14.6 +/- 5.5) range. Mean (+/- SD) CBG-binding capacity was significantly (p less than 0.001) lower in EH (14.4 +/- 3.0), NR (17.5 +/- 2), HR (17.6 +/- 2.2) as compared to controls (20.9 +/- 2.1), indicating that the decline in EH and in most relatives was mainly in plasma CBG-bound cortisol. The plasma CBG-binding capacity for cortisol was significantly negatively correlated with mean arterial pressure (MAP) in both controls (p less than 0.001) and NR (p less than 0.01) but not in either HR (r = 0.02) or never-treated EH patients. Total afternoon plasma aldosterone was higher (p less than 0.01 vs. controls) in 93 untreated EH patients (11.2 +/- 4.8 ng/dl) than in either 161 first-degree relatives (8.1 +/- 3.4 ng/dl) or 117 controls (7.6 +/- 3.5 ng/dl). The respective aldosterone-binding globulin (ABG) binding capacities for aldosterone were 21.2 +/- 6.7, 20.1 +/- 9.3 and 9.8 +/- 4.0%. In all these subjects taken together, there was a positive correlation between MAP and ABG-binding capacity (r = 51; p less than 0.001). The association of reduced plasma cortisol and decreased CBG binding capacity in EH may be closely related to altered steroid metabolism, which may be partly explained by an abnormality resembling a relative deficiency in adrenal 17 alpha- and 11 beta-hydroxylation. In some EH patients, hypertension may be the result of the ineffectiveness of plasma cortisol in preventing slightly elevated endogenous ACTH levels leading to an increase in ACTH-sensitive steroids.     

Relationship between clinical, 24-hour, average day-time and night-time blood pressure and measures of arterial stiffness in essential hypertension

Arterial wall stiffness is considered an independent cardiovascular risk factor. Aim of this study was to evaluate relationship between clinical, 24-hour, average day-time and night-time blood pressure (BP) and measures of arterial stiffness assessed by pulse wave velocity (PWV) (using SphygmoCor applanation tonometer) in essential hypertension (severe-resistant (RH, n=29) and moderate hypertension (EH, n=35)) and in normotensive control subjects (n-29) (NCS) matched by age. After multiple regression analysis, PWV remains significantly correlated mainly with night-time pulse pressure and to a lesser extent with age. PWV was significantly higher in RH compared to moderate EH and NCS.     

高血压不同并发症患者动态血压特点分析

目的:探讨高血压不同并发症患者动态血压特点。方法:选取123例确诊为高血压病的患者,根据合并不同的并发症分为四组,即单纯高血压(EH)组、高血压合并心房颤动(EH-AF)组、高血压合并腔隙性脑梗死(EH-LI)组和高血压合并左室肥厚(EH-LVH)组,行24H动态血压监测,分析动态血压各参数的变化。结果:合并有各种并发症的原发性高血压患者,其3级高血压所占百分比明显高于单纯原发性高血压,其平均收缩压和平均舒张压及收缩压、舒张压负荷值及血压昼夜波动节律异常均高于单纯原发性高血压患者;高血压合并左室肥厚患者,与高血压合并心房颤动及腔隙性脑梗死患者比较,平均收缩压和平均舒张压及收缩压、舒张压负荷值及血压昼夜波动节律异常均升高。结论:血压水平、血压负荷及血压昼夜波动节律异常与高血压并发症密切相关;高血压病合并不同并发症,其动态血压参数有不同特点。     

Effect of somatostatin on plasma renin activity and blood pressure in patients with essential hypertension

The effects of somatostatin on plasma renin activity (PRA) and blood pressure were evaluated in patients with essential hypertension (EH) and in normotensive subjects. All subjects examined were hospitalized and placed on a diet containing 7-8 g/day sodium chloride and received an intravenous infusion of somatostatin (500 microgram/20 ml of saline, for 60 min) in the basal condition. During somatostatin infusion, the mean blood pressure (MBP) remained unaffected in all patients with EH and the normotensive subjects, while the PRA decreased slightly in the EH group. When the patients with EH were classified according to their renin levels (low, normal and high), parallel significant decreases in MBP and PRA were found only in the high renin group during the somatostatin infusion. No significant change in MBP and PRA was observed in the other groups including the normotensive subjects. To assess the activity of synthetic somatostatin, the plasma levels of growth hormone (GH) and cyclic AMP were measured. These levels were lowered significantly during the infusion and the GH levels showed a rebound 15 min after cessation of the infusion. The cyclic AMP returned to the basal levels, but no rebound was observed. The above data indicate that the fall in blood pressure in the high renin group in the basal condition was probably due in part to reduced renin release by somatostatin, and the maintenance of high blood pressure especially in high renin EH.