盐敏感性高血压患者同型半胱氨酸水平与血压及心率变异性的相关性

目的 探讨盐敏感性高血压患者同型半胱氨酸(Hcy)水平与血压变异性（BPV）和心率变异性（HRV）之间的关系。 方法 收集2015年至2016年入住中国中医科学院广安门医院131例盐敏感高血压患者,以Hcy≥15 μmol/L为Hcy升高组,<15 μmol/L为正常组。通过对患者血压及心率的动态监测,采用SPSS 26.0统计学软件对数据进行处理,分析比较两组间血压和心率变异性相关参数。 结果 两组患者的年龄和性别构成的差异均无统计学意义。升高组Hcy水平显著高于正常组（P<0.01）;升高组24 h平均收缩压（24HASBP）、24 h平均舒张压（24HADBP）、24 h收缩压变异性(24HSBPV)和24 h舒张压变异性(24HDBPV)均显著高于正常组（P<0.01,P<0.01,P<0.05,P<0.01）;而升高组心率变异性指标所有相邻心搏R-R间期之差的标准差(RMSDD)、所有心搏的R-R间期的标准差(SDNN)、每5 min心搏 R-R 间期均值的标准差(SDANN)则显著低于正常组（P<0.05,P<0.01,P<0.01）。其中Hcy水平与24HADBP、24HDBPV、RMSSD、SDNN之间有相关性（P<0.01）,其中与RMSSD和SDNN呈负相关。且多元线性逐步回归分析显示,上述二者与Hcy水平之间具有显著影响（P<0.05）。 结论 盐敏感性高血压患者Hcy水平与BPV和HRV之间具有相关性。     

原发性高血压患者血清同型半胱氨酸水平与靶器官损害的关系

目的探讨原发性高血压患者血清同型半胱氨酸(Hcy)水平与靶器官损害的关系。方法入选原发性高血压患者155例,按Hcy水平分为两组:Hcy10μmol/L及Hcy≥10μmol/L。两组患者均接受24小时动态血压、颈动脉超声、超声心动图、血肌酐及尿微量白蛋白等检测。结果 Hcy≥10μmol/L患者发生动脉粥样硬化(颈动脉内膜中层增厚或粥样斑块)及肾功能异常(肾小球率过滤降低或血肌酐升高)的比例明显高于Hcy10μmol/L患者(P0.05)。两组患者左心室质量指数及尿微量蛋白升高比例差异无统计学意义(均P0.05)。多因素Logistic回归分析显示Hcy≥10μmol/L患者发生动脉粥样硬化的风险是Hcy10μmol/L患者的1.36倍。结论血中同型半胱氨酸水平升高与原发性高血压患者靶器官损害相关,以动脉粥样硬化更为明显。     

高同型半胱氨酸血症相关疾病诊治

<正>1969年Mccully~([1])在遗传性同型半胱氨酸血症死亡儿童尸检中发现广泛的动脉血栓形成及动脉粥样硬化(AS),首次提出高同型半胱氨酸血症(HHcy)可导致AS性血管疾病的假说。Hcy通过氧化应激反应导致内皮细胞和内质网损伤,破坏机体凝血和纤溶之间的平衡,使机体处于血栓前状态,引起血管平滑肌细胞增殖和胶原合成,加速AS进程。2006年美国心脏协会脑卒中指南~([2])将HHcy作为脑卒中独立危险因素,确定诊断     

高血压病患者盐敏感性与高胰岛素血症之间的关系

目的：探讨高胰岛素血症（ＨＩＳ）与盐敏感性高血压病肾脏排钠障碍间的关系。方法：根据盐敏感性（盐负荷试验Ｓｕｌｉｖａｎ标准），将５３例高血压病患者分为２组：盐敏感型（ＳＳ）组２２例、盐不敏感型（ＳＲ）组３１例。测定患者在盐负荷试验中血糖和血胰岛素浓度变化，计算胰岛素抵抗。结果：ＳＳ组与ＳＲ组相比较，基础状态、盐负荷和服呋喃苯胺酸（速尿）后各时点血糖及血胰岛素变化明显（血糖：５．１２±１．２５、５．９７±１．５９、５．２１±１．２８ｍｍｏｌ／Ｌ比４．９６±１．１４、５．４８±１．３８、５．０７±１．２３ｍｍｏｌ／Ｌ，Ｐ＞０．０５；血胰岛素：１２．４６±４．１４、３１．６８±１２．２１、１４．３５±４．４５ｍＵ／Ｌ比１０．１５±３．６２、２２．１４±８．６４、１０．８９±３．９１ｍＵ／Ｌ，Ｐ＜０．０１），ＳＳ组中胰岛素抵抗发生率显著高于ＳＲ组（６３．６％比３２．３％，Ｐ＜０．０５）。结论：ＳＳ高血压病肾脏排钠障碍与高胰岛素血症有关。     

老年人盐敏感性与高血压

老年人高血压通常表现为盐敏感性单纯收缩期高血压。这种盐敏感性并非由于盐摄入量增加,而部分是由于适当排钠减少。与年龄相关的膜钠/钾 ATP酶活性降低,也可促发老年人高血压。钙ATP酶活性降低,细胞内钙外流减少,从而使细胞内钙增加和血管阻力增加。钙对盐敏感性高血压的作用机理为:①抑制甲状旁腺激素而减少钙内流;②增加钠/钾ATP酶的活性;③钙致钠利尿而减少血容量。     

高同型半胱氨酸血症与心房颤动

同型半胱氨酸是蛋氨酸代谢的中间产物,高同型半胱氨酸血症是心房颤动的独立危险因素,近年来一系列临床研究表明,高同型半胱氨酸血症通过氧化应激、参与心房离子通道重构、促进血栓形成等机制参与房颤的发生发展。高同型半胱氨酸血症与心房颤动密切相关,本文旨在阐述高同型半胱氨酸血症与房颤发生的潜在机制,以期寻找防治心房颤动的新途径,为临床进一步研究提供参佐。     

高同型半胱氨酸血症与高血压及临床处理

同型半胱氨酸（homocysteine,Hcy）是体内的一种含硫氨基酸,是甲硫氨酸和半胱氨酸代谢过程中一个重要的中间产物。高同型半胱氨酸血症（hyperhomocysteinemia,Hh—cy）是指血浆中游离的及与蛋白结合的同型半胱氨酸和混合性二硫化物的水平升高。     

盐敏感性高血压特点及防治

盐敏感性是连接盐与高血压的遗传基础, 其涉及一系列病理生理改变: 钠代谢异常、交感神经活性增强、胰岛 素抵抗、内皮功能不良、氧化应激及炎症激活等。盐敏感性高血压有其独特的临床特点: 盐负荷后血压明显升高, 血 压的昼夜差值缩小, 血压的应激反应增强, 靶器官损害出现早。在盐敏感性高血压的防治中, 限盐是关键, 其次包 括补充钾离子、钙离子摄入以及替代低钠盐的应用。钙拮抗剂和利尿剂是治疗盐敏感性高血压的首选药物。     

Increased insulin resistance in salt sensitive essential hypertension

OBJECTIVE: To determine the possible relationship between insulin resistance and salt sensitivity in essential hypertension. DESIGN AND METHODS: We studied 17 non-obese, essential hypertensive patients (24-h blood pressure: 149 +/- 15/94 +/- 5 mm Hg) with normal glucose tolerance. Salt sensitivity was diagnosed in the presence of a significant increase (P < 0.05, more than 4 mm Hg) in 24-h mean blood pressure (MBP) when patients switched from a low-salt intake (50 mmol/day of Na(+)) to a high-salt intake (240 mmol/day of Na(+)), each period lasting 7 days. The insulin sensitivity index was determined by the euglycaemic hyperinsulinaemic clamp. RESULTS: Six patients were classified as salt sensitive (24-h MBP increase: 6.2 +/- 1.1 mm Hg), and 11 as salt resistant (24-h MBP increase: -1.2 +/- 3.8 mm Hg). No significant differences were observed between salt sensitive and salt resistant patients regarding baseline characteristics, fasting serum insulin, fasting serum glucose, glycosylated haemoglobin, total cholesterol, HDL-cholesterol, LDL-cholesterol, triglycerides, uric acid and microalbuminuria. Salt sensitive patients exhibited a reduced insulin sensitivity index compared with salt resistant patients (1.7 +/- 1.1 vs 3.5 +/- 1.2 mg/kg/min; P = 0.009). An inverse relationship (r -0.57; P = 0.016) between the insulin sensitivity index and 24-h MBP increase with high salt intake was found. CONCLUSION: Salt sensitive essential hypertensive patients are more insulin resistant than salt resistant patients when both salt sensitivity and insulin resistance are accurately measured. Indirect measures of both insulin and salt sensitivity and/or the presence of modifying factors, such as obesity or glucose intolerance, may account for differences in previous studies.     

Calcium metabolism and dietary calcium in salt sensitive hypertension

Evidence has accumulated over the past decade that suggests a relationship between low calcium intake, abnormalities in cation metabolism and hypertension in certain segments of the essential hypertension population. This evidence has been developed from epidemiological data, calcium intervention trials and observations related to biochemical alterations suggestive of a calcium deficiency in certain patients with hypertension and in animal models of essential hypertension. It is becoming increasingly evident that salt sensitive individuals are especially likely to be characterized by abnormalities of calcium metabolism and blood pressure responses to dietary calcium. In this review the role of calcium in the regulation of blood pressure is examined with an emphasis on epidemiological, biochemical, hemodynamic and dietary intervention data in the salt sensitive hypertensive patient.     

Calcium and calcium regulating hormones in the "prehypertensive" Dahl salt sensitive rat (calcium and salt sensitive hypertension)

The purpose of this study was to determine if alterations of calcium and calcium regulating hormones precede the onset of NaCl induced hypertension in the Dahl salt sensitive (S) rat. After a 5 day balance study, serum ionized calcium, PTH, and 1,25 dihydroxy vitamin D concentrations were measured in Dahl-S and salt resistant (R) rats that had been maintained on a "normal" (1%) or high (7%) NaCl intake. Blood pressure was higher in Dahl-S than R (P less than .01), but was not affected by 5 days of high NaCl. On both NaCl intakes, urine calcium excretion was increased, serum calcium was decreased, and serum PTH and 1,25 dihydroxy vitamin D were increased in Dahl-S compared to Dahl-R (P less than .01). On the high NaCl intake, fecal calcium was greater in Dahl-S than in Dahl-R, and net 5 day calcium balance was less positive in Dahl-S (P less than .05). In contrast to NaCl, a high dietary intake of sodium with anions other than chloride (NaAA) fails to produce hypertension in the Dahl-S rat. NaAA loading resulted in decreased urine calcium excretion (P less than .01), and after 5 days of the high NaAA diet, serum calcium and PTH did not differ in Dahl-S and Dahl-R. Thus, alterations of calcium, PTH, and vitamin D precede NaCl-induced hypertension in Dahl-S. These alterations may contribute to the development of hypertension in this animal model.     

Modest salt reduction lowers blood pressure in isolated systolic hypertension and combined hypertension

Many randomized trials have shown that a reduction in salt intake lowers blood pressure in hypertensive individuals. However, few have looked at the effects according to hypertension category. A recent analysis of the third and fourth National Health and Nutrition Examination Survey suggests that salt intake may not be related to blood pressure in isolated systolic or combined hypertension. To look at this further, we reanalyzed the data of our previous salt reduction trials. Hypertensive individuals were studied in randomized double-blind crossover studies: 1 month of usual salt intake compared with 1 month of reduced salt intake. In isolated systolic hypertension (n=24), blood pressure was reduced from 166+/-19/86+/-7 to 156+/-20/85+/-7 mm Hg (systolic P<0.001; diastolic P=0.459) with a reduction in urinary sodium from 175+/-51 to 87+/-38 mmol per 24-hour period (10.3 to 5.1 g per day of salt). In combined hypertension (n=88), blood pressure was reduced from 161+/-16/100+/-9 to 154+/-17/96+/-9 mm Hg (P<0.001) with a reduction urinary sodium from 176+/-65 to 98+/-51 mmol per 24-hour period (10.4 to 5.8 g per day of salt). These results demonstrate that salt reduction has a significant effect on blood pressure in isolated systolic and combined hypertension. The fall in systolic observed in isolated systolic hypertension would be predicted to reduce stroke by approximately one third, ischemic heart disease by one quarter, and heart failure by one quarter in the population between 60 and 80 years of age, in whom isolated systolic hypertension is the predominate form of hypertension and carries the highest risk. These results provide strong support for universal salt reduction in all hypertensives.     

子宫肌瘤合并高血压56例临床分析

目的探讨子宫肌瘤合并高血压的关系。方法选择2008-03～2009-06收治的子宫肌瘤合并高血压患者56例,对其治疗前后的血压变化进行回顾性的比较分析。结果 56例患者术后血压恢复正常者51例(91.07%),降低者3例(5.36%),无明显改变者2例(3.57%)。与手术前比较,收缩压和舒张压均明显降低,差别均具有统计学意义(P0.05)。结论本组结果表明,子宫肌瘤并发高血压者在行子宫肌瘤切除后血压可得到有效控制,具体原因有待进一步研究。     

Increased concentration of plasma immunoreactive atrial natriuretic factor in Dahl salt sensitive rats with sodium chloride-induced hypertension

In order to determine whether there is a relationship between genetically determined salt-induced hypertension and atrial natriuretic factor (ANF), a radio-immunoassay for ANF was applied to the determination of immunoreactive ANF in plasma, atrium, hypothalamus and pons of Dahl salt-sensitive (S) and -resistant (R) rats which were fed high- or low-salt diet for 7 weeks. A twofold higher concentration of plasma ANF was observed in high-salt S rats, which developed hypertension, compared with low-salt S rats or R rats on high or low salt, which were normotensive. No significant difference was seen in atrial concentrations of ANF between S and R rats. The brain ANF concentration of the high-salt group was lower than that of the low-salt group in both S and R rats. It is proposed that the elevation of plasma ANF in the hypertensive rats may reflect a compensatory mechanism induced by volume expansion in the salt-fed S rats.     

缬沙坦合并吲达帕胺治疗高血压疗效观察

目的研究分析采用缬沙坦合并吲达帕胺治疗高血压的临床效果。方法选取2011年9月至2013年11月,在我院接受治疗的72例高血压患者,随机分为观察组和对照组,每组36例。观察组患者采用缬沙坦合并吲达帕胺治疗,对照组单纯采用缬沙坦治疗,比较两组患者的治疗效果、治疗前后的血压变化及不良反应情况。结果观察组的治疗总有效率要优于对照组的总有效率(P0.05);治疗2周后,观察组的收缩压和舒张压下降幅度均要优于对照组(P0.05),治疗4周后,观察组的收缩压先于对照组降至正常(P0.05),治疗6周后,两组患者的舒张压差距加大,整个治疗期间观察组的舒张压下降幅度均低于对照组(P0.05);两组患者的不良反应情况比较无显著差异(P0.05),不具有统计学意义。结论高血压患者采用缬沙坦合并吲达帕胺治疗的临床效果显著,而且不良反应少,值得临床推广和应用。     

扩张型心肌病合并肺动脉高压的临床特点分析

目的 探讨扩张型心肌病（DCM）合并肺动脉高压的临床特征.方法 连续选取我院诊断DCM的住院患者98例,根据超声数据分为正常肺动脉压组（43例）和肺动脉高压组（55例）.回顾性分析两组的一般资料、生化和超声心动图等检查数据.结果 肺动脉高压组一般资料与正常组患者比较差异均无统计学意义.超声心动图检查肺动脉高压组患者的左心室舒张末径、左心房内径、右心室内径显著大于正常组[分别为（72.36±11.14）mm比（66.82±10.54）mm、（51.76±9.25）mm比（43.13±8.93）mm和（27.93±6.85）mm比（21.47±5.09）mm,P均＜0.05],左心室射血分数显著低于正常组[（28.51±9.36）％比（35.73±10.51）％,P＜0.05],脑利钠肽（BNP）水平显著高于正常组[（1254.73±569.36）ng/ml比（573.26±257.14） ng/ml,P＜0.05].结论 DCM合并肺动脉高压的患者心脏扩张较显著,心功能更差,临床预后可能较差.