黄芪、全蝎、红花、丹参、葛根混合剂抑制自发性高血压大鼠阻力血管肥厚

目的观察黄芪、全蝎、红花、丹参、葛根混合剂(脑心通)对自发性高血压大鼠(SHR)阻力血管结构和血压的影响。方法选择12周龄雄性 SHR 大鼠(二级)32只,随机分成4组,脑心通大剂量组[1.5 g/(kg·d)]、脑心通小剂量组[0.5 g/(kg·d)]、氯沙坦组[30 mg/(kg·d)]和 SHR 组(给等量蒸馏水)。另选周龄、性别相匹配的Wistar Kyoto(WKY,给等量蒸馏水)大鼠8只。各组每日灌胃给药。12周后尾袖法测定动脉血压,称质量后处死。HE 染色,计算机图像分析计算血管壁腔比,以观察各组大鼠肠系膜三级动脉的结构变化。结果 1)大、小剂量脑心通治疗后,两组 SBP 均显著低于 SHR 组[脑心通大剂量:(153.6±12.2)比脑心通小剂量:(159.2±5.8)比 SHR:(178.6±12.0)mmHg,P<0.01];大剂量脑心通组 SHR 治疗后 SBP 较治疗前明显降低[(153.6±12.2)比治疗前(163.6±11.8)mmHg,P<0.01],与小剂量组比较能更进一步降低血压(P<0.05)。2)与 SHR 组相比,小剂量脑心通治疗对肠系膜三级动脉血管的管壁面积/管腔...     

软脉灵对自发性高血压大鼠心肌纤维化的作用

目的 观察软脉灵对自发性高血压大鼠(SHR)心肌纤维化的影响.方法 选择12周龄雄性SHR 36只,随机分为4组,软脉灵大剂量和小剂量组、空白组、阳性对照组.血压正常的京都Wistar大鼠(WKY)为正常对照组(WKY组).治疗前及治疗12周后用尾袖法测定动脉血压,称重后处死,取心脏,计算左心室重量与体重比(LVM/BW),天狼星红染色,计算心肌胶原容积分数.结果 软脉灵大剂量、小剂量组治疗12周后,收缩压(SBP)均显著低于空白组(P<0.01).与空白组相比,软脉灵大剂量组对SHR心肌外斜层纤维化有明显抑制作用(P<0.01),而软脉灵小剂量组则无影响;与空白组相比,软脉灵大剂量和小剂量组对SHR心肌中环层纤维化及心肌血管周围纤维化均有明显抑制作用(P<0.01).结论 软脉灵可以抑制SHR血压的发展,抑制SHR的心肌纤维化.     

黄芪、全蝎、红花、丹参、葛根混合剂抑制自发性高血压大鼠阻力血管肥厚

目的 观察黄芪、全蝎、红花、丹参、葛根混合剂(脑心通)对自发性高血压大鼠(SHR)阻力血管结构和血压的影响.方法 选择12周龄雄性SHR大鼠(二级)32只,随机分成4组,脑心通大剂量组[1 5 g/(kg·d)]、脑心通小剂量组[0 5 g/(kg·d)]、氯沙坦组[30 mg/(kg·d)]和SHR组(给等量蒸馏水).另选周龄、性别相匹配的Wistar Kyoto(WKY,给等量蒸馏水)大鼠8只.各组每日灌胃给药.12周后尾袖法测定动脉血压,称质量后处死.HE染色,计算机图像分析计算血管壁腔比,以观察各组大鼠肠系膜三级动脉的结构变化.结果 1)大、小剂量脑心通治疗后,两组SBP均显著低于SHR组[脑心通大剂量:(153 6±12 2)比脑心通小剂量:(159 2±5 8)比SHR:(178 6±12 0)mmHg,P<0 01];大剂量脑心通组SHR治疗后SBP较治疗前明显降低[(153 6±12 2)比治疗前(163 6±11 8)mmHg,P<0 01],与小剂量组比较能更进一步降低血压(P<0 05).2)与SHR组相比,小剂量脑心通治疗对肠系膜三级动脉血管的管壁面积/管腔面积及管壁厚度/管腔半径比值无影响,而大剂量脑心通可显著降低肠系膜三级动脉血管的管壁面积/管腔面积(W/L:脑心通大剂量:0 29±0 01比脑心通小剂量:0 37±0 06比SHR:0 44±0 04,P<0 01)及管壁厚度/管腔半径(Tw/RI:脑心通大剂量:0 12±0 01比脑心通小剂量:0 17±0 03比SHR:0 20±0 02,P<0 01).结论 脑心通可剂量依赖地抑制SHR大鼠血压的发展,减轻SHR阻力血管的肥厚.     

缬沙坦治疗对自发性高血压大鼠心肌纤维化的影响

目的　观察缬沙坦对自发性高血压大鼠 (SHR)心肌纤维化的影响。方法　 3 0只 12周龄雄性SHR大鼠 ,随机分成3组 :(1)大剂量缬沙坦组 (n =10缬沙坦 3 0mg/kg·d) ;(2 )小剂量缬沙坦组 (n =10缬沙坦 10mg/kg·d) ;(3 )SHR空白对照组 (n =10 ) ;(4)同龄雄性正常血压WKY大鼠对照组 (n =10 )。给药 4周 ;天狼星红染色法使胶原特殊染色 ,计算机图象分析测量心肌切片的胶原容积分数和心肌小动脉周围胶原面积与小动脉面积比表示心肌纤维化程度。结果　与SHR组相比大小剂量缬沙坦组 ,均能有效降低SHR血压 (P <0 0 5)。并能改善SHR大鼠左心室肥厚 (P <0 0 5)并使心室内、外膜及心肌小动脉周围的胶原减少 ,其中大剂量组各指标均较SHR有显著差异 (P <0 0 5)。结论　缬沙坦对SHR大鼠的心肌纤维有显著的抑制作用     

厄贝沙坦对SHR左心室肥厚和心肌纤维化的影响

目的 探讨厄贝沙坦对自发性高血压大鼠(SHR)左心室肥厚(LVH)和心肌纤维化的影响。方法 16只16周龄雄性SHR,随机分为厄贝沙坦治疗组和SHR空白对照组;另设同源的WKY大鼠8只为正常对照组。治疗组予厄贝沙坦15 mg/（kg·d）灌胃给药,8周后处死动物,测量左心室心肌厚度并称质量,计算左心室质量/体质量比(LVM/BM);通过Van Gieson染色法观察左心室心肌胶原变化,对左心室心肌胶原容积分数(CVF)和血管周围胶原面积(PVCA)进行定性和半定量分析;HE染色光镜观察左心室心肌病理变化。结果 与WKY组相比,SHR对照组的尾动脉收缩压(SBP)、LVM/BM、左心室壁厚度、CVF、PVCA、均显著增高(P<0.01);与SHR对照组相比,厄贝沙坦治疗组能有效降低SHR的SBP,改善LVH(P<0.01),减少心肌间质及心肌小动脉周围的胶原(P<0.01)。结论 厄贝沙坦可有效降低SHR血压,减轻心肌纤维化和LVH。     

胰激肽原酶对自发性高血压大鼠氧化损伤和心肌纤维化的影响

目的探讨胰激肽原酶对自发性高血压大鼠(SHR)抗氧化损伤和心肌纤维化的影响。方法15周龄雄性SHR大鼠24只,随机分成SHR对照组、胰激肽原酶小剂量组、大剂量组,每组8只。另取8只WKY大鼠作为正常血压对照组。小剂量组(7.2 U.kg-1.d-1)和大剂量组(14.4 U.kg-1.d-1)给予胰激肽原酶腹腔注射。治疗4 w后,测量各组收缩压(SBP)、左心室重量指数(LVM I)、心肌胶原容积分数(CVF)和心肌血管周围胶原面积(PVCA),同时测定血清中超氧化物岐化酶(SOD)、丙二醛(MDA)含量。结果治疗组SBP、CVF、PVCA与SHR对照组比较明显降低(P<0.05),仍未达到WKY组水平(P<0.05)。治疗组血清中SOD含量明显上升,MDA含量下降,与WKY组差异无显著性。结论胰激肽原酶能降低血压,减轻过氧化损伤,逆转心肌纤维化。且无明显毒副作用,有望成为治疗高血压左室肥厚新的有效药物。     

依那普利或氯沙坦对SHR左室肥厚和心肌纤维化的影响

目的:观察自发性高血压大鼠(SHR)左室肥厚和心肌纤维化各指标的改变,以及依那普利和氯沙坦的保护作用.方法:雄性SHR(n=30)自第10周始服用依那普利(20mg@kg-1@d-1),或氯沙坦(25mg@kg-1@d-1),或二者合用(依那普利10mg@kg-1@d-1,氯沙坦12.5mg@kg-1@d-1)至第16周,并以年龄、性别、数量配对的未治疗SHR和Wistar-kyoto(WKY)大鼠作对照.测定收缩压(SBP)、左室重量(LVM)以及左室重量指数(LVMI)和左室心肌胶原含量;计算机图象分析心肌细胞大小、心肌胶原容积分数(CVF)和血管周围胶原面积(PVCA).结果:SHR的SBP、LVM、LVMI、心肌胶原含量、心肌细胞的横截面积、CVF和PVCA均显著高于WKY对照组(P＜0.001).SHR治疗组上述指标显著低于SHR未治疗组(P＜0.01),依那普利与氯沙坦之间无显著差别(P＜0.05).二者合用比单用依那普利或氯沙坦更有效(P＜0.05).结论:依那普利和氯沙坦可显著的降低血压、逆转SHR早期左室肥厚和心肌纤维化,而且二者合用在逆转左室肥厚和心肌纤维化方面效果更明显.     

依贝沙坦对自发性高血压大鼠左心室肥厚和心肌纤维化的影响

目的探讨依贝沙坦对自发性高血压大鼠(SHR)左心室肥厚(LVH)和心肌纤维化的影响。方法18只16周龄SHR,随机分为依贝沙坦治疗组(SHR-I)和SHR空白对照组(SHR-C);另设同源的WKY大鼠8只为正常对照组。治疗组口服依贝沙坦50mg.kg-1.d-1给药8周后处死动物,取左心室心肌称重,计算左心室/体重比(LVW/BW),Masson三色法染色观察左心室心肌胶原变化,计算机图象分析测量心肌切片的胶原容积分数(CVF)和血管周围胶原面积(PVCA)。结果SHR空白对照组的收缩压(SBP),LVW/BW,CVF,PVCA均显著高于WKY对照组(P<0.01),与SHR空白对照组相比,依贝沙坦治疗组能有效降低SHR的SBP,改善左心室肥厚(P<0.01)并使左心室内膜及心肌小动脉周围的胶原减少(P<0.01)。结论依贝沙坦可有效降低SHR血压,部分逆转心肌纤维化和左心室肥厚。     

依那普利或氯沙坦对SHR左室肥厚和心肌纤维化的影响

目的 :观察自发性高血压大鼠 (SHR)左室肥厚和心肌纤维化各指标的改变 ,以及依那普利和氯沙坦的保护作用。方法 :雄性 SHR(n=30 )自第 1 0周始服用依那普利 (2 0 mg.kg- 1 .d - 1 ) ,或氯沙坦 (2 5 mg.kg - 1 .d - 1 ) ,或二者合用 (依那普利1 0 mg.kg - 1 .d - 1 ,氯沙坦 1 2 .5 mg.kg - 1 .d - 1 )至第 1 6周 ,并以年龄、性别、数量配对的未治疗 SHR和 Wistar- kyoto(WKY)大鼠作对照。测定收缩压 (SBP)、左室重量 (L VM)以及左室重量指数 (L VMI)和左室心肌胶原含量 ;计算机图象分析心肌细胞大小、心肌胶原容积分数 (CVF)和血管周围胶原面积(PVCA)。结果 :SHR的 SBP、L VM、L VMI、心肌胶原含量、心肌细胞的横截面积、CVF和 PVCA均显著高于 WKY对照组 (P<0 .0 0 1 )。 SHR治疗组上述指标显著低于 SHR未治疗组 (P<0 .0 1 ) ,依那普利与氯沙坦之间无显著差别 (P<0 .0 5 )。二者合用比单用依那普利或氯沙坦更有效 (P<0 .0 5 )。结论 :依那普利和氯沙坦可显著的降低血压、逆转 SHR早期左室肥厚和心肌纤维化 ,而且二者合用在逆转左室肥厚和心肌纤维化方面效果更明显     

缬沙坦治疗对自发性高血压大鼠心肌纤维化的影响

目的观察缬沙坦对自发性高血压大鼠(SHR)心肌纤维化的影响.方法 30只12周龄雄性SHR大鼠,随机分成3组(1)大剂量缬沙坦组(n=10 缬沙坦30 mg/kg*d);(2)小剂量缬沙坦组(n=10 缬沙坦10 mg/kg*d); (3)SHR空白对照组(n=10);(4) 同龄雄性正常血压WKY 大鼠对照组(n=10).给药4周; 天狼星红染色法使胶原特殊染色,计算机图象分析测量心肌切片的胶原容积分数和心肌小动脉周围胶原面积与小动脉面积比表示心肌纤维化程度.结果与SHR组相比大小剂量缬沙坦组,均能有效降低SHR血压(P<0.05).并能改善SHR大鼠左心室肥厚(P<0.05)并使心室内、外膜及心肌小动脉周围的胶原减少,其中大剂量组各指标均较SHR有显著差异(P<0.05).结论缬沙坦对SHR大鼠的心肌纤维有显著的抑制作用.     

Hypertension prevalence and control in Ulaanbaatar,Mongolia

This study examines the prevalence, awareness, treatment, and control of hypertension in Ulaanbaatar, Mongolia, using both the American Heart Association and conventional thresholds (130/80 and 140/90 mm Hg, respectively). In this randomized cross‐sectional study, two‐stage cluster sampling was used to obtain a sample of 4515 individuals aged ≥20 years. Hypertension was defined by the use of antihypertensives in the last 2 weeks or a blood pressure at or above the thresholds of 140/90 and 130/80 mm Hg. The mean age of the participants was 41.1 ± 14.0 years and 54.5% were women. Hypertension prevalence was 25.6% (using 140/90 mm Hg) and 46.5% (using 130/80 mm Hg). Prevalence increased with age and below 50 years men were consistently more likely to be hypertensive. Among hypertensive participants, the rates of awareness, treatment, and control were 69.7%, 46.8%, and 24.0% (using 140/90 mm Hg) and 49.1%, 25.8%, and 6.4% (using 130/80 mm Hg, respectively). Men had lower rates of awareness, treatment, and control compared with women, with the most pronounced differences at younger ages. This study shows that awareness, treatment, and control rates in Ulaanbaatar are better than in most low‐ and middle‐income countries but are still suboptimal. The largest “care gap” was in young men where a regulatory requirement for annual workplace blood pressure screening has the potential to enhance care. A major hypertension control program has just been initiated in Ulaanbaatar.     

Redefining primary hyperaldosteronism as “The Syndrome of Inappropriate Aldosterone Secretion (SIALDS)”: A common but unrecognized cause of hypertension

The current screening and diagnostic recommendations for detecting Primary Hyperaldosteronism (PHA) focus on diagnosing the more severe and overt instances of renin-independent aldosterone production. However, milder forms of autonomous aldosterone secretion have been demonstrated to exist below the diagnostic thresholds of current PHA guidelines, and associate with clinically relevant cardiovascular risk. PHAencompasses a spectrum of renin independent aldosterone production, progressing from a subclinical state in normotensives to a full-blown clinical syndrome representing the resistant hypertension population. The authors propose the Syndrome of Inappropriately Elevated Aldosterone Secretion (SIALDS) concept as a potential new paradigm for understanding and diagnosing PHA and expanded diagnostic approach to improve early detection even in well-controlled hypertension. The authors also delve into the impact of treatments, including mineralocorticoid receptor antagonists and emerging aldosterone synthase inhibitors. Furthermore, The authors outline future research directions, proposing clinical trials to investigate the long-term identification and treatment outcomes of SIALDS.     

Is tinnitus an early voice of masked hypertension? High masked hypertension rate in patients with tinnitus

Objectives: Tinnitus is hearing a sound without any external acoustic stimulus. There are some clues of hypertension can cause tinnitus in different ways. The aim of the study was to evaluate the relationship between tinnitus and masked hypertension including echocardiographic parameters and severity of tinnitus.

Methods: This study included 88 patients with tinnitus of at least 3 months duration and 85 age and gender-matched control subjects. Tinnitus severity index was used to classify the patients with tinnitus. After a complete medical history, all subjects underwent routine laboratory examination, office blood pressure measurement, hearing tests and ambulatory blood pressure monitoring. Masked hypertension is defined as normal office blood pressure measurement and high ambulatory blood pressure level.

Results: Baseline characteristics in patients and controls were similar. Prevalence of masked hypertension was significantly higher in patients with tinnitus than controls (18.2% vs 3.5%, p = 0.002). Office diastolic BP (76 ± 8.1 vs. 72.74 ± 8.68, p = 0.01), ambulatory 24-H diastolic BP (70.2 ± 9.6 vs. 66.9 ± 6.1, p = 0.07) and ambulatory daytime diastolic BP (73.7 ± 9.5 vs. 71.1 ± 6.2, p = 0.03) was significantly higher in patients with tinnitus than control group. Tinnitus severity index in patients without masked hypertension was 0 and tinnitus severity index in patients with masked hypertension were 2 (1–5).

Conclusion: This study demonstrated that masked hypertension must be kept in mind if there is a complaint of tinnitus without any other obvious reason.     

老年高血压病患者血液流变学分析

对48例老年高血压患者（合并冠心病21例，糖尿病10例）进行血液流变学测定。结果老年高血压组纤维蛋白原（Fg）、血浆粘度（ηP）与对照组比较，P＜0．01。全血粘度（ηb）、全血还原粘度（ηh）、血沉（ESR）、血小板粘附率（PAD）及体外血栓干重（DW）与对照组比较，P＜0．05；高血压合并冠心病组与单纯高血压组比较，ηb，ηh，PAD及体外血栓长度（L）、湿重（MW）（P＜0．05），DW（P＜0．01）；高血压合并糖尿病组与单纯高血压组比较，Fg（P＜0．01），ηh，ηh，ESR，PAD，L，DW，（P＜0．05）。结果提示，老年高血压病患者血液流变学改变表现为纤维蛋白原增高、红细胞刚性增加、红细胞变形能力降低，致红细胞聚集性增强。高血压合并冠心病或糖尿病组，均以血小板反应性增高、红细胞聚集性增强、内皮功能受损及体外血栓形成能力增强更为突出。     

Portopulmonary hypertension

Portopulmonary hypertension (PPHT) is defined as precapillary pulmonary hypertension accompanied by hepatic disease or portal hypertension. Pulmonary hypertension results from excessive pulmonary vascular remodeling and vasoconstriction. These histological alterations have been indistinguishable from those of other forms of pulmonary arterial hypertension. Factors involved in the pathogenesis of PPHT include volume overload, hyperdynamic circulation, and circulating vasoactive mediators. The disorder has a substantial impact on survival and requires focused treatment. Liver transplantation in patients with moderate to severe PPHT is associated with a significantly reduced survival rate. The best medical treatment for patients with PPHT is controversial; most authors currently regard continuous intravenous application of prostacyclin as the treatment of choice for patients with severe PPHT. There is only very limited reported experience with inhaled prostacyclin or its analog, iloprost. Increasing evidence of the efficacy of the endothelin-receptor antagonist bosentan and of the phosphodiesterase-5 inhibitor sildenafil is emerging in highly selected patients with PPHT. In the future, a combination therapy of the above-mentioned agents might become a therapeutic option. Other agents such as β-blockers seem to be harmful to patients with moderate to severe portopulmonary hypertension. Up-to-date, randomized, double-blind, controlled clinical trials are lacking and are needed urgently. An erratum to this article is available at .     

Relationship between Blood Pressure and Nocturia in Hypertensive Patients

Objective: We investigated the relationship between the pattern of hypertension and nocturia. Methods: Seventy‐seven patients who were being treated for hypertension completed a questionnaire regarding the number of times they urinated during the day and at night, and measured their blood pressure at home immediately after rising in the morning and just before going to sleep at night. The patients' blood pressure was also measured at the clinic. The patients were divided into groups according to their blood pressure patterns. The relationship between blood pressure pattern and number of urinations during the day and at night was investigated. Results: When the patients were divided into white coat hypertension, masked hypertension, sustained hypertension, and normotension groups, the number of daytime urinations was significantly lower in the sustained hypertension group compared with the normotension and white coat hypertension groups. When the subjects were divided into morning blood pressure surge and non‐morning surge groups or into morning hypertension and non‐morning hypertension groups, the numbers of nighttime urinations was significantly higher in the morning surge group or the morning hypertension group compared with the non‐morning surge group or non‐morning hypertension group, respectively. Conclusion: Sustained hypertension and elevation of blood pressure in the early morning influence the frequency of daytime and nighttime urination, respectively. It is important to control both the blood pressure and nocturia of hypertensive patients to improve their prognosis.     

Masked hypertensives: A disguised arterial stiffness population

The aim of this study was to determine whether masked hypertension (MHT) and white coat hypertension (WCHT) could be related to increased arterial stiffness and to identify the best office cutoff values of office BP for the diagnosis of MHT and WCHT. A total of 542 consecutive patients (50.2% male, age 42.5 ± 26.2 years) were included in the study. Patients were never treated before for hypertension. Patients were classified as true normotensives (44%), true hypertensives (30%), WC hypertensives (19%), and masked hypertensives (7%). Carotid‐femoral pulse wave velocity (c‐f PWV) was 9.91 ± 0.20 m/s in true normotension, 10.26 ± 0.27 m/s in WCHT, 11.28 ± 0.47 m/s in MHT, and 11.86 ± 0.23 m/s in true hypertension after adjustment for age and sex. Decision limits yielding 65% sensitivity were 130 mm Hg for office systolic BP with 72% specificity for the diagnosis of MHT. The optimal cutoff value of 80 mm Hg for office diastolic BP provides 60% sensitivity and 68% specificity. Decision limits yielding 63% sensitivity were 150 mm Hg for office systolic BP with 72% specificity for the diagnosis of WCHT. The optimal cutoff value of 95 mm Hg for office diastolic BP provides 75% sensitivity and 51% specificity. The presence of MHT should be taken into account when increased c‐f PWV is detected in the absence of office hypertension. The optimal office BP of 130/80 mm Hg provides the best sensitivity and specificity for the diagnosis of MHT. As regards the diagnosis of WCHT, the cutoff value of 150/95 mm Hg seems to provide the best option.     

Resistant hypertension, secondary hypertension, and hypertensive crises: diagnostic evaluation and treatment

Hypertension is a very common modifiable risk factor for cardiovascular morbidity and mortality. Patients with hypertension represent a diverse group. In addition to those with primary hypertension, there are patients whose hypertension is attributable to secondary causes, those with resistant hypertension, and patients who present with a hypertensive crisis. Secondary causes of hypertension account for less than 10% of cases of elevated blood pressure (BP), and screening for these causes is warranted if clinically indicated. Patients with resistant hypertension, whose BP remains uncontrolled in spite of use of 3 or more antihypertensive agents, are at increased cardiovascular risk compared with the general hypertensive population. After potentially correctible causes of uncontrolled BP (pseudoresistance, secondary causes, and intake of interfering substances) are eliminated, patients with true resistant hypertension are managed by encouraging therapeutic lifestyle changes and optimizing the antihypertensive regimen, whereby the clinician ensures that the medications are prescribed at optimal doses using drugs with complementary mechanisms of action, while adding an appropriate diuretic if there are no contraindications. Mineralocorticoid receptor antagonists are formidable add-on agents to the antihypertensive regimen, usually as a fourth drug, and are effective in reducing BP even in patients without biochemical evidence of aldosterone excess. In the setting of a hypertensive crisis, the BP has to be reduced within hours in the case of a hypertensive emergency (elevated BP with evidence of target organ damage) using parenteral agents, and within a few days if there is hypertensive urgency, using oral antihypertensive agents.