依那普利逆转Ⅱ型糖尿病合并高血压左心室肥厚效果的临床观察

近几年研究表明依那普利对原发性高血压所致的左室肥厚(LVH)有逆转作用,但对合并Ⅱ型糖尿病时是否仍具有同样的作用研究较少,我们对30例Ⅱ型糖尿病并高血压LVH患者予以6个月的依那普利治疗,旨在观察其逆转LVH的效果与非糖尿病患者是否具有相同作用。     

依那普利、福辛普利对自发性高血压大鼠心肌超微结构逆转的实验研究

目的:观察血管紧张素转换酶抑制剂enalapril和fosinopril对SHR心肌超微结构的逆转作用.方法:将10月龄18只SHR随机分为Enalapril(SHRE)、Fo sinopril(SHRF) 和生理盐水(SHRc) 三组,给药剂量为10 mg/kg/d腹腔内注射8周.测定血压、心室重量指数,电镜观察心肌超微结构改变.结果:两药物组心室肥厚均不同程度消退,部分逆转心肌超微结构改变,而且Fosinopril降低LVW/BW比Enalapril更好(P<0.05).结论:福辛普利和依那普利不同程度改善心肌细胞超微结构损害.     

依那普利对高血压左室肥厚的逆转效应

本文对依那普利治疗原发性高血压时的左室肥厚逆转效应进行观察。根据心超LVMI分为肥厚组 (2 4例 )和非肥厚组 (13例 )。疗程 4周 ,剂量 10～ 40mg/d。结果显示左室肥厚的逆转效应在短期 (4周 )治疗后可出现 ,首先是IVST的下降。对左室无肥厚者起相反效应     

卡托普利逆转高血压左室重构的实验研究

１４周龄的自发性高血压大鼠（ＳＨＲ）已形成左室肥厚（ＬＶＨ），心肌胶原浓度及心肌Ｃａ￣（２＋）增加，左室顺应性下降，经卡托普利治疗５０ｍｇ／ｋｇ·ｄ１４周后，ＬＶＨ消退。心肌胶原及Ｃａ￣（２＋）消退，左室舒张期弹性硬度改善，表明卡托普利治疗高血压能逆转左室肥厚及心肌胶原重构，并改善心功能。     

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。     

苯磺酸氨氯地平联合依那普利治疗中度原发性高血压疗效观察

目的观察苯磺酸氨氟地平联合依那普利治疗中度原发性高血压的疗效、不良反应及对心肌肥厚的影响。方法68例中度原发性高血压患者,随机分为对照组和观察组各34例,对照组单用苯磺酸氨氯地平5mg晨服每日1次;观察组在对照组基础上加用依那普利10mg晨服每日1次。两组疗程均为24周,观察治疗前后的血压变化、心肌肥厚状况、不良反应及生化指标。结果两组患者总有效率间差别有统计学意义（P〈0．05）;观察组中22例有心肌肥厚患者的左心室舒张末期内径、室间隔厚度和左心室后壁厚度均值较治疗前显著缩小,差异有统计学意义（P〈0．05）;而对照组中21例心肌肥厚患者的相应指标间差异无统计学意义（P〉0．05）。两组的不良反应主要为头晕、头痛、面红或轻微干咳,患者均能耐受。结论苯磺酸氨氯地平联合依那普利治疗中度原发性高血压可显著提高降压疗效,且可以明显逆转心肌肥厚。     

丹参预防自发性高血压大鼠左心室肥厚

目的　观察丹参对自发性高血压大鼠左室肥厚的作用。方法　 18只 8周龄的自发性高血压大鼠随机分成 3组 :一组于 8周处死 ,另两组分别经腹腔注射丹参和蒸馏水 (1g/kg·d) ,共 10周。测量大鼠尾动脉收缩压 (SBP)及左心室重量指数 (LVMI)。应用HE、VG染色 ,结合计算机图像分析技术 ,检测心肌细胞的直径 (TDM)、面积 (CA)、心肌组织胶原体积比例 (CVF)、血管周围胶原面积和管腔面积比例 (PVCA)。结果　与 8周龄的自发性高血压大鼠相比 ,18周龄大鼠的SBP、LVMI、心肌细胞的直径、面积、CVF、PVCA显著增加 (P <0 0 1) ,丹参治疗组大鼠反映左室肥厚的各项指标上升不明显 (P >0 0 5 ) ,但收缩压仍显著升高 (P <0 0 1)。结论　长期应用丹参治疗可预防自发性高血压大鼠左室肥厚的形成。     

依那普利对高血压心肌细胞凋亡影响的实验研究

目的　探讨依那普利对自发性高血压大鼠心肌细胞凋亡的影响。方法　选用 1 2周龄自发性高血压大鼠 (SHR) 4 0只 ,雌雄不拘 ;随机分为治疗组 (2 0只 )和对照组 (2 0只 ) ,并以正常血压大鼠 (WKY)作为对照。治疗组大鼠服用依那普利 (30mg/kg·d- 1 ) 1 2w。每周测体重 1次 ,每 2w测血压 1次 ;治疗结束时测左心室重量 ,并以Tunel方法对三组大鼠心脏作凋亡细胞检测。结果　依那普利治疗后2个月SHR治疗组血压明显低于SHR对照组血压 (P <0 0 1 ) ,与WKY组血压相近似 (P >0 0 5) ;SHR治疗组左心室重量亦明显低于SHR对照组 (P <0 0 1 ) ,略高于WKY组 ,但无统计学差异 (P >0 0 5)。Tunel检查结果表明 ,依那普利治疗组SHR左心室心肌细胞凋亡指数(1 9 5± 3 0 )明显高于SHR对照组 (1 2 6± 1 2 )和WKY组 (7 9± 1 9) ;三组间差异显著 (P <0 0 5)。结论　自发性高血压大鼠心肌细胞凋亡明显高于正常对照WKY ;长期服用依那普利能促进SHR心肌细胞的凋亡。     

氯沙坦对自发性高血压大鼠左心室结构改变的实验研究

目的 :探讨氯沙坦 (Los)对自发性高血压大鼠 (SHR)左心室结构的影响。方法 :6周龄Los治疗组 (SHRlos)管饲法给予Los3 0mg kg天。治疗 17周后 ,观察 3组大鼠动脉收缩压 (SBP)、左心室 (LV)壁的厚度、左心室重量 体重 (LVW BW)以及左心室结构的变化 ;血浆放免法测肾素活性和AngⅡ含量。结果 :1 SBP :治疗结束后 ,SHRlos组血压 10 9 15± 11 3 1mmHg( 1mmHg =0 .13 3kPa) ,与对照组 (SHR)血压167 4± 13 0 1mmHg相比明显下降 (P <0 0 1)。 2 SHRlos组的LVW BW、LV壁厚度与SHR组相比明显减少 (P <0 0 1)。SHRlos心肌的超微结构与正常对照组 (WKY)相似。 3 血浆肾素活性在WKY组和SHR组之间无明显差异 (P >0 0 5 )。SHRlos组肾素活性及AngⅡ水平分别高于SHR组 (P <0 0 5 ,P <0 0 1)。结论 :Los能有效地降低SHR的血压 ,具有预防高血压LVH的作用。     

自发性高血压大鼠左室肥厚及心肌纤维化的动态变化

目的 生高血压大鼠（ＳＨＲ）血压增高的初期。增高期和稳定期左室肥厚和心肌纤维化参数的改变,探讨高血压左室肥厚和心肌纤维化的动态演化规律。方法 应用生化测定、病一检查结合计算机分析等方法,检测ＳＨＲ及其照ＷＫＹ在６周、１４周和２４周的收缩压、左室重量及左室重量指数、心肌细胞面积及横径、民胶原只分数（ＣＶＦ）、血管周围胶原面积（ＰＶＣＡ）及心肌组织内羟脯氨酸浓度。结果ＳＨＲ左室重量及左室重量指数、心肌     

Epidemiology of Hypertension and Cardiovascular Disease China Experience

Epidemiological studies show higher BP level, lipid level and higher prevalence of coronary atherosclerosis and stenosis, in north than in south China. Urban populations have higher prevalence of HT than rural, high altitude dwellers usually have lower prevalence. Genetic differences start to affect BP from early childhood, children fromhigher BP parents are found more salt sensitive. Higher Na and Na/K, lower protein and Ca in the north, are importnat dietary factors in explaining north-south difference. Low prevalence of high altitude dwellers is found to be related with low salt intake, less stress perhaps also hypoxia.

CVD Community control program has started since 1969, from 1969—1989, eleven such programs have been established in Beijing covering a total population of 750,000. Encouraging results in reduction of CVD mortality and morbidity rates have been obtained. Primary prevention by restriction of Na and supplementation of calcium has been tried and found to be eligible preventive measures.     

Regression of Chronic Hypoxia-Induced Pulmonary Hypertension, Right Ventricular Hypertrophy, and Fibrosis: Effect of Enalapril

Chronic hypoxia induces pulmonary hypertension and right ventricular hypertrophy. These changes are completely reversible, except for persistent myocardial fibrosis. The aim of the present study was to determine whether treatment with the angiotensin-converting enzyme (ACE) inhibitor enalapril can reduce the ventricular collagen content in animals recovering from chronic hypoxia. Adult male Wistar rats were exposed to intermittent high-altitude hypoxia simulated in a barochamber (7000 m, 8 hr/day, 5 days a week, 24 exposures), then transferred to normoxia and divided into two groups: (a) treated with enalapril (0.1 g/kg/day for 60 days) and (b) without treatment. The corresponding control groups were kept under normoxic conditions. Enalapril significantly decreased the heart rate, systemic arterial pressure, and absolute left and right ventricular weights in both hypoxic and control rats; on the other hand, the pulmonary blood pressure was unchanged. The content and concentration of collagen was reduced in both ventricles of enalapril-treated hypoxic and control animals by 10–26% compared with the corresponding untreated groups. These data suggest that the partial regression of cardiac fibrosis due to enalapril may be independent of the pressure load.     

培哚普利,卡托普利和硝苯地平对高血压左心室肥厚及心功能影响

目的观察培哚普利、卡托普利和硝苯地平对老年高血压心室肥厚（ＬＶＨ）及心功能的影响。方法将９４例老年轻、中度高血压ＬＶＨ病人随机分为培哚普利、卡托普利和硝苯地平３组。服用安慰剂２周后分别用药３个月，剂量递增，于实验前、用药前、用药后每月分别测定动脉血压，超声心动图左室舒张末内径、舒张期室间隔厚度、左室后壁厚度，并由此计算左室质量指数（ＬＶＭＩ），同时测定左室缩短分数，Ｅ／Ａ比值和射血分数。结果３组病人用药前一般情况无明显差别，用药后血压均有显著下降（Ｐ＜０．００１），组间无差异。ＬＶＭＩ培哚普利组（Ｐ＜０．０１）和卡托普利组（Ｐ＜０．００１）用药后有显著减低，Ｅ／Ａ比值明显升高（均Ｐ＜０．００１）。而硝苯地平组仅有Ｅ／Ａ比值升高（Ｐ＜０．０５）。左室缩短分数和射血分数３组均未见明显变化。结论对老年轻中度高血压ＬＶＨ病人，三药均可有效降低血压，卡托普利和培哚普利明显减轻ＬＶＨ，并改善左室舒张功能，硝苯地平亦可改善左室舒张功能     

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     

Effect of Chronic Treatment with Angiotensin I Converting Enzyme Inhibitors on Circulating Atrial Natriuretic Polypeptide in Spontaneously Hypertensive Rats

We have recently shown that circulating atrial natriuretic polypeptide (ANP) in adult spontaneously hypertensive rats (SHR) is higher than that in age-matched Wistar-Kyoto rats (WKY). The present experiment was designed to examine the possible effects of chronic treatment with angiotensin I converting enzyme inhibitors (ACEI) on plasma ANP levels in SHR. Captopril and enalapril lowered blood pressure and reduced relative ventricular weight in SHR but not to the level of WKY. Plasma ANP levels were decreased by captopril and enalapril compared with untreated SHR. These results suggest that the ANP release may be suppressed in ACEI-treated SHR compared with untreated SHR. We speculate that a reduction of cardiac overload by ACEI may in part explain the decline of circulating ANP.     

Ultrastructural changes during myocardial hypertrophy and its regression: Long-term effects of nifedipine in adult spontaneously hypertensive rats

Summary Nifedipine (20mg/kg/day) was given to 15-week-old spontaneously hypertensive rats for 20 weeks (SHR-N,n=8). Comparison was done with sex-matched 15-week-old SHR (SHR-15,n=7), untreated 35-week-old SHR (SHR-C,n=10), 15-week-old normotensive Wistar-Kyoto rats (WKY-15,n=15), and 35-week-old WKY (WKY-15,n=5). Light and electron microscopic data on the subepicardial, middle, and subendocardial layers and papillary muscles of the left ventricle were compared among the five rat groups. In SHR-N, blood pressure was significantly reduced by nifedipine, but was higher than in WKY-35 (199±11 mmHg vs 121±13mmHg). The left ventricular weight/body weight ratio was much lower in SHR-N than in SHR-C, and was even below the baseline value in SHR-15. In addition, cardiac myocyte diameter was much smaller in each myocardial layer of SHR-N than in SHR-C, and was similar to the findings in SHR-15, but still larger than in WKY-35. The interstitial area ratio was markedly reduced in SHR-N and did not differ from that in SHR-15 or even WKY-15, while capillary density was significantly greater than in SHR-C and comparable to that in WKY-35. In SHR-C, large fibrotic foci were common, and many hypertrophic cardiac myocytes showed various degenerative changes including those of mitochondria and widening of the intermyofibrillar spaces. These changes were rarely seen in SHR-N. The intracellular volume ratio of myofibrils did not differ between SHR-N and WKY-35, but was significantly decreased in SHR-C, whereas that of mitochondria did not differ between SHR-N and SHR-C or WKY-35. These findings indicate that despite only a moderate suppression of hypertension, long-term nifedipine treatment caused regression of left ventricular hypertrophy, with cardiocyte hypertrophy, interstitial fibrosis, degenerative changes, and subcellular remodeling being reversed to the baseline levels in SHR-15. In addition, the capillary density was increased to that seen in WKY-35.     

Changes in Brain Angiotensinogen During Development of Hypertension

Angiotensinogen was measured in the brain and cerebrospinal fluid (CSF) of spontaneously hypertensive rat (SHR) and the normotensive Wistar-Kyoto strain at 4, 7 and 16 weeks of age. Levels of angiotensinogen were elevated in a number of areas of SHR, primarily in the 4 and 7 week old animals. CSF levels did not correlate with the brain levels. These results suggest that the regulation of the brain angiotensin system maybe altered during the development of hypertension.