氯沙坦治疗高血压病伴左室肥厚患者的疗效观察

目的观察氯沙坦对高血压病伴左室肥厚患者降压及左室肥厚的治疗效果。方法高血压病伴左室肥厚患者60例,随机分为氯沙坦组（30例）和卡托普利组（30例）,用药前及用药后3个月测量血压和计算患者左室质量指数。结果2组用药后血压和左室质量指数均比用药前有显著的下降（P〈0.01）,但组间差异无统计学意义（P〉0.05）。结论氯沙坦可有效降低高血压病伴左室肥厚患者的血压,逆转左心室肥厚。     

洛沙坦与苯那普利治疗原发性高血压左室肥厚的对比研究

评价洛沙坦治疗高血压左室肥厚的疗效并与苯那普利作比较。原发性高血压左室肥厚患者５０例,随机分为洛沙坦治疗组（２５～５０ｍｇ／ｄ）、苯那普利治疗组（５～２０ｍｇ／ｄ）,疗程４个月,结果洛沙坦或苯那普利治疗后血压比治疗前显著降低,两组对左室肥厚的逆转率分别为８０％与７２％,逆转作用无差别,不良反应发生率洛沙坦比苯那普利明显减少。本文资料显示,洛沙坦是降低血压、逆转左室肥厚疗效较好的药物。     

坎地沙坦的抗高血压及对左室肥厚的逆转作用

目的观察坎地沙坦降压疗效及其对原发性高血压(EH)左室肥厚(LVH)的逆转作用。方法 83例患者口服坎地沙坦8mg,1次/d,治疗8周,用动态血压仪记录坎地沙坦治疗EH患者的降压效果,用超声心动图测量LVH患者的左心肥厚的改善情况。结果坎地沙坦可使24h血压平稳下降且左室质量指数较治疗前减低(P<0.01)。结论坎地沙坦能有效地控制血压的升高,对EH的LVH有逆转作用。     

缬沙坦逆转高血压患者左心室肥厚的临床观察

目的：观察血管紧张素Ⅱ受体拮抗剂－缬沙坦（代）的降压效果及其对高血压病合并左室肥厚的影响。方法：对32例轻，中度高血压病左心室肥厚患进行6mon的缬沙坦治疗，通过治疗前后对血压，超声多普勒心动图检测的对比，探讨缬沙坦对逆转左室肥厚的作用。结果：经过6mon的治疗，血压从162／102mmHg降至135／84mmHg(P＜0．01），左室心肌重量指数（LVMI）也明显下降（P＜0．01）。结论：缬沙坦长期治疗可使高血压患左室肥厚逆转。     

奥美沙坦酯对原发性高血压患者血压及左心室肥厚的影响

目的观察血管紧张素Ⅱ型受体拮抗剂奥美沙坦酯对高血压患者血压及左心室肥厚的影响。方法采用前瞻性、随机双盲、阳性药物对照研究方法,将54例原发性高血压合并左心室肥厚的患者随机分为奥美沙坦组(治疗组)27例,口服奥美沙坦酯20mg/d,1次/d;缬沙坦组(对照组)27例,口服缬沙坦80mg/d,1次/d,共24周,服药前后分别测量血压,并行心脏超声检查。结果2组治疗前后血压明显下降(P<0.05);左室后壁厚度(PWT)、左心室舒张期室间隔厚度(IVST)、左室重量指数(LVM I)与治疗前相比有明显的统计学意义(P<0.05),2组间比较无差异性(P>0.05)。结论奥美沙坦酯在降低原发性高血压患者血压的同时,可逆转左心室肥厚。     

血管紧张素Ⅱ受体拮抗剂治疗高血压左心室肥厚的临床分析

目的观察血管紧张素Ⅱ受体拮抗剂———缬沙坦(代文)的降压效果及其对高血压合并左心室肥厚的影响。方法对95例轻、中度高血压左心室肥厚患者进行24周的缬沙坦治疗(80～160mg/d,顿服),并对治疗前后的血压、超声多普勒心动图检测结果进行分析。结果经过24周的治疗,血压从165/112mmHg降至130/84mmHg(P<0.01),左室后壁厚度、室间隔厚度、左室心肌重量指数也明显下降(P<0.01)。结论缬沙坦作为血管紧张素Ⅱ受体拮抗剂,可用于治疗轻、中度高血压左室肥厚。     

科素亚对高血压病左室肥厚逆转作用的临床研究

目的 评价科素亚对高血压病左室肥厚的逆转作用。方法 测量36例高血压病患者在科素亚治疗前和治疗后12周的血压、心功能及左室重量指数、左室壁厚度。结果 12周治疗后血压明显下降，LVMI、PWTd明显减少，心功能指标改善。结论 科素亚在降压的同时能逆转左心室肥厚。     

坎地沙坦联合曲美他嗪治疗原发性高血压左室肥厚的临床观察

目的观察坎地沙坦联合曲美他嗪治疗原发性高血压左室肥厚的疗效。方法原发性高血压患者115例,随机分为两组,A组采用坎地沙坦口服,B组采用坎地沙坦联合口服曲美他嗪,比较两组降压效果、超声心动图指标的改变。结果两组患者血压均较治疗前明显下降(P<0.05),但两组间降压效果比较无统计学差异(P>0.05);两组LVEDd、LVPWT、IVST、LVMI、LVEF及E/A均显著改善,且B组均优于A组(P<0.05)。结论采用坎地沙坦联合曲美他嗪较单纯采用坎地沙坦治疗可更明显逆转原发性高血压左室肥厚、改善心功能。     

洛沙坦联合吲达帕胺对重度高血压与左心室肥厚的治疗作用

目的 观察联合洛沙坦、吲达帕胺对重度高血压并左心室肥厚患者的降压疗效及对左心室肥厚(LVH)的影响. 方法 60例原发性高血压并左心室肥厚的患者口服洛沙坦50～100 mg/d,吲达帕胺1.5～3.0 mg/d,6个月为疗程,观察治疗前后血压、心率、彩色多普勒超声心动图(UCG)及血尿常规电解质、肝肾功能、血脂、血糖、生化指标变化;同时观察药物不良反应.结果 治疗前后对比,联合治疗方案对收缩压、舒张压均有明显降压作用(P<0.01)、对心率无影左心室响(P>0.05);左心室舒张末期室间隔厚度、舒张末期左心室后壁厚度明显降低(P<0.01),左心室重量和左心室重量指数(LVMI)明显降低(P<0.01),而舒张末期左心室内径(LVDd)无改变(P>0.05),各项生化指标无明显改变,不良反应轻.结论 应用洛沙坦、吲达帕胺联合治疗能很好控制血压的同时逆转左心室肥厚,耐受性好,无明显副作用,是临床严重高血压值得推荐的联合治疗方案.     

百乐眠胶囊治疗高血压病伴睡眠障碍对血压的影响

目的：观察中成药百乐眠治疗高血压病伴睡眠障碍对血压的影响。方法：入选高血压病合并中、重度睡眠障碍的患者,在常规降压等治疗的基础上加服百乐眠,2次/d,4粒/次,治疗7d。观察百乐眠治疗后的血压变化及不良反应。结果：百乐眠治疗一周后,41例睡眠障碍改善,平均动脉压下降10mmHg,收缩压、舒张压均明显下降（P＜0.01）,差异具有统计学意义。5例血压下降不明显,5例血压轻度升高,有效率89.36%,2例出现轻度不良反应,未经处理停药后自动缓解。结论：百乐眠胶囊治疗高血压病伴睡眠障碍,能明显改善失眠,有效降低血压。     

Beneficial effects of the combination of nifedipine and losartan in hypertensive Dahl salt-sensitive rats

BACKGROUND: The antihypertensive and organ-protective effects of the combination of the angiotensin II type 1 receptor blocker losartan and the calcium channel blocker nifedipine were examined in Dahl salt-sensitive rats. METHODS: The rats fed with a high-salt diet developed hypertension accompanied by aorta and heart hypertrophy, and impaired renal function. The animals were treated with losartan (30 mg/kg/day), nifedipine (7.8 mg/kg/day) or with a combination of both drugs for 8 weeks. At the end of the study systolic blood pressure, kidney function, organ weight, and mRNA expression were investigated. RESULTS: Losartan reduced significantly the systolic blood pressure as well as the aorta and left ventricular hypertrophy. Nifedipine and its combination with losartan had similar effects on the systolic blood pressure, aorta and left ventricular hypertrophy but only the combination treatment reduced the expression of transforming growth factor-beta1 in aorta and brain natriuretic peptide in left ventricle significantly. Nifedipine and the combination therapy reduced proteinuria and improved urine creatinine excretion. The expression of collagen III and IV in the kidney was significantly reduced by the combination therapy. CONCLUSION: These results indicate that although losartan and nifedipine were effective in lowering blood pressure and showed moderate organ protection, additional benefits can be expected by combination therapy with both compounds.     

氯沙坦对老年高血压者左室肥厚逆转及血浆内皮素水平的影响

目的 :了解氯沙坦对老年高血压性左室肥厚的逆转作用及对血浆内皮素 (ET)水平的影响。方法 :以 2 0例健康老年人为对照组 ,观察单纯高血压 32例 (EH组 )、高血压伴左室肥厚 2 6例 (LVH组 )在每日服氯沙坦 50mg前及 16wk后血压、ET的变化。用超声心动图观察LVH组在用药前后的左室舒张末期内径 (LVDd)、室间隔厚度 (IVST)、左室后壁厚度 (LVPWT)、左室重量 (LVM )、左室重量指数 (LVMI)的变化。结果 :经氯沙坦治疗后 ,EH组、LVH组的平均动脉压 (MAP)及ET水平有显著性下降 ;LVH组的ET水平与LVM ,LVMI呈正相关 ,LVH组在治疗后IVST ,LVPWT ,LVDd ,LVM ,LVMI亦有显著性下降。结论 :氯沙坦对老年高血压病人不仅有良好的降压效果 ,同时具有逆转LVH及降ET的作用     

氯沙坦钾与螺内酯合用对大鼠急性心肌梗死后心室重构的影响

目的观察氯沙坦钾与螺内酯合用对大鼠急性心肌梗死后心室重构的影响。方法建立大鼠急性心肌梗死模型,将存活鼠随机分为氯沙坦钾组、螺内酯组、联合用药组及安慰剂组,并设假手术组。心肌梗死后6周,对各组大鼠均进行心功能、心室重构指标的检测;并同时测定各组大鼠非梗死区心肌组织中血管紧张素Ⅱ(AngⅡ)、醛固酮(Ald)水平。结果①氯沙坦钾组、螺内酯组及联合用药组全心重量/体重(VW/BW)、左室重量(LVW)、左室重量指数(LVWI)及心肌细胞横径(TDM)均较安慰剂组降低;联合用药组各指标降低更明显(P<0.05)。②氯沙坦钾组、螺内酯组及联合用药组AngⅡ、Ald水平较安慰剂组降低;联合用药组AngⅡ、Ald水平进一步降低(P<0.05)。结论急性心肌梗死后非梗死区心肌组织发生重构,螺内酯和氯沙坦钾均可通过抑制局部心肌组织AngⅡ和Ald水平而减轻心肌细胞的肥大程度、延缓心肌梗死后心室重构过程,而且螺内酯和氯沙坦钾合用还具有明显的协同效果。     

Losartan: a review of its use, with special focus on elderly patients

Losartan is an orally active, nonpeptide, selective angiotensin subtype 1 (AT1) receptor antagonist. It provides a more specific and complete blockade of the actions of angiotensin II than renin or ACE inhibitors. Short term (up to 12 weeks' duration) clinical trials have shown losartan to be as effective at lowering blood pressure (BP) [causes a decrease in BP < or = 26/20 mm Hg] in elderly patients with hypertension as recommended dosages of captopril, atenolol, enalapril, felodipine and nifedipine. In patients with isolated systolic hypertension (ISH) the efficacy of losartan was similar to that of atenolol. The addition of hydrochlorothiazide to losartan therapy provides greater antihypertensive efficacy, equivalent to that seen with captopril plus hydrochlorothiazide. Preliminary evidence also indicates that losartan therapy contributes to the regression of left ventricular hypertrophy associated with chronic hypertension. Exercise capacity is increased by losartan in patients with either asymptomatic or symptomatic heart failure. Results from the Losartan Heart Failure Survival or ELITE II (Evaluation of Losartan in the Elderly II) study indicate that there was no statistically significant difference between losartan and captopril in reducing overall deaths or in reducing sudden cardiac death and/or resuscitated cardiac arrest in patients with heart failure. Other than ELITE II, little conclusive long term mortality and morbidity data exist for losartan. Additional long term trials to evaluate the survival benefits of losartan in elderly patients with hypertension, renal disease or after an acute myocardial infarction are currently in progress. In elderly patients with hypertension, the incidence of treatment-related adverse events associated with once daily losartan (alone or in combination with hydrochlorothiazide) [19 to 27%] was similar to felodipine (23%) and nifedipine (21%), however, losartan tended to be better tolerated than captopril (11 vs 16%). Losartan was also better tolerated than atenolol in patients with ISH (10.4 vs 23%). In patients with heart failure the renal tolerability of losartan was similar to that of captopril, but losartan was associated with a lower withdrawal rate because of adverse events. No dosage adjustment is required in elderly or in patients with mild to moderate renal dysfunction, and the risk of first-dose hypotension is low. Conclusions: comparative data have shown losartan to be as effective as other antihypertensive agents in the treatment of elderly patients with hypertension. Treatment with losartan is therefore an option for first-line therapy in all patients with hypertension, particularly those who are not well managed with or who are intolerant of their current therapy. Morbidity and mortality data from the Losartan Heart Failure Survival (ELITE II) study show that losartan has potential in the treatment of heart failure.     

N(G)-nitro-L-arginine methyl ester-induced hypertension and natriuretic peptide gene expression: inhibition by angiotensin II type 1 receptor antagonism

This study examined the role of angiotensin II in the increase of blood pressure, activation of cardiac natriuretic peptide gene expression, left ventricular hypertrophy, and vascular changes in nitric oxide-deficient hypertension. N(G)-nitro->L-arginine methyl ester (>L-NAME, 20 mg/kg/d), angiotensin II type 1 receptor (AT ) antagonist losartan (20 mg/kg/d), or their combination were administered orally for 8 weeks in Wistar rats. >L-NAME elevated systolic blood pressure, which reached its maximum within 4 weeks (200 +/- 4 mm Hg). Despite hypertension, >L-NAME administration for 8 weeks did not induce left ventricular hypertrophy. Losartan treatment significantly decreased the development of hypertension induced by >L-NAME and decreased left ventricular hypertrophy in untreated rats. In contrast, losartan did not prevent the hypertrophic remodeling of the mesenteric resistance arteries induced by >L-NAME. >L-NAME treatment increased ventricular atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) mRNA levels and immunoreactive BNP levels significantly. Losartan therapy decreased the >l-NAME-induced ventricular ANP gene expression by 69% (p < 0.05) and also reduced ventricular BNP mRNA levels so that it did not differ from control. Losartan treatment alone decreased ventricular immunoreactive ANP and BNP levels by 30% (p < 0.05). These results show that ventricular ANP and BNP gene expression are dissociated from the increased ventricular mass in nitric oxide deficiency-induced hypertension. Results suggest that >l-NAME-induced hypertension and the associated activation of ventricular ANP and BNP gene expression are, at least in part, mediated by angiotensin II, whereas the resistance vessel hypertrophy following nitric oxide synthase inhibition is angiotensin II independent.     

Losartan: a review of its use in stroke risk reduction in patients with hypertension and left ventricular hypertrophy

Losartan (Cozaar) is an angiotensin AT1 receptor antagonist. It is approved in numerous countries for the treatment of hypertension and has been approved in the UK, the US and several European countries for stroke risk reduction in patients with hypertension and left ventricular hypertrophy (LVH). Losartan is recommended for use alone or with hydrochlorothiazide, but it can also be administered with other antihypertensive medications. In patients with hypertension, losartan effectively lowers blood pressure and also leads to regression of LVH. In the large, well designed LIFE (Losartan Intervention For Endpoint reduction in hypertension) study in patients with hypertension and LVH, losartan was more effective than atenolol in reducing the composite primary endpoint of cardiovascular (CV) mortality, stroke or myocardial infarction (MI). This was mainly due to a significant 25% reduction in the risk of stroke in the losartan group. Losartan recipients also had a significantly lower incidence of new-onset diabetes mellitus compared with atenolol recipients. Similar benefits were observed in several patient subgroups from the LIFE study, but not in the subgroup of Black patients. Losartan is well tolerated and is a cost effective alternative to atenolol in the setting of stroke reduction. Comparative data on clinical outcomes in hypertensive patients for losartan versus other antihypertensive agents would be of interest. Nonetheless, in addition to its established antihypertensive and end organ effects, the LIFE study indicates that, with the possible exception of Black patients, losartan can reduce the risk of stroke in patients with hypertension and LVH.     

氯沙坦和雷米普利对压力过载引起的左心室肥厚作用的比较观察

目的：应用氯沙坦和雷米普利来探讨血管紧张肽Ⅱ对压力过载引起的左心室肥厚的相关作用。方法：采用缩窄大鼠肾动脉间腹主动脉的方法造成后负荷过载所致的左心室肥厚模型。造模后12 wk,分别给予灌服氯沙坦(1.0 mg·kg~(-1))和雷米普利(1.0 mg·kg~(-1))。给药12 wk后,应用形态测量学测定左室重量指数；Langendorff离体心脏灌流法测定离体心功能和右颈总动脉插管法测定在体心功能及血流动力学；应用酶联免疫吸附法测定大鼠血浆血管紧张肽Ⅱ(AngⅡ)、醛甾(固)酮(Ald)含量和心肌组织AngⅡ含量。结果：与模型动物比较,氯沙坦和雷米普利均能降低左室重量指数；在体大鼠血流动力学的测定中发现,压力过载造成大鼠动脉血压和左室收缩压显著升高,应用氯沙坦和雷米普利治疗后,明显改善大鼠心脏收缩功能,降低左室收缩压和外周动脉血压；离体大鼠心功能测定发现,压力过载引起离体大鼠心脏左室舒张压和左室最大上升速率下降,氯沙坦和雷米普利不能改善左室舒张压和左室最大上升速率下降。此外,氯沙坦和雷米普利能够降低心室重构过程中血浆和心肌组织中AngⅡ的含量以及血浆中Ald含量。结论：应用氯沙坦和雷米普利均能够降低缩窄大鼠腹主动脉造成的左心室肥厚,进一步提示AngⅡ在慢性压力过载导致左心室重构中起着关键性作用。     

Beneficial effects of the combination of amlodipine and losartan for lowering blood pressure in spontaneously hypertensive rats

A combination of antihypertensive agents can better control blood pressure and reduce the number and severity of side effects than a monotherapy. Since both CCBs (calcium channel blockers) and ARBs (angiotensin II receptor type-1 blockers) are current and effective antihypertensive drugs, this study assessed the synergistic antihypertensive effects as well as the optimal combination ratio of these two drugs. Amlodipine (3 mg/kg) or losartan (30 mg/kg) alone or a combination of each drug at a ratio 1:10 and 1:20 was administered orally to spontaneously hypertensive rats (SHR). A four-week treatment of either 3 mg/kg amlodipine or 30 mg/kg losartan alone decreased the systolic blood pressure (SBP). However, their combination significantly lowered the SBP from the 3^rd week, and there was a positive correlation between this reduction in blood pressure and the improvement in arterial endothelium-dependent relaxation. In addition, the combination therapy (1:20) decreased both the cardiac mass and left ventricular weight to a greater extent than with either amlodipine or losartan alone. The collagen content in the cardiac tissue was also significantly lower after the 4-week combination therapy (1:10). These results suggest that the combined use of amlodipine and losartan might be more effective in treating hypertension than a monotherapy.     

氯沙坦逆转自发性高血压大鼠心血管肥厚作用的研究

目的：探讨氯沙坦逆转心血管肥厚的作用与心血管局部组织中内皮素（ET）的关系。方法：16周龄的自发性高血压大鼠（SHR）随机分成氯沙坦治疗组（SHR－L）与对照组（SHR－C）。另设同源正常血压大鼠（WKY）组，饲养共6周。大鼠的收缩压和心率用尾套法测量，左室重量指数（LVI）及主动脉中膜与内径比率测微计测量，血浆，心肌和主动脉含量用放免法测定，以SHR－C组做直线相关分析。结果：氯沙坦能显著降低SHR的收缩压，SHR－L与SHR－C组比较LVI及主动脉中膜内内径比值下降，左室及主动脉ET，SHR－C组高于WKY组，且分别与LVI及主动脉中膜和内径比值呈正相关。结论：左室及主动脉组织中ET升高是造成左室及主动脉肥厚的重要因素，氯沙坦通过阻断受体和降低血浆及血管组织中的含量产生降压及逆转心血管肥厚的作用。