匹伐他汀对高血压患者高敏C反应蛋白水平的影响

目的观察口服匹伐他汀对高血压患者血清高敏C反应蛋白(hs-CRP)水平的影响。方法 60例高血压患者,随机分为对照组和匹伐他汀组,每组30例,分别单服用硝苯地平30 mg.d-1和服用匹伐他汀2 mg.d-1及硝苯地平30 mg.d-1,疗程为3 mo。观察治疗前和治疗3 mo后血压、血脂、血清hs-CRP和补体的变化。结果 2组患者用药3 mo后血压均明显下降(P<0.01),匹伐他汀组与对照组相比血压下降幅度有增大趋势,但无显著差异(P>0.05)。对照组患者治疗前后血脂各项指标无显著变化(P>0.05),匹伐他汀组治疗3 mo后总胆固醇、低密度脂蛋白胆固醇和三酰甘油水平较治疗前均明显降低(P<0.01),与对照组比较有显著差异(P<0.01)。2组治疗前后补体C3、C4水平无显著差异。治疗3 mo后对照组hs-CRP水平与治疗前相比无显著变化(P>0.05),匹伐他汀组hs-CRP水平较治疗前显著降低(P<0.05),与对照组相比差异显著(P<0.05)。结论匹伐他汀可以在调脂的同时降低高血压患者血清高敏C反应蛋白的水平。     

多剂量口服硝苯地平缓释片的药动学及生物等效性

目的：研究多剂量口服硝苯地平缓释片在人体内的药动学特点和国产硝苯地平缓释片的生物等效性.方法：健康志愿受试者20名,口服硝苯地平试验品和参比品20mg,用标准二阶段交叉设计自身对照试验方法,采用液相色谱串联质谱方法（LC-MS/MS）测定服药后不同时刻的血药浓度,计算主要药动学参数,并采用方差分析和双单侧t检验（1-2a）90%置信区间进行生物等效性评价.结果：受试者分别口服受试品和参比品后,其主要药动学参数Tmax,Cmax,T1/2和AUCss分别为：（4.10±1.07）,（4.55±1.23）h;（52.64±15.80）,（51.54±12.87）μg/L;（8.44±1.69）,（8.33±2.27）h;（352.96±85.12）,（367.96±71.28）ng/（h·mL）;受试品的相对生物利用度为（96.2±17.3）%.结论：硝苯地平缓释片和硝苯地平缓释片（1）制剂具有生物等效性.     

缬沙坦联合硝苯地平缓释片治疗原发性高血压的临床疗效观察

目的：探讨缬沙坦联合硝苯地平缓释片治疗原发性高血压的临床疗效。方法：选择我院内科门诊治疗的86例原发性高血压患者,随机分为缬沙坦联合硝苯地平缓释片治疗组（A组,n=43）和单用缬沙坦对照组（B组,n=43）。对两组患者治疗4周后的有效性和安全性进行比较。结果：两组血压均有下降,A组下降明显,治疗总有效率95．3％,B组总有效率76．7％,两组比较差异有统计学意义（P〈0．05）。结论：缬沙坦联合硝苯地平缓释片治疗原发性高血压降压有效率优于单用缬沙坦。     

特拉唑嗪在治疗老年顽固性高血压中的疗效观察

目的探讨特拉唑嗪在治疗老年原发性顽固性高血压的临床疗效。方法将我院收治的80例顽固性高血压患者随机分成两组,均为原发性高血压。对照组36例使用拜新同及安博诺治疗,治疗组44例在对照组的基础上加用特拉唑嗪治疗,两组疗程均为6周。结果治疗组的总有效率明显高于对照组,两组相比较差异有统计学意义（P〈0.05）;两组治疗后的收缩压与舒张压均较治疗前有明显下降,治疗前后差异具有统计学意义（P〈0.05）,治疗组的降压效果明显优于对照组。结论盐酸特拉唑嗪联合多种降压药治疗老年顽固性高血压效果良好,副作用少,值得临床推广。     

氯沙坦联合硝苯地平对老年2型糖尿病肾病合并高血压患者肾功能的影响

目的 观察氯沙坦联合硝苯地平对老年2型糖尿病肾病合并高血压的疗效及对肾功能的影响.方法 将2009年12月至2010年12月收治的86例2型糖尿病肾病合并高血压患者随机均分为两组,观察组43例服氟沙坦片联合硝苯地平控释片治疗,对照组43例仅口服硝苯地平控释片治疗,观察两组的降压效果及对肾功能的影响.结果 观察组的降压总有效率为72.09%,明显高于对照组的51.16%(P<0.05).与治疗前比较,观察组治疗后血尿素氮、血肌酐、血尿酸和尿微量白蛋白水平明显下降(P<0.05),且均明显低于对照组(P<0.05).结论 氯沙坦联合硝苯地平治疗老年2型糖尿病肾病合并高血压,降压效果明显,且可保护肾脏功能,值得临床推广.     

心痛定与克甫定联合应用对100例高血压降压疗效和冠心病危险因素的影响

联合应用心痛定与克甫定对100例高血压降压疗效和冠心病危险因素的影响观察。用药七天后,总有效率93％,(P<0.01)。81％的患者服药后2—4天就能稳定在下降后的水平。服药后三大常规,肝肾功能无异常发现,血电解质,血尿酸及BUN不受影响。血糖明显降低(P<0.01),总胆固醇(TC)和甘油三脂(TG)降低,低密度脂旦白胆固醇(LDL—ch)降低和高密度脂旦白胆固醇(HDL—ch)升高非常显著(P<0.01)对心功能有良好的改善,血浆肾素(PRA)活性升高,而血管紧张素Ⅱ(AngⅡ)及醛固酮(PAC)降低。服药前后心率无明显变化(P>0.05)。无发现明显和严重副作用。是治疗高血压较理想的配伍方法。     

Clinical application of quantitative coronary angiography using the CAAS system: Preliminary results of the INTACT study (international nifedipine trial on antiatherosclerotic therapy)

Summary It is the objective of the INTACT-study to test in man, whether a significant retardation of the progression of coronary artery disease is attainable with the Ca-antagonist nifedipine; this may be possible on the basis of numerous animal experiments. INTACT is a prospective, randomized, double blind, placebo controlled investigation in 423 patients with preferably early stages of coronary sclerosis in whom a progression of the disease seems likely. A proper coronary angiogram led to inclusion of the patients in the study (October 1983–June 1985). Over the following 3-years-period patients received either nifedipine 80 mg/day or placebo. The study is concluded by a control coronary angiogram with angiographic projections which are identical to those of the first coronary angiography. The extent of coronary sclerosis is objectivated by computer-assisted quantitative measurement of the entire coronary arterial system with the CAAS-system (Rotterdam). For definition purposes the coronary artery system subdivided into 25 segments. Parameters for progression assessment will be mean segment diameter, minimal obstruction diameter, percentage severity of obstruction, length of obstruction and plaque area.So far 4826 coronary segments have been analyzed from the first angiograms of 383 patients. Per patient an average of 12.6 different segments could be evaluated in at least one angiographic projection. The major coronary segments could be measured in 72–93% of the patients in one or more angiographic projections (at the average about 2 different projections). Five hundred and forty-six coronary obstructions were analyzed; 131 of these were total occlusions. Only 9% of the length of the vessel contours detected by the computer algorithm required manual correction by the operators, suggesting a high reliability of the system. It can be concluded that quantitative measurement of the complete coronary artery system can indeed be obtained in a large angiographical multicenter study such as INTACT.     

Interactions of a new beta-blocker,celiprolol, with the calcium antagonists,diltiazem and nifedipine,on atrioventricular conduction

Summary The influence of a new beta-blocker, celiprolol, on the direct dromotropic effects of the Ca antagonists, diltiazem and nifedipine, on atrioventricular (AV) conduction was estimated in the canine isolated, blood-perfused AV node preparation. Diltiazem (1–10 µg) and nifedipine (0.3–3 µg) injected i.a. into the AV node artery dose dependently prolonged the atrio-His (AH) interval (5–39 msec and 7–51 msec) in the AV mode preparation. When celiprolol (1 and 10 mg/kg) was given i.v. in the support dog, the AH interval in the AV node preparation was transiently shortened and then maintained constant as a control. These doses of i.v. celiprolol completely abolished the isoproterenol-induced decrease in the AH interval (28 msec at 0.03 µg, i.a.) and AV nodal tachycardia. In the presence of celiprolol, the same doses of i.a. diltiazem and nifedipine increased the AH interval by the same amounts (6–43 msec and 8–53 msec) as the control. The incidence of second degree AV conduction block produced by diltiazem (2 in 5 AV node preparations at 10 µg) and nifedipine (2 in 6 preparations at 3 µg) was not changed by celiprolol. In the second experiments, diltiazem (30–300 µg/kg) and nifedipine (3–30 µg/kg), given i.v. in an open-chest in situ vagotomized dog, dose dependently increased AV conduction time (AVCT; 2–30 msec and 1–12 msec). Celiprolol 1 and 10 mg/kg i.v., which suppressed the isoproterenol-induced decrease in AVCT (32 msec at 0.3 µ/kg i.v.) and AV nodal tachycardia (4 in 6 in situ hearts), potentiated the prolongation of AVCT by the same doses of diltiazem (11–50 msec) and nifedipine (3–40 msec). The incidence of second degree AV conduction block produced by i.v., diltiazem (1 in 5 in situ hearts at 300 µg/kg) and nifedipine (0 in 6 in situ hearts at 30 µg/kg) was aggravated (4 in 5 and 3 in 6 in situ hearts) after i.v. celiprolol. These results indicate that although celiprolol does not affect thedirect negative dromotropic effects of the Ca antagonists, AV block could easily be produced when celiprolol eliminates tonic adrenergic influences in vivo.     

Hemodynamic interactions of a new beta blocker,celiprolol, with nifedipine in angina pectoris

The hemodynamic consequences of blockade at both beta-adrenoceptors and slow calcium channels is of therapeutic importance for patients with angina pectoris. The hemodynamic interaction of a new cardioselective beta blocker, celiprolol, and nifedipine was examined in an acute hemodynamic study using three prospectively matched groups with angiographically confirmed coronary artery disease (n = 10/group). Patients were randomly allocated to intravenous celiprolol (8 mg), sublingual nifedipine (20 mg), or their combination. Rest and exercise (supine bicycle) hemodynamics were determined before and following each therapy. At rest, celiprolol did not alter pumping function; nifedipine reduced diastolic blood pressure and systemic vascular resistance index (SVRI), with a small increase in heart rate. Combination therapy reduced systemic arterial pressure and SVRI; heart rate and cardiac stroke volume index increased. During exercise celiprolol tended to reduce heart rate and cardiac index; nifedipine reduced exercise SVR and cardiac stroke work indices. Combination therapy reduced all components of blood pressure; cardiac stroke work and SVR indices fell. These hemodynamic data suggest that beta blockade with celiprolol may result in a slight depression of cardiac pumping during exercise; however, such effects are offset by the vasodilating actions of nifedipine (reflex sympathetic action offsetting cardiodepression). Thus the acute hemodynamic effects of this combination were seemingly safe in these patients; the longer term effects during maintained therapy should be further assessed.     

Nisoldipine tablets once daily versus nifedipine capsules three times daily in patients with stable effort angina pectoris pretreated with atenolol

Summary Treatment with nisoldipine (2×10 mg tablets once daily) and nifedipine (2×10 mg capsules three times daily) in patients with severe, but stable effort angina pretreated with atenolol (100 mg once daily in 19 patients and 50 mg once daily in one patient) were compared for their effects on bicycle exercise tolerance and their adverse effects in a randomized 2×4 week, double-blind, double-dummy crossover study. All patients had multivessel disease, 16 patients had occlusion of at least one vessel, and eight patients had a history of myocardial infarction. Two patients left the study during the initial nisoldipine period, one because of aggravation of the angina and the other because of suspected allergic reaction. Addition of nifedipine to atenolol treatment significantly improved the variables measured for severity of angina, such as time of exercise until 1 mm and 2 mm ST-segment depression, total exercise time and total workload. In contrast, no such improvement was noted after the addition of nisoldipine to atenolol. However, nisoldipine resulted in a significant prolongation of the time to the initiation of chest discomfort, the maximum heart rate, and the double product.In atenolol-treated patients with severe effort angina pectoris, nifedipine 20 mg tid improved exercise capacity, while nisoldipine 20 mg once daily did not have a similar effect.