卡托普利与小剂量氢氯噻嗪合用治疗高血压疗效观察

目的：研究卡托普利与小剂量氢氯噻嗪合用对高血压患者的疗效及对代谢的影响。方法：５０例原发性高血压患者随机分为两组,第１组：单用卡手早１２．５ｍｇ～７５ｍｇ,每日２～３次。第２组,卡手早１２．５ｍｇ,每日２次,加服氢氯噻嗪１２．５ｍｇ,每日１次,两组治疗时间均为８周,测定治疗前后的基础血压,空腹血糖、血脂、血、血 到、 纱氮、肌酐以及有后的２４小时动态血压。 托普利加小剂量氢氯噻嗪组的总有效率及２４     

卡托普利与小剂量氢氯噻嗪合用治疗高血压疗效观察

目的:研究卡托普利与小剂量氢氯噻嗪合用对高血压患者的疗效及对代谢的影响.方法:50例原发性高血压患者随机分为两组,第1组:单用卡托普利12.5 mg～7 5 mg,每日2～3次.第2组:卡托普利12.5 mg,每日2次,加服氢氯噻嗪12.5 mg,每日1次,两组治疗时间均为8周,测定治疗前后的基础血压,空腹血糖、血脂、血钾、血尿酸、尿素氮、肌酐, 以及治疗前后的24小时动态血压.结果:卡托普利加小剂量氢氯噻嗪组的总有效率及24小时动态血压结果均明显优于单用卡托普利组,而且两组治疗前后的代谢指标均无明显改变.结论:卡托普利与小剂量氢氯噻嗪合用治疗高血压较单用卡托普利更有效,而且对代谢无明显影响.     

氢氯噻嗪、阿替洛尔、卡托普利对高血压病人24小时脉压的影响

目的 探讨不同降压药对高血压病患者24小时平均脉压的影响。方法符合1999年中国高血压联盟颁布的《中国高血压防治指南》中诊断标准的高血压病1、2级患者300例，随机分成三组，分别服用氢氯噻嗪、阿替洛尔、卡托普利，服药前及服药后8周分别进行动态血压检查。结果用药8周后收缩压(SBP)、舒张压(DBP)、脉压(PP)较用药前均有明显下降，但氢氯噻嗪组脉压下降比其它组明显。结论氢氯噻嗪对高血压病人不但降低收缩压及舒张压，对其24小时平均脉压的降低也有明显的作用。     

卡托普利与吲达帕胺或氢氯噻嗪合用的降压疗效观察

目的研究和评价卡托普利与吲达帕胺或氢氯噻嗪合用的降压疗效及对代谢的影响。方法选择60例轻、中度原发性高血压病患者,随机分成三组,每组各20例。卡托普利组:单用卡托普利12.5～50mg,3次/d;卡托普利与吲达帕胺合用组:卡托普利12.5—25mg,3次/d,加吲达帕胺2.5mg,1次/d;卡托普利与氢氯噻嗪合用组:卡托普利12.5~25mg,3次/d,加氢氯噻嗪12.5mg,2次/d。三组疗程均为12周。观察三组治疗前后的随测血压和24h动态血压及生化指标。结果卡托普利加吲达帕胺或加氢氯噻嗪组降压总有效率及随测血压、24h动态血压的变化均明显优于卡托普利单用组,且治疗前后心率和生化指标无明显改变。结论 卡托普利与吲达帕胺或氢氯噻嗪联合应用降压效果较单用卡托普利更有效,且对代谢无影响。     

小剂量氢氯噻嗪联合卡托普利治疗原发性高血压

目的 评价卡托普利联合小剂量氢氯噻嗪(HCTZ)治疗原发性高血压的疗效和安全性.方法 选择原发性高血压患者120例,随机分为A、B两组,其中A组用卡托普利25 mg,3次/d,口服,氢氯噻嗪25 mg,1次/d,口服.B组用卡托普利,用法用量与A组相同,氢氯噻嗪12.5 mg,1次/d,口服,共治疗8周,分别测定治疗前、后偶测血压(OBP)、24 h动态血压(ABP)、血生化指标并评价降压效果及安全性.结果 治疗8周末,A组和B组治疗后OBP、ABP监测的血压值较治疗前均明显下降(P＜0.01),组间比较差异无统计学意义.A、B两组降压总有效率分别为86.7%、85%,A组降压总有效率略高于B组,但组间差异无统计学意义.A、B两组降压达标率分别为61.7%、60%,两组间比较差异无统计学意义.A、B两组低血钾发生率分别为15%、5%,两组间比较,差异有统计学意义,两组间其他不良反应发生率,差异无统计学意义.结论 应用小剂量氢氯噻嗪联合卡托普利治疗原发性高血压安全、经济、有效.     

小剂量氢氯噻嗪联合卡托普利治疗原发性高血压

目的评价卡托普利联合小剂量氢氯噻嗪(HCTZ)治疗原发性高血压的疗效和安全性。方法选择原发性高血压患者120例,随机分为A、B两组,其中A组用卡托普利25mg,3次/d,口服,氢氯噻嗪25mg,1次/d,口服。B组用卡托普利,用法用量与A组相同,氢氯噻嗪12·5mg,1次/d,口服,共治疗8周,分别测定治疗前、后偶测血压(OBP)、24h动态血压(ABP)、血生化指标并评价降压效果及安全性。结果治疗8周末,A组和B组治疗后OBP、ABP监测的血压值较治疗前均明显下降(P<0·01),组间比较差异无统计学意义。A、B两组降压总有效率分别为86·7%、85%,A组降压总有效率略高于B组,但组间差异无统计学意义。A、B两组降压达标率分别为61·7%、60%,两组间比较差异无统计学意义。A、B两组低血钾发生率分别为15%、5%,两组间比较,差异有统计学意义,两组间其他不良反应发生率,差异无统计学意义。结论应用小剂量氢氯噻嗪联合卡托普利治疗原发性高血压安全、经济、有效。     

卡托普利配伍氢氯噻嗪治疗原发性高血压30例疗效观察

近年来我国高血压病的发病率逐年上升，寻找有效、安全、经济的降压治疗方法是目前研究的热点。2000年2月～2002年10月，我们应用卡托普利配伍氢氯噻嗪治疗高血压病30例，取得良好效果，现报告如下。     

氯沙坦与吲哒帕胺或氢氯噻嗪合用的降压疗效观察

目的：研究和评价氯沙坦与吲哒帕胺或氢氯噻嗪合用降压疗效及对代谢的影响。方法：选择４５例轻一中度原发性高血压患者,随机分成３组,氯沙坦与吲达帕胺合用组：氯沙坦５０ｍｇ,每日一次,加吲达帕胺２．５ｍｇ,每日一次;氯沙坦与氢氯噻嗪合用组：氯沙坦５０ｍｇ,每日一次,加氢氯噻嗪１２．５ｍｇ,每日二次。三组疗程均为１２周。观察三组治疗前后的随测血压（ＣＢＰ）和２４小时动态血压（ＡＢＰＭ）及生化指标。结果：氯沙坦加吲达帕胺或加氢氯噻嗪组降压总有效率及随测血压、２４小时动脉血压的变化均明显优于氯沙坦单用组,且治疗前后心率和生化指标无明显改变。结论：氯沙坦与吲达帕胺或氢氯噻嗪联合应用降压效果较单用氯沙坦更有效,且对代谢无影响。     

氢氯噻嗪及氢氯噻嗪与依那普利合用对轻中度高血压病患者血脂及电解质的影响

目的评价氢氯噻嗪以及氢氯噻嗪与依那普利合用对轻、中度高血压病患者血脂及电解质的影响。方法对166例轻、中度高血压患者应用小剂量氢氯噻嗪（12.5mg/d）治疗2周,根据血压达标情况（≥140/90mmHg）决定加用依那普利（83例,A组）,或继续维持（〈140/90mmHg）小剂量氢氯噻嗪（83例,B组）治疗。随访3个月,观察用药前后两组血压、心率、血脂、电解质等的变化。结果两组治疗后血压、心率较治疗前均明显下降（P〈0.05）;治疗3个月后,A组患者总胆固醇（TC）、三酰甘油（TG）、低密度脂蛋白胆固醇（LDL-C）、高密度脂蛋白胆固醇（HDL-C）无显著变化。B组患者TC、HDL-C、TG水平无显著改变,LDL-C稍有升高（P〉0.05）。治疗3个月后A组、B组两组患者的血钾、血钠、血氯无明显变化。结论小剂量的氢氯噻嗪和氢氯噻嗪加用依那普利两种治疗方案对高血压患者血脂均较有效,且安全无明显副反应。     

长期小剂量氢氯噻嗪的降压疗效观察

目的观察原发性高血压病患者长期服用小剂量氢氯噻嗪的降压疗效。方法232例轻、中度高血压病患者服用氢氯噻嗪12.5mg,每日1次,每月发放一次药物并测量血压,观察1年。比较服药6周及1年的降压疗效及生化指标的变化。结果(1)观察结束时资料完整的观察对象为231例,治疗后6周的收缩压、舒张压、平均动脉压下降值分别为(6.01±16.05)mmHg(1mmHg=0.133kPa)、(2.90±10.33)mmHg、(3.94±10.68)mmHg;治疗1年的收缩压、舒张压、平均动脉压下降值分别为(10.45±17.28)mmHg、(8.45±11.06)mmHg、(9.12±10.88)mmHg。1年时血压下降值高于6周时血压下降值,差异有统计学意义(P<0.05)。治疗6周时的降压达标率为20.3%,治疗1年时降压达标率为35.1%,差异有统计学意义(P<0.05)。(2)观察结束时未发现有症状的低钾血症,但血尿酸值明显增加,与基线值比较差异有统计学意义(P<0.05)。结论长期服用小剂量氢氯噻嗪可有效降低轻、中度原发性高血压患者的血压,对电解质、糖、脂代谢无明显不良影响。     

缬沙坦与卡托普利联合应用对扩张型心肌病的疗效

目的:探讨缬沙坦与卡托普利联合应用对扩张型心肌病的疗效。方法:50例扩张型心肌病患者在应用洋地黄、利尿剂、β-受体阻断剂的基础上,随机分为:观察组(n=25):口服缬沙坦80 mg/d及卡托普利18.75~150mg/d;对照组(n=25):口服卡托普利18.75~150 mg/d。治疗前、后分别行血清电解质、肾功能和超声心动图检查。结果:治疗3个月后两组左室舒张末期容积(LVEDV)、左室收缩末期容积(LVESV)、左心室射血分数(LVEF)与短轴缩短率(FS)均有显著改善(P<0.05),但观察组较对照组改善更显著(P均<0.05)。治疗前、后两组血清电解质与肾功能无显著性变化(P>0.05)。结论:缬沙坦与卡托普利联合应用治疗扩张型心肌病的疗效优于单用卡托普利。     

Influence of captopril on the arterial baroreceptor reflex in patients with heart failure

In 16 male patients with heart failure (NYHA II-III), the influenceof a single dose of 25 mg captopril on the carotid sinus baroreceptorreflex was examined. Blood presure fell significantly by 11± 1.7 mm Hg (P < 0.001), whereas heart rate remainedunchanged (85 ± 3 vs. 83 ± 3 beats min^–1).Carotid sinus baroreceptors were stimulated by means of an airtightneck chamber. Two indices of baroreflex sensitivity were calculated.(1) The sensitivity to reflex heart rate slowing was increasedby captopril from –2.9 ± 0.7 to –5.0 ±1.3 ms mmHg^–1 (P <0.002). The higher the initial sensitivitythe more pronounced was the change after captopril with an increaseof sensitivity by 46% (y = 1.46x –0.17, P <0.01). Thisincrease in sensitivity cannot be explained by haemodynamicchanges induced by captopril. (2) In eight patients the sensitivityof the baroreflex to increased transmural pressure gradientsof the carotid sinus was evaluated by registration of the bloodpressure response to neck suction; this demonstrated an unchangedresponsiveness following captopril administration. From thesedata it can be concluded that captopril selectively augmentsa reflex bradycardia which is mediated by an increase in vagalefferent tone. The change in the reflex response depends onthe initial reflex sensitivity and cannot be explained by haemodynamicchanges caused by captopril.     

比索洛尔加小剂量双氢克尿噻治疗高血压病的疗效观察

目的:观察比索洛尔加小剂量双氢克尿噻治疗高血压病的疗效和安全性。方法:86例高血压患者被随机均分为两组:对照组(单用比索洛尔2.5mg,晨服,1次/d)和观察组(在对照组治疗基础上再加用小剂量双氢克尿噻12.5mg,晨服,1次/d),疗程均为1月,观察治疗前、后血压,心率,血脂,血糖,肝、肾功能,电解质含量的变化。结果:治疗1个月后血压下降,总有效率对照组72%,观察组93%,两组有显著差异(P<0.05)。两组均无不良事件发生。结论:比索洛尔加小剂量双氢克尿噻治疗高血压病安全、有效。     

缬沙坦联合氨氯地平或氢氯噻嗪对老年高血压患者血压变异性的影响

目的 观察比较缬沙坦分别联合氨氯地平或氢氯噻嗪对老年高血压患者血压及其变异性的影响.方法 选取138例老年高血压患者,随机分为两组,A组70例给予口服缬沙坦80 mg联合氨氯地平5mg qd;B组68例给予口服缬沙坦80 mg联合氢氯噻嗪12.5 mg qd.分别在治疗前、治疗8w时进行24 h动态血压监测,观察24 h、白天与夜间收缩压变异性(systolic blood pressure variability,SBPV)和舒张压变异性(diastolic blood pressure variability,DBPV);24h、白天与夜间平均收缩压(systolic blood pressure,SBP)和平均舒张压(diastolic blood pressure,DBP).结果 与治疗前比较治疗后第8周A组与B组24 h、白天、夜间SBP、DBP、SBPV均下降(P＜0.05),A组下降幅度均大于B组(P＜0.05).A组治疗8w后,DBPV均有下降(分别地,P＜0.05),而B组无变化,组间比较差异有统计学意义(P＜0.05).结论 缬沙坦联合氨氯地平或氢氯噻嗪治疗均能有效控制老年高血压患者的血压,但缬沙坦联合氨氯地平具有更佳的血压达标率和更低的血压变异性.     

Effect of captopril on renal function in patients with essential hypertension

The glomerular filtration rate (creatinine clearance), glomerular permeability (qualitative and quantitative proteinuria), tubular reabsorption (k-λ chains of immunoglobulins and lysozyme) and indexes of tubular cell lysis (alpha-glucosidase and gamma-glutamyltranspeptidase) were measured in the urine of 10 patients with moderate, uncomplicated essential hypertension during placebo therapy and after captopril given at increasing doses of 25, 50, 100 and 200 mg twice daily, the first three doses being given for 3 days and the last one for 4 weeks in all patients and for an additional 6 months in 5 patients. During placebo therapy, proteinuria was absent in eight patients and detectable (glomerular and selective) in two; selective proteinuria appeared in two and a decrease in selectivity was observed in two patients with previous proteinuria after 4 weeks of captopril therapy. No proteinuria was detectable in the five patients followed up for 6 months, not even in the one in whom a decrease in glomerular selectivity had occurred after 4 weeks. The glomerular filtration rate was unchanged as were lysozyme and gamma-glutamyltranspeptidase values, while light chains were always undetectable. Alpha-glucosidase showed some increase; however, increments were transient and always much lower than those observed with known tubular toxic drugs. These data show that under our experimental conditions captopril caused no evident changes in glomerular and tubular function.     

卡托普利对高血压病及非胰岛素依赖型糖尿病患者运动血压及微蛋白尿的短期作用

对血压正常的非胰岛素依赖型糖尿病（ＮＩＤＤＭ）患者１４例（ＮＩＤＤＭ组）、高血压病（ＥＨ）患者１２例（ＥＨ组）、ＥＨ合并ＮＩＤＤＭ患者１２例（ＥＨ并ＮＩＤＤＭ组）给予卡托普利口服２５ｍｇｂｉｄ，在１ｄ半内共服３次，服药前后做踏车运动试验测定血压、心率、尿白蛋白排泄率（ｕＡＥＲ）及尿转铁蛋白排泄率（ｕＴＥＲ），并以１０例正常人作对照（对照组）。结果：①服卡托普利后ＥＨ组血压明显下降，ｕＡＥＲ及ｕＴＥＲ无明显改变，而ＥＨ并ＮＩＤＤＭ组却相反；②运动状态下，三组患者服卡托普利后尿白蛋白均明显下降，但与血压互不相关；③ＥＨ组服药后，运动血压有所下降，但血压变化的绝对值服药前后相似；④血压正常的ＮＩＤＤＭ组运动后血压明显升高，服药后这种异常消失。提示：①运动状态下，早期ＥＨ和ＮＩＤＤＭ有不同的病理生理机理，似乎糖尿病更依赖于肾素－血管紧张素系统，卡托普利有较好的疗效。②对于正常血压、尿白蛋白（－）的ＮＩＤＤＭ患者，运动激发是观察尿白蛋白及血压改变的灵敏方法，若被运动激发，应当考虑给予卡托普利治疗。     

Effect of captopril on plasma prolactin in patients with essential hypertension

The effects of the angiotensin-converting enzyme inhibitor captopril on blood pressure, heart rate, plasma prolactin, and renin activity were examined in a single-blind, placebo-controlled trial on 30 patients with essential hypertension (15 given drug, 15 placebo). Captopril, 25 mg administered orally, reduced the blood pressure and increased the plasma renin activity. Captopril decreased mean plasma prolactin from 17.5 +/- 1.4 ng/mL to 9.1 +/- 1.0 ng/mL (p less than 0.001). Significant correlation was found between captopril-induced change from control values of plasma prolactin (delta plasma prolactin) vs delta plasma renin activity (r = -0.688, p less than 0.001). These results suggest that acute administration of captopril was accompanied by a reduction in plasma prolactin and that this reduction may be of clinical significance during therapy of hypertension.     

地尔硫缓释剂对原发性高血压患者肾功能的影响

目的 :探讨地尔硫缓释剂对原发性高血压 (EH)患者肾功能的影响。方法 :6 2例 EH患者 (EH组 )随机分为两亚组 :A组 (地尔硫缓释剂组 )和 B组 (卡托普利组 ) ,疗程均为 10周。治疗前后观察肾功能指标变化。2 0例健康体检者作为对照组。结果 :1治疗前 EH组患者内生肌酐清除率 (Ccr)显著低于对照组 ,血尿 β2 -微球蛋白 (β2 - m)及尿白蛋白 (Alb)显著高于对照组 ,且上述指标改变程度与 EH的病程相关 ;2地尔硫缓释剂和卡托普利治疗 EH患者 ,可明显降低血压、血尿 β2 - m与尿 Alb,其中病程较长者下降幅度较大 ,B组尿 Alb降低程度 >A组 (P <0 .0 5 )。结论 :1EH患者早期即有肾功能损害 ,且随病程延长损害加重 ;2地尔硫缓释剂可保护 EH患者早期损害的肾功能 ,且病程较长者获益较大 ,其效果可能与卡托普利相似     

Effects of captopril on prostaglandin and natriuresis in patients with essential hypertension

The antihypertensive, renal and hormonal effects of captopril were studied in 10 patients with essential hypertension. Captopril significantly decreased arterial blood pressure with a concomitant increase in glomerular filtration rate, natriuresis and kaliuresis and a significant selective increase in urinary (renal) prostaglandin E₂; other plasma and urinary prostaglandins (F_2α 6-keto-prostaglandin F_1α, thromboxane B₂) were not significantly changed. The urinary prostaglandin E₂ increase was observed even in patients with pretreatment subnormal prostaglandin E₂ excretion. Increases in urinary prostaglandin E₂ were significantly positively correlated with increases in urinary sodium concentration. It is concluded that the antihypertensive effect of captopril is mediated, at least partially, by prostaglandin E₂ release from renal and extrarenal tissues. Captopril enhances natriuresis at a lower perfusion pressure.