乐卡地平与氨氯地平治疗老年原发性高血压的比较

目的：以氨氯地平作对照，观察乐卡地平的降压疗效。方法：选择Ⅰ-Ⅱ级老年高血压患者46例，经停用降血压药1周后，随机分成A组（23例）；口服乐卡地平10mg/d；B组（23例）；口服氯氯地平5mg/d，连续治疗4周，观察血压、心率、血糖，血脂、肝肾功能，不良反应等指标。结果：（1）乐卡地平与氨氯地平降压作用明显（P＜0．05），对偶测血压，脉压有下降作用（P＜0．05），两组之间降压疗效无明显差异（P＞0．05）；（2）用药前后心率无明显差异（P＜0．05）；（3）两组生化指标治疗前后无明显差异（P＞0．05）。患者耐受性好，不良反应较少。结论：乐卡地平是治疗Ⅰ-Ⅱ级高血压的有效而安全的药物，是适合老年高血压患者降压治疗的药物。     

卡托普利含服治疗高血压急症的疗效观察

目的以卡托普利舌下含服治疗高血压急症，并与利血平肌注治疗对照。方法卡托普利３７．５ｍｇ舌下含服治疗高血压急症６０例为治疗组，６０例用利血平１．０ｍｇ肌注作对照。结果卡托普利组用药后１５ｍｉｎ即开始有显著的降压作用（Ｐ＜０．００１），３０，６０，１２０ｍｉｎ后疗效更显著（Ｐ＜０．００１）。对照组利血平用药后１５ｍｉｎ血压无显著下降（Ｐ＞０．０５），３０，６０，１２０ｍｉｎ血压明显下降（Ｐ＜０．００１）。二组比较，卡托普利组降压作用明显（Ｐ＜０．００１）。结论卡托普利舌下含服是治疗高血压急症较迅速、有效、安全、简便的降压方法，无明显不良反应     

乌拉地尔治疗高血压急症的疗效和安全性研究

目的：观察乌拉地尔、硝普钠治疗高血压急症的降压效果及安全性。方法：86例高血压急症患者被随机分成：乌拉地尔组（43例），持续静脉泵人乌拉地尔；硝普钠组（43例），持续静脉泵人硝普钠作为对照。监测两组血压，观察治疗效果，同时了解达到治疗高血压急症的最初目标的安全性。结果：乌拉地尔、硝普钠组在用药前血压无显著差异[（219．21±27．92）／（148．79±14．15）mmHg比（226．98±23．00）／（148．03±11．49）mmHg，P〉0．05]；两组在用药5min后血压开始明显下降，用药后各时间段血压均较治疗前明显下降，（P〈0．01），于用药后360min乌拉地尔、硝普钠组血压分别降至[（143．53±11．16）／（89．56±8．01）mmHg]、[（143．88±8．09）mmHg／（90．16±6．44）mmHg]，两种药物疗效差异无显著性（P〉0．05），都能达到治疗的最初目标。乌拉地尔、硝普钠组用药前心率无显著差异[（98．28±11．52）次／min比（98．09±9．23）次／mini，于用药后360min乌拉地尔组心率显著降至（96．95±11．37）次／min，而硝普钠组心率却显著上升至（100．33±10．96）次／min，乌拉地尔组对心率影响显著优于硝普钠组（P〈O．05）。结论：乌拉地尔对高血压急症有显著疗效，安全性高，值得推广。     

拜新同对高血压病患者血压变异性、胰岛素敏感性及免疫球蛋白的影响

目的 评价拜新同在降压的同时对高血压病患血压变异性、胰岛素敏感性及免疫球蛋白的影响。方法 60例高血压病患随机分成拜新同组和卡托普利组各30例,治疗前后分别测24h动态血压、空腹血糖、胰凫素及免疫球蛋白,以血糖与胰岛素乘积的倒数并取其自然对数为胰岛素敏感性指数。结果 两组高血压病患在血压下降的同时胰岛素敏感性提高、免疫球蛋白下降（P＜0．05）;拜新同组血压变异性下降（P＜0．05）,卡托普利组血压变异性下降明显（P＜0．05）。结论 皋新同 可显降低高血压病患的血压变异性、免疫球蛋白及提高胰岛素敏感性。     

卡托普利联合舒血宁治疗老年原发性高血压急症的疗效

目的 观察卡托普利联合舒血宁治疗老年原发性高血压（高血压）急症的临床疗效.方法 选择老年高血压急症患者共106例,分为治疗组和对照组各53例.两组患者均舌下含服卡托普利25 mg,治疗组加用舒血宁注射液20 mL加入250 mL 5％葡萄糖注射液（糖尿病患者改为0.9％氯化钠注射液）静脉注射.比较两组治疗前、后的血压、心率、心电图、临床症状及不良反应等.结果 治疗组治疗后不同时间点的舒张压和收缩压下降均比对照组明显,差异有统计学意义（P＜0.05）.治疗组治疗总有效率明显高于对照组,差异有统计学意义[94.33％（50/53）vs.67.92％（36/53）,P＜0.05].结论 卡托普利联合舒血宁治疗老年高血压急症较单纯应用卡托普利治疗更具优势,疗效较好.     

卡托普利与美多心安对肥胖高血压病患者左心室重量及糖、胰岛素代谢的影响

目的：观察卡托普利与美多心安对肥胖高血压病患者左心室重量（LVM及糖及胰岛素代谢（GIM）的影响。方法：对46例肥胖高血压病并且无糖尿病患者分别应用卡托普利（25－50mg,2次／d)和美多心安（12．5－50mg,2次／d)治疗24周，比较治疗前、后血压、LVM、口服葡萄糖耐量试验（OGTT）以及GIM相关指标的变化。结果：卡托普利与美多心安均能有效降低收缩压（P＜0．01）及舒张压（P＜0．05）。卡托普利显著影响血胰岛素Δ峰值（P＜0．05）和血胰岛素曲线下面积（P＜0．01）；美多心安显著升高空腹血糖（P＜0．01）、空腹胰岛素（P＜0．05）、血胰岛素Δ峰值（P＜0．05）和血胰岛素曲线下面积（P＜0．05）。卡托普利明显降低LVM（P＜0．05）和左心室重量指数（LVMI）（P＜0．05）；美多心安对LVM及LVMI无明显影响。结论：对肥胖高血压病患者，卡托普利与美多心安均能显著降压，此外卡托普利尚能降低LVM，并改善GIM。     

丹参对肝硬变犬门脉压力及胃粘膜血流的影响

通过胆总管结扎法，制造犬肝硬变门脉高压模型，并直接测定丹参注射液对肝硬变犬门脉压力及胃粘膜血流（GMBF）的影响。结果表明，静注丹参注射液后，肝硬变犬的门脉压力（PpV）、嵌塞肝静脉压（WHVP）、肝静脉压力梯度（HVPG）显著下降（P＜0．01），平均动脉压（MAP）、心率（HR）无显著变化（P＞0．05）。给药后10min，肝硬变及正常犬的GMBF显著增加（P＜0．05）．用药后30min达最高值（P＜0．01），60min后GMBF稍有下降．但与用药前比较仍有显著差异（P＜0．05）。说明丹参在降低肝硬变犬门脉压力的同时改善GMBF，对血压、心率无显著影响。为副作用小，兼具降低门脉压力与保护胃粘膜作用的药物。     

利喜定在高血压急症治疗中的临床应用

目的　评价利喜定静脉注射治疗高血压急症的降压效果。方法　 4 0例高血压急症患者予 2 5mg利喜定 5min内静脉注射 ,然后以 2 0 0 μg/min速度微泵静注 ,观察用药前后血压、心率变化及左心衰改善情况。结果　血压在用药后 5min即明显下降 ,2 0～ 30min达到高峰 ,至 12 0min均保持稳定 ,显效率 92 5 % ,有效率10 0 % ,心率无明显变化 ,2 5例高血压合并急性左心衰患者 ,急性左心衰控制满意。结论　利喜定治疗高血压急症起效快 ,降压效果显著、平稳、副作用少。     

卡托普利并小剂量双氢克尿噻治疗高血压的疗效

目的：研究卡托普利与小剂量双氢克尿噻合用对高血压患的疗效。方法：选择68例原发性高血压患随机分为两组，其中对照组单用卡托普利25mg，3次／日，口服；研究组卡托普利法相同，加服双氢克尿噻12．5mg，1次／日，口服，治疗8周，测定治疗前、后基础血压，24小时动态血压。结果：较之对照组，研究组的降压总有效率及24小时动态血压下降情况更优（P＜0．01，P＜0．05）.结论：卡托普利与小剂量双氢克尿噻合用治疗高血压较单用卡托普利更有效。     

乌拉地尔对高血压急症的疗效及安全性研究

目的评价静脉注射乌拉地尔对高血压急症的疗效及安全性。方法80例高血压急症病人以12．5mg～25．0mg乌拉地尔静脉注射（5min内），观察用药前后血压、心率变化。结果血压在用药后5min明显下降，30min达到高峰并保持稳定，心率无明显变化。结论静脉注射乌拉地尔治疗高血压急症安全、有效。     

美托洛尔静脉注射治疗快速心房颤动疗效评价

目的:观察美托洛尔(商品名:倍他乐克)注射液治疗快速心房颤动(房颤)的疗效及安全性。方法:42例快速房颤患者随机分为美托洛尔组与西地兰组,美托洛尔组21例予美托洛尔注射液5～15mg静脉注射,西地兰组21例予西地兰注射液0.4～0.8mg静脉注射,分别观察治疗前及治疗后40min、60min及120min患者心率及血压的变化。结果:1.2组患者分别有12例和8例在120min内心室率降至<100次/min,2组比较差异无显著性(57.14%vs38.09%,P>0.05)。2.美托洛尔组患者心室率降至<100次/min所需的时间为(18.33±12.31)min,西地兰组心室率降至<100次/min所需的时间为(65.00±35.05)min,2组比较差异有显著性(P<0.01)。3.美托洛尔静注起效平均时间(14.00±9.95)min,西地兰静注起效平均时间为(62.50±41.66)min,二者比较差异有显著性(P<0.01)。4.美托洛尔组总有效率85.71%(18/21),西地兰组总有效率47.62%(10/21),2组比较差异有显著性(P<0.01)。5.美托洛尔组治疗主要不良反应为低血压,无心力衰竭及严重心律失常。结论:美托洛尔静脉注射治疗快速房颤安全有效,为急诊科治疗快速房颤的可靠方法。     

Plasma renin activity and norepinephrine as predictors for antihypertensive effects of nifedipine and captopril

To examine predictors for the efficacy of antihypertensive agents, we investigated the effects of nifedipine and captopril on blood pressure (BP) and humoral factors in patients with essential hypertension. Eleven essential hypertensive patients (mean age: 54) were treated with long acting nifedipine at 20 to 40 mg/day for 8 weeks and 25 essential hypertensives (mean age: 51) were treated with captopril at 37.5 to 75 mg/day. Blood pressure was measured every 2 weeks. Plasma renin activity (PRA), and plasma concentrations of aldosterone, epinephrine and norepinephrine were determined before and at the end of treatment. Both nifedipine and captopril decreased BP (nifedipine: mean BP 119 +/- 3 to 101 +/- 2 mm Hg, captopril: 124 +/- 2 to 100 +/- 2, P less than .01 for each), whereas neither of them affected heart rate. The 8-week treatment of nifedipine showed no significant effect on humoral factors. Captopril increased PRA by 63% (P less than .05) and decreased plasma epinephrine by 42% (P less than .01) and norepinephrine by 35% (P less than .01). The change in mean BP was positively correlated with pretreatment PRA (r = 0.68, P less than .01) in nifedipine-treated patients and inversely with pretreatment norepinephrine (r = -0.53, P less than .01) in captopril treatment. The results suggest that both nifedipine and captopril were effective antihypertensive agents and that the long term treatment of nifedipine is more effective in essential hypertensives with lower PRA, while captopril is more effective in those with higher plasma norepinephrine concentration.     

Combined captopril and hydrochlorothiazide therapy in severe hypertension: long-term haemodynamic changes at rest and during exercise

Captopril is an orally active converting enzyme inhibitor lowering blood pressure (BP) in different types of hypertension. A combination of captopril and a diuretic is often used in the treatment of severe hypertension. We have examined the chronic haemodynamic effect of combined captopril and hydrochlorothiazide treatment at rest and during 50 and 100 W dynamic exercise in 12 patients with severe therapy resistant essential hypertension. Blood pressure was measured intra-arterially before and after a mean treatment period of 8.7 months. Cardiac index (CI) was measured by dye dilution (Cardiogreen) and body fluid volumes by radioisotope dilution techniques. During rest sitting BP was reduced by 31/17 mmHg (15%) from a pretreatment value of 205/119 mmHg. Total peripheral resistance index (TPRI) fell 17% whereas CI, heart rate (HR) and stroke index (SI) did not show any significant changes. The fall in mean arterial pressure (MAP) was slightly less during exercise (12%) and the BP reduction was associated with a fall in CI and SI of 15 and 17%, respectively and no fall in TPRI. No significant changes were observed in body fluid volumes.     

The influence of physical activity on the variability of ambulatory blood pressure

The aim of this study was to assess the contribution of physical activity levels to blood pressure (BP) variability, and to assess the effect age, gender, body mass index, and use of antihypertensive medications on this relationship. We simultaneously monitored 24-h ambulatory BP by automated recorder and activity by actigraphy in 431 patients. Mean activity scores for the 5, 10, 15, and 20 min preceding each BP measurement were calculated, and BP and heart rate were related to these variables using linear mixed model regression. Various patient characteristics were added to the mixed model as covariates. Patients were heterogeneous in age (48 +/- 13 years), sex (49% men), and average 24-h BP (132/81 +/- 15/10 mm Hg). Mean daytime activity level was 44 +/- 15 U. During the daytime, systolic BP (r = 0.33), diastolic BP (r = 0.29), and heart rate (r = 0.42) correlated best with the average activity for the 15 min preceding each measurement (P < .001). Variance was very high, with activity explaining from 0% to 62% of BP variability for different individuals. Men and the obese had a greater reactivity of systolic BP to activity; older patients and those on antihypertensive therapy had a lower reactivity of heart rate. Blood pressure level is significantly associated with physical activity, but the percentage of variance of BP explained by physical activity varies greatly between individuals. Correlation is strongest between BP and average activity integrated over the previous 15 min. Much of the variance in blood pressure remains unexplained.     

Long-term effects on central haemodynamics and body fluid volumes of ketanserin in essential hypertension studies at rest and during dynamic exercise

The long-term haemodynamic effects of ketanserin, a new serotonin-antagonist, was examined in 13 patients of both sexes (age range 24-62 years) with mild and moderate essential hypertension (EH). Cardiac output (CO) and intra-arterial blood pressure (BP) were measured at rest and during exercise before and after nine months of therapy. On ketanserin the mean casual BP was lowered by 15/21 mmHg to 152/91 mmHg and five of the 13 patients became 'normotensive' (BP less than 140/90 mmHg). The intra-arterial systolic pressure fell by 5-8% and the diastolic pressure by 5-11% from pretreatment levels at rest supine, sitting and during 50, 100 and 150 W exercise. The fall in BP was associated with a reduction in CO at rest while during exercise both a fall in CO and in total peripheral resistance contributed to the hypotensive effect. The fall in CO was due to a reduction in heart rate (average: -4 to 8 beats/min). The stroke volume remained unchanged in all settings and oxygen consumption was not affected by the drug. Body weight and body fluid volumes did not change significantly. Eight patients complained of drowsiness and lack of concentration. It is concluded that in mild and moderate EH ketanserin induces a moderate BP reduction associated with a fall in CO. There is no large vasodilating effect after long-term ketanserin treatment either at rest or during exercise. Ketanserin does not influence body fluid balance. The incidence of side-effects is high.     

Blood pressure elevation after phenylephrine infusion may adversely affect myocardial perfusion in patients with coronary artery disease

BACKGROUND: Although blood pressure is a major determinant of myocardial oxygen-demand, little information is currently available regarding the changes in blood pressure (BP) during myocardial ischemia. Since BP elevation may cause left ventricular (LV) wall stress and an increase in oxygen demand, infusion of an alpha-adrenergic agonist, such as phenylephrine (PH), may provoke changes in myocardial perfusion in coronary artery disease (CAD) patients. As the effects of BP changes alone on myocardial perfusion have never been assessed by thallium-201 (Tl) scintigraphy, we investigated the effects of BP elevation after PH infusion, in order to study the hypothesis that pressure loading alone without increases in heart rate, may provoke transient impairment of regional myocardial perfusion, in CAD patients. PATIENTS AND METHODS: Forty-one (41) patients with angiographically documented CAD, aged 54+/-8 years, were included in our study. Each patient was given, without any complications, a PH (0.1 mg/ml) dose infused at a rate of 0.8 ml/mm, determined by a standardisation procedure and producing a mean blood pressure elevation of approximately 30% above baseline levels and a heart rate response to levels of no less than 50 bpm. One minute after the desired blood pressure and heart rate responses were reached, 2 mCi of Tl were injected and the PH infusion continued until the termination of the test. Tl scintigraphy was performed both 2 min after Tl injection and 4 h later, while the results were correlated to coronary angiography findings. RESULTS: PH scintigraphy produced 152 total defects. The mean perfusion defect size (%) was 14+/-12 and was directly related to the number of diseased vessels, i.e., 2% for one-vessel disease, 15% for two-vessel disease and 25% for three-vessel disease (P<0.05). The lowest percentage Tl activity values were 56+/-14 and were inversely related to the number of diseased vessels (P<0.01). The mean Tl lung counts/pixel values were 25+/-8 while it increased as the number of diseased vessels increased (P<0.01). The mean lung/heart ratio values were 0.31+/-0.08 while it increased as the number of diseased vessels increased (P<0.01). CONCLUSION: BP elevation after PH loading, produces a significant impairment of myocardial perfusion, that correlates well with the extend of angiographic findings.     

Hemodynamic and clinical effects of captopril in congestive heart failure

The acute and chronic effects of Captopril were evaluated in 8 patients (5 males and 3 females, age 49 +/- 17 years) with chronic severe congestive heart failure. Acute hemodynamic effects were studied according to a randomized, double blind, placebo controlled protocol, by using two doses of Captopril (25 and 50 mg). The usual diuretic and digitalis treatment was kept unchanged throughout the trial. The acute administration of placebo associate with the usual doses of diuretic and digitalis was followed after 2 hours by a significant reduction of mean pulmonary wedge pressure (-23%, p less than 0.05). One hour following a single administration of Captopril, the following significant (p less than 0.05) changes were observed, respectively for the doses of 25 and 50 mg: heart rate -9% and -6%, cardiac index +13% and +10%, mean pulmonary wedge pressure -27% and -35%, mean pulmonary arterial pressure -29% and -26%, systemic vascular resistances -20% and -17%. A longer duration of effects on heart rate and cardiac index was noted after the 50 mg dose. All patients received long-term treatment with Captopril 75 or 150 mg daily. The NYHA functional class improved in all cases and there was a significant decrease of the cardio-thoracic ratio (from 0.61 +/- 0.05 to 0.55 +/- 0.09, p less than 0.01). A repeated hemodynamic study after a mean period of 6.5 months (range 2.5-22 months) revealed in 7 cases a sustained effect of the drug.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of endurance training on blood pressure at rest, during exercise and during 24 hours in sedentary men

The effect of 4 months of physical training on resting, exercise and 24-hour blood pressure (BP) was studied using a randomized crossover design in 26 healthy, sedentary men, with an average age of 39 +/- 10 (standard deviation) years. Peak oxygen uptake increased by 14% (p less than 0.001) and the physical working capacity at a heart rate of 130 beats/min by 25% (p less than 0.001). The heart rate was reduced by 7 beats/min at night (p less than 0.01) and by 6 beats/min during the day (p less than 0.001). Training-induced changes of BP varied according to measuring conditions. A decrease in BP at rest while sitting in the morning in the laboratory was significant for diastolic (-5 mm Hg, p less than 0.01) but not for systolic BP. During exercise, systolic BP was significantly lower after training, when measured at the same submaximal workloads. However, when workload was expressed as a percentage of peak oxygen uptake, systolic BP was not different before and after training. When measured during 24 hours, the training-induced change in BP was not significant at night either for systolic or diastolic BP. During the day the decrease in diastolic BP was significant (-5 mm Hg, p less than 0.001), but the change in systolic BP was not.     

Cardioprotective Effects of Angiotensin II Type 1 Receptor Blockade with Olmesartan on Reperfusion Injury in a Rat Myocardial Ischemia‐Reperfusion Model

We determined the effects of olmesartan on infarct size and cardiac function in a rat ischemia/reperfusion model. Rats underwent 30 min of left coronary artery (CA) occlusion followed by 2 h of reperfusion. In protocol 1, the rats received (by i.v.) 1 mL of vehicle at 10 min after CA occlusion (Group 1, n = 15); olmesartan (0.3 mg/kg) at 10 min after CA occlusion (Group 2, n = 15); 1 mL of vehicle at 5 min before CA reperfusion (Group 3, n = 15); or olmesartan (0.3 mg/kg) 5 min before CA reperfusion (Group 4, n = 15). In protocol 2, the rats received (by i.v.) 1 mL of vehicle at 5 min before CA reperfusion (Group 5, n = 21); or olmesartan (3 mg/kg) at 5 min before CA reperfusion (Group 6, n = 21). Systemic hemodynamics, left ventricular (LV) function, LV ischemic risk zone, no‐reflow zone, and infarct size were determined. In protocol 1, olmesartan (0.3 mg/kg) did not affect blood pressure (BP), heart rate, LV ± dp/dt or LV fractional shortening during the experimental procedure, and did not alter no‐reflow or infarct size. In protocol 2, olmesartan (3 mg/kg) significantly reduced infarct size to 21.7 ± 4.1% from 34.3 ± 4.1% of risk zone in the vehicle group (P= 0.035), but did not alter the no‐reflow size. Prior to CA reperfusion, olmesartan (3 mg/kg) significantly reduced mean BP by 22% and LV ±dp/dt, but did not affect heart rate. At 2 h after reperfusion, olmesartan significantly decreased heart rate by 21%, mean BP by 14%, and significantly increased LV fractional shortening from 54.1 ± 1.4% to 61.3 ± 1.6% (P= 0.0018). Olmesartan significantly reduced myocardial infarct size and improved LV contractility at a dose (3 mg/kg) with systemic vasodilating effects but not at a lower dose (0.3 mg/kg) without hemodynamic effects.     

右旋美托咪啶用于覆膜支架腔内隔绝术中镇静的随机双盲对照研究

目的:探讨观察右美旋托咪啶用于B型主动脉夹层覆膜支架腔内隔绝术中的镇静效果及安全性。方法:局麻复合强化麻醉下行覆膜支架腔内隔绝手术的患者60例,随机分为右旋美托咪啶组(D组)和芬太尼+咪达唑仑组(C组),每组30例,采用静脉注射,给药时间持续10 min,观察给药后即刻(基础值),5 min(T1)、8 min(T2)、10 min(T3)、12 min(T4)、15 min(T5)、20 min(T6)、25 min(T7)及30min(T8)的血压、心率(HR)、呼吸频率、经皮血氧饱和度(SpO2)、脑电双频谱(BIS)值及改良警觉、镇静观察评分变化并记录有无术中不良反应。结果:与基础值比较,D组T3～T8时收缩压(SBP)降低和舒张压(DBP)降低,T3～T8时HR降低,T4～T7时镇静评分降低,T5、T6时BIS值降低;C组T3时SBP降低,T4时镇静评分降低(P<0.05或P<0.01)。与C组比较,D组在T5～T7时SBP降低,在T6、T7时DBP降低,T3～T6时HR降低,T5、T6时镇静评分降低,T5、T6时BIS值降低,发生呼吸抑制及恶心呕吐的发生率降低(P<0.05或P<0.01)。2组各时点呼吸频率(RR)和血氧饱和度(SpO2)比较,差异无统计学意义(P>0.05)。结论:右旋美托咪啶具有良好的镇静效果,对呼吸影响小,不良反应轻微,可安全用于覆膜支架腔内隔绝术中镇静。