盐酸奥昔麻黄碱治疗冠心病心绞痛的临床疗效

本文应用盐酸奥昔麻黄碱治疗110例冠心病心绞痛患者,用法:wk1给安慰剂,wk2,3口服奥昔麻黄碱,8mg,tid,wk4,5给安慰剂。结果:奥昔麻黄碱组症状疗效为88.2％,安慰剂组为35.4％(P<0.01),奥昔麻黄碱组心电图疗效为51.8％。本药并可使收缩时间间期(STI)缩短,心率加快,副作用小,可作为治疗冠心病心绞痛有效药物之一。     

盐酸奥昔麻黄碱对家兔血小板聚集功能的影响及临床效应

本文对10只家兔用奥昔麻黄碱1mg/kg,静注,测定血浆血小板聚集率(％),并以同法与阿司匹林进行对比观察,发现奥昔麻黄碱与阿司匹林同样具有显著对抗血浆血小板聚集作用,P<0.01;并结合内蒙及上海协作组的290例与本院治疗的21例冠心病心绞痛作一临床应用评价。     

纳多洛尔随机双盲法治疗心绞痛30例

本文采用随机、双盲、安慰剂对照、交叉试验,观察口服纳多洛尔片剂4wk(40mg,qd),治疗30例(男19,女11,年龄60±6yr)冠心病心绞痛患者.用药后,临床总有效率为93％,心电图总有效率为80％,均显著高于安慰剂(P<0.01)。     

冠脉扩张药奥昔麻黄碱的药理作用及临床应用

奥昔麻黄碱(麻黄苯丙酮)是较好的冠脉扩张药,口服吸收。其特点为:作用温和、维持时间较长、疗效高、副作用小,长期应用也较安全。本文综述奥昔麻黄碱的药代动力学、心血管作用、临床应用及不良反应。     

注射用奥扎格雷钠治疗不稳定型心绞痛的临床观察

目的 观察奥扎格雷钠治疗不稳定型心绞痛的临床疗效及治疗前后血液黏稠度、凝血因子的变化规律。方法 将86例入选病人随机分为治疗组与对照组,对照组应用抗凝、扩冠、降低心肌耗氧等治疗措施。治疗组在对照组治疗的基础上加用奥扎格雷钠60mg静滴。每日2次,2周为一疗程。比较两组疗效及治疗前后相关指标的变化。结果 心绞痛缓解总有效率：治疗组93％,对照组65．1％（两组比较P〈0．05）;心电图恢复总有效率分别为83．7％和53．5％（P〈0．05）。结论 奥扎格雷钠治疗不稳定心绞痛疗效显著优于对照组,并能改善血液黏稠度,预防血栓形成。     

西布曲明片治疗单纯性肥胖的临床研究

目的 :评价西布曲明 (sibutramine)对单纯性肥胖或体重指数 (BMI)≥ 2 5的超重者的减肥疗效及安全性。方法 :以安慰剂作为对照进行 8wk的随机双盲、多中心临床研究 ;试验组、对照组各纳入受试者 10 4例 ,每日 1次饭前或饭后 1h口服西布曲明片 10mg或相同片数的安慰剂。 8wk启盲后 ,试验组继续用药观察至 2 4wk。结果 :西布曲明可明显减少受试者的腰围、臀围、BMI、体重 (P <0 .0 1) ,总有效率为 73.8% ,对照组为 15 .5 % ,P <0 .0 1。对血脂及血糖的影响 2组间差异无显著意义。治疗至 8wk末西布曲明不良反应发生率为5 8.6% ,对照组为 4 1.4 %。 2 4wk末西布曲明不良反应发生率为 35 .7%。未发现严重的不良反应。结论 :西布曲明片是疗效肯定、不良反应较轻、给药方便、依从性高的减肥药     

尼可地尔治疗心绞痛115例

本文用尼可地尔治疗心绞痛115例,其中男93例、女22例;年龄45-75岁,平均58±6岁。口服剂量5mg,tid,连续4wk为一疗程。对各种类型心绞痛症状的总有效率为89.6％;心电图ST-T总改善率为62.6％。它能有效地减少心绞痛的发作次数,具有速效、长效的优点;且无严重不良反应。随机对30例心绞痛患者用异山梨醇作对照观察,两者疗效无显著差异。     

西地那非治疗骨盆骨折尿道损伤后并发勃起功能障碍

目的 :观察西地那非治疗骨盆骨折尿道损伤后阴茎勃起功能障碍 (ED)的疗效和安全性。方法 :采用随机、交叉、双盲和安慰剂对照方法 ,将 5 2例骨盆骨折尿道损伤后ED病人 ,分为A ,B 2组 ,A组 2 8例 ,性交前 1h口服西地那非 5 0～ 10 0mg ,2～3日口服 1次 ,连续 4wk ;B组 2 4例 ,同时给予安慰剂治疗 4wk。间隔 1wk后 ,2组用药顺序进行自身前后交叉治疗。采用勃起功能国际问卷 (IIEF 5 )进行评价。结果 :A ,B 2组服用西地那非总有效率分别为 79%与 71% (P >0 .0 5 )。A ,B 2组在交叉服药后 ,其治疗ED总有效率西地那非治疗组为75 % ,而安慰剂组为 2 1% (P <0 .0 5 )。不良反应较轻微而且短暂。结论 :西地那非治疗骨盆骨折尿道损伤后阴茎勃起功能障碍疗效确切 ,且无明显不良反应     

前列腺素E1治疗不稳定型心绞痛疗效观察

目的 观察前列腺素E1对不稳定型心绞痛的临床疗效。方法 将72例不稳定型心绞痛患者随机分为2组。治疗组36例,采用前列腺素E1治疗1对照组36例,采用硝酸甘油治疗。观察前列腺素E1对不稳定型心绞痛改善临床症状、体征、心电图及心律失常、心功能情况。结果心绞痛疗效:治疗组总有效率为94.4％,对照组为77.7％。改善心电图、心律失常;治疗组总有效率为88.89％,对照组总有效率为63.9％,P<0.05。结论 治疗组优于对照组。     

硝苯地平控释片3种剂量治疗稳定性心绞痛疗效比较

目的 :比较硝苯地平控释片小、中和大剂量治疗稳定性心绞痛的疗效。方法 :1 0 2例病人被随机分为 4组 ,分别接受硝苯地平控释片 30mg·d-1(n =2 7) ,60mg·d-1 (n =2 5) ,90mg·d-1 (n =2 6)和安慰剂 (n =2 4 )治疗 ,为期 6wk。结果 :经过 6wk的治疗后 ,硝苯地平控释片 3种剂量均能显著减少心绞痛发作次数及硝酸甘油消耗量 ;均能延长运动至ST压低 1mm时间和总运动时间 ;各治疗组治疗前后或与对照组比较 ,差异均有显著或非常显著意义 (P <0 .0 5或P <0 .0 1 )。临床症状总有效率分别为 81 % ,88%和 89% ;心电图总有效率分别为56 % ,60 %和 65 %。不良反应发生率 90mg组高于其余 3组。结论 :硝苯地平控释片 30 ,60和 90mg·d-1 短期治疗均能有效改善稳定性心绞痛病人的临床症状、心电图及运动能力 ,但每日剂量以低于60mg为宜     

The haemodynamic effects of prolonged oral administration of oxyfedrine, a partial agonist at β-adrenoceptors: Comparison with propranolol

1 Haemodynamic changes have been studied in cats after the chronic oral administration of oxyfedrine (14 mg/kg for 3-4 weeks) or of placebo (lactose). The initial part of the study was carried out under double-blind conditions. The arterial blood pressure was between 19 mmHg (diastolic) and 27 mmHg (systolic) higher in the oxyfedrine treated animals, but there were no differences between the two groups with regard to cardiac output, left ventricular dP/dt max, heart rate or systolic ejection time.2 In cats similarly treated with propranolol (4 mg/kg) there was a slight (12%), but significant, reduction in cardiac output.3 Isoprenaline dose-response curves were shifted to the right in the cats administered oxyfedrine as well as in those administered propranolol. The degree of shift was five-fold (positive chronotropic response) and 20-fold (decrease in diastolic blood pressure) in the oxyfedrine group and 10- and 80-fold, respectively, in the propranolol group.4 In contrast to the partial blockade of the effects of isoprenaline, the haemodynamic response to oxyfedrine was largely unaltered, both in the cats pretreated with propranolol and in those pretreated with oxyfedrine. The pressor response to noradrenaline was potentiated in the cats pretreated with oxyfedrine.5 These results provide an explanation for the anti-anginal action of oxyfedrine. Some degree of beta-adrenoceptor blockade is achieved without a reduction in cardiac output or left ventricular dP/dt max. The relevance of these findings to the haemodynamic situation in angina is discussed.     

The effect of prolonged treatment with oxyfedrine on intracellular potentials and on other features of cardiac function in rabbits and guinea-pigs

1. Previous work in acute experiments has shown that the main pharmacological action of oxyfedrine is stimulation of beta-adrenoceptors, yet there have been clinical reports that the drug is beneficial in the treatment of angina pectoris.2. In the present experiments rabbits and guinea-pigs were treated for several weeks with daily i.p. injections of oxyfedrine.3. A daily dosage of 15 mg/kg oxyfedrine had no effect on growth rate for 4 weeks, but thereafter the growth rate of treated animals fell below that of controls.4. The heart weights of the treated animals, expressed as a percentage of body weight, were significantly lower than those of controls.5. Measurement of intracellular potentials in hearts taken from treated rabbits showed that the main effects were a reduction in the maximum rate of depolarization and a prolongation of the plateau of the action potential.6. Guinea-pigs treated for 6 weeks with 15 mg/kg oxyfedrine daily i.p. were protected to some extent from the toxic effect of ouabain infused intravenously.     

Effects of oxyfedrine on left ventricular function in patients several months after myocardial infarction.

Left ventricular (LV) function was investigated by left heart catheterization at rest and during exercise in 15 men 3--5 months after acute myocardial infarction. The effect of 8 mg oxyfedrine i.v. in 10 patients was compared to placebo in 5. The administration of oxyfedrine led to a significant decrease of LV end-diastolic pressure; an increase of LV dp/dt max, heart rate, LV ejection fraction and LV stroke work; and a shift of LV function curve indicating its improvement. These results give evidence for a positive inotropic effect of this drug which could have therapeutic implications in patients with impaired LV function after myocardial infarction.     

Oxyfederine and propranolol--a controlled trial in angina pectoris.

1 A double-blind-crossover randomised trial was performed to compare the effects of oxyfedrine (maximum dose 32 mg three times daily), propranolol (maximum dose 120 mg three times daily) and placebo in 30 patients with chronic stable angina pectoris. Assessment was by means of symptom level, ECG responses to graded exercise and haematological and biochemical investigation. 2 Oxyfedrine and propranolol resulted in similar significant improvements in symptom level (P < 0.05 in both cases), and ST index (propranolol P < 0.02; oxyfedrine P < 0.05). Neither drug produced any significant changes in haematologaical or biochemical investigations and only infrequent minor side effects were noted. 3 These results indicate that oxyfedrine is a safe and well-tolerated drug with an efficacy comparable with that of propranolol in the treatment of patients with angina pectoris.     

The effect of 2 weeks treatment with cetirizine on bronchial reactivity to methacholine in asthma.

1. We investigated the effect of 2 weeks therapy with oral cetirizine (10 mg twice daily) on methacholine bronchial reactivity in 14 asthmatics. All had bronchial hyperreactivity to methacholine on entry to the study, with a geometric mean cumulative PC20 of 0.83 mg ml-1 (range 0.1-3.61 mg ml-1) and eight were atopic on skin prick testing. 2. The study was placebo-controlled and in randomised order, with a minimum 1 month washout period between cetirizine and placebo study periods. Four methacholine challenges were performed in all, at the beginning and at the end of each study period. 3. No significant change in methacholine reactivity was found following 2 weeks therapy with cetrizine. The repeatability coefficient for the PC20 methacholine over 2 weeks was found to be 2.90 doubling dilutions for the placebo period and 1.73 doubling dilutions for the cetirizine period. The study had a 80% power at the 5% significance level (two-tailed) to detect a 1.16-doubling concentration change in methacholine reactivity. 4. We conclude that 2 weeks therapy with cetirizine has no significant effect on non-specific bronchial hyperreactivity.     

Potentation of the cardiac response to aminophylline by oxyfedrine

Summary The influence of oxyfedrine on the cardiostimulatory effects of aminophylline was studied in the isolated perfused guinea-pig heart. It was found that oxyfedrine potentiated the stimulatory effects of aminophylline on isometric contraction,dF/dt, coronary flow and heart rate. This potentation was abolished after pretreatment with propranolol. Histamine, though to a lesser extent, also potentiated the effects of aminophylline. When oxyfedrine and histamine were infused simultaneously in the presence of propranolol, the response of the heart to aminophylline was also potentiated; the magnitude of this potentiation was comparable to that obtained with histamine alone, indicating that propranolol abolished only the action of oxyfedrine but not that of histamine. The mechanical effects of aminophylline were accompanied by a slight (15%) but significant inhibition of phosphodiesterase, which was not further augmented by oxyfedrine.The results suggest that the potentiating effects of oxyfedrine or histamine on the cardiostimulatory actions of aminophylline are elicited by their stimulatory actions on adenylate cyclase activity.Supported by Fonds zur Förderung der wiss. Forsch. in Österreich (Proj. 1301/1453).     

A controlled comparison of oxyfedrine, isosorbide dinitrate and placebo in the treatment of patients suffering attacks of angina pectoris.

1 In a group of 23 patients with documented ischaemic heart disease who experienced angina pectoris, oral oxyfedrine (24 mg three times daily) was compared with isosorbide dinitrate (10 mg three times daily) and placebo in a double-blind double-crossover clinical trial. 2 Isosorbide dinitrate appeared no better than placebo, either in terms of symptomatic relief or ECG responses to exercise. Thirty eight per cent of patients complained of headaches and 28% had to cease taking the drug for this reason. 3 Oxyfedrine produced statistically significant improvements in both symptom level (P < 0.01) and ECG ST-segment responses to exercise (P < 0.01). The only side effect noted was a reversible loss of taste sensation by one patient. 4 Neither drug produced any adverse changes in any haematological or biochemical parameters. 5 Oxyfedrine is, therefore, to be preferred to isosorbide dinitrate, being both much better tolerated and more efficacious.     

Excretion of norephedrine by man after oral administration of oxyfedrine

Summary After oral administration of oxyfedrine to healthy volunteers, norephedrine was identified in the urine by thin layer chromatography and gas liquid chromatography and mass spectrography. 30 hours after single oral doses of 8, 16 or 24 mg of oxyfedrine, about 4, 8 and 9 mg, respectively, of norephedrine were found in the urine, i.e. on a molar base 75–100% of the dose was excreted as norephedrine. The peak of excretion occurred within 2–4 hours after administration of the drug. No accumulation of oxyfedrine and/or its metabolite was observed after administration of 16 mg of oxyfedrine t.i.d. for three days. It could not be decided whether oxyfedrine was metabolized to norephedrine by liver enzymes, as in rats, or was spontaneously degraded to norephedrine, e.g. in duodenal fluid before absorption. 30–150 min after oral oxyfedrine (24 mg) norephedrine was demonstrable in duodenal fluid. Thus, in addition to the direct-sympathomimetic effects of oxyfedrine, it may also have indirect sympathomimetic effects because of the noradrenaline-releasing properties of its metabolite norephedrine.Presented in part at the 79. Tag.Dtsch.Ges.Inn.Med., Wiesbaden, 1973 (Appelet al., 1973^b). The work was supported by grants from the Deutsche Forschungsgemeinschaft     

Effects of oxyfedrine on isolated portal vein and other smooth muscles

1. Oxyfedrine (0.01-1.0 mug/ml), inhibited spontaneous myogenic activity in rat isolated portal vein and carbachol-induced contractions of rat isolated uterus, and relaxed the rabbit duodenum and the guinea-pig tracheal chain preparation. These actions were prevented by the beta-adrenoceptor blocking drug alprenolol. Oxyfedrine was a relatively weak beta-adrenoceptor stimulant (10-100 times less active than isoprenaline) but its actions were more prolonged.2. In the same concentrations, oxyfedrine reduced or prevented the inhibition of myogenic activity of the rat portal vein induced by isoprenaline and by repeated doses of oxyfedrine itself, acting as a partial agonist at beta-adrenoceptor sites.3. Oxyfedrine, 1-12 mug/ml increased myogenic activity in the rat portal vein. This effect was not due to direct or indirect stimulation of alpha-adrenoceptors (because it was unaffected by phentolamine) or to potentiation of acetylcholine or 5-hydroxytryptamine.4. Oxyfedrine (>20 mug/ml) inhibited spontaneous myogenic activity in the portal vein and relaxed the saphenous vein contracted with noradrenaline. This spasmolytic effect of the drug was not due to beta-adrenoceptor stimulation or to inhibition of phosphodiesterase since it was unaffected by alprenolol and by concentrations of imidazole which antagonized the effects of the active phosphodiesterase inhibitor, papaverine. In the portal vein this effect of oxyfedrine was similar to that of the calcium inhibitor iproveratril; some of the effects of oxyfedrine on venous smooth muscle may be mediated through effects on calcium transport.