奥昔麻黄碱治疗冠心病

本文报道25例冠心病心绞痛患者应用奥昔麻黄碱的近期疗效。wk1给安慰剂,wk2一3口服奥昔麻黄碱8mg,tid,wk4-5给安慰剂。结果,症状疗效总有效率88％,安慰剂组36％(P<0.O1),心电图总有效率80％。说明本药有一定的抗心绞痛作用,且副作用小、安全、有效,值得推广应用。     

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。     

单硝酸异山梨酯缓释片与缓释胶囊治疗冠心病心绞痛的比较

目的 :比较单硝酸异山梨酯的缓释片与缓释胶囊治疗冠心病心绞痛的疗效。方法 :冠心病心绞痛病人 58例 ,随机分为缓释片组 30例 ,给缓释片60mg ,po ,qd ,共 4wk ;缓释胶囊组 2 8例 ,给缓释胶囊 50mg ,po ,qd ,共 4wk。结果 :缓释片组心绞痛有效率及心电图改善率分别为 93%和 57% ;缓释胶囊组依次为 93%和 61% ,组间比较差别无显著意义 (P >0 .0 5)。 2药不良反应均轻微。结论 :2种单硝酸异山梨酯缓释剂型治疗冠心病心绞痛疗效相近     

灯盏细辛注射液治疗冠心病心绞痛31例

本文报道应用灯盏细辛注射液治疗冠心病心绞痛31例(男性18例,女性13例;年龄60±11yr)的疗效。结果:灯盏细辛注射液(80mg/d)静脉滴注2wk后,临床疗效为87％,心电图疗效为71％。另外,对15例冠心病心绞痛患者采用复方丹参16mL加入葡萄糖液500mL静脉滴注,qd,2wk后,临床疗效80％,心电图疗效40％;2组比较,疗效相似。     

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。     

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)。     

安非他酮缓释片戒除尼古丁依赖的多中心随机双盲对照试验

目的:评价国产安非他酮缓释片戒除尼古丁依赖的有效性及安全性。方法:多中心、随机、双盲、安慰剂平行对照研究。共入组自愿戒烟者143例,安非他酮组72例与安慰剂组71例。受试者分别口服安非他酮缓释片150～300 mg·d-1或安慰剂,疗程4 wk,观察12 wk。结果:治疗后4,12 wk安非他酮组戒烟率分别为39％,31％,高于安慰剂组(13％,9％),差异有非常显著意义(P<0．01);治疗后1 wk起安非他酮组吸烟量的减少值均大于安慰剂组,差异有非常显著意义(P<0．01)。安非他酮常见不良反应为注意力不集中、乏力、腹部不适等,其发生率高于安慰剂组,差异有显著意义(P<0．05),2组均未发生严重不良反应。结论:国产安非他酮缓释片是一种安全、有一定疗效的戒除尼古丁依赖(烟瘾)的药物。     

麝香保心丸治疗冠心病心绞痛临床体会

目的：探讨在常规西药治疗冠心病心绞痛基础上加用麝香保心丸的临床疗效。方法：72例冠心病心绞痛患者,在常规抗心绞痛治疗基础上加用麝香保心丸治疗,3次／d,每次2粒。选择同期冠心病心绞痛69例患者作为对照组,接受常规西药抗心绞痛治疗。两组疗程均为8wk。结果：治疗组心绞痛症状和心电图改善的总有效率分别为86．1％和77．8％,均明显高于对照组（82．6％和72．5％,P值均〈0．05）。治疗组在减少心绞痛发作次数、硝酸甘油消耗量以及改善心肌缺血方面均优于对照组（P〈0．05）。结论：麝香保心丸治疗冠心病心绞痛安全、有效、副作用较轻,值得推广应用。     

舒心饮治疗冠心病心绞痛的随机双盲多中心临床研究

目的:评价中药舒心饮治疗冠心病心绞痛的临床疗效及安全性。方法:采用随机双盲多中心的方法,将133例冠心病心绞痛患者分为治疗组与对照组,分别给予舒心饮、生脉饮治疗4wk,观察患者心绞痛发作情况、中医证候、心电图等指标。结果:治疗组心绞痛的总有效率为90.91%,明显优于对照组的74.63%(P<0.01);治疗后2组患者胸闷、心悸、气短等证候均获得改善,治疗组对胸闷的改善尤为明显(P<0.05);2组患者心电图ST-T的变化均改善;2组间不良反应发生率无显著性差异(P>0.05)。结论:舒心饮治疗冠心病心绞痛安全、有效。     

氨氯地平治疗心绞痛55例

冠心病心绞痛55例(男性39例,女性16例;年龄58±7a)采用单项药物氨氯地平5mg, po, qd共治疗4wk。结果:心绞痛症状总缓解率为91％(心绞痛次数与治疗前比较明显减少P<0.05),心电图改善为51％;22例伴高血压者降压疗效为86％;并有增加运动耐量、降低血小板聚集的作用;对心率无明显影响;高密度脂蛋白胆固醇比治疗前明显增加(P<0.05);不良反应轻微。可作为治疗冠心病或高血压的有效药物。     

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).     

Effects of oxyfedrine and ouabain on the heart-lung preparation of the dog

Summary The actions of l-3-methoxy--(1-hydroxy-1-phenylisopropylamino) propiophenone hydrochloride (oxyfedrine) and ouabain in the canine heart-lung preparation (HLP) were studied taking particular notice of the changes of competence index and cardiac output. Both of these drugs caused potent cardiotonic effects in pentobarbital-induced heart failure but only slight effect on the normal heart. 280 g of oxyfedrine corresponded with 64 g of ouabain in this respect. Increasing doses of ouabain resulted in ventricular extrasystoles and fibrillation at 76 and 125 g respectively on the average, but no arrhythmia was observed even with 5 mg of oxyfedrine. Cardiotonic effect of oxyfedrine was prevented by pretreatment of the heart with propranolol but was intact in reserpinized HLP.     

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.     

Positive and negative chronotropic response of the S-A node to oxyfedrine.

Direct perfusion of the sinus node artery under a constant pressure of 100 mmHg was carried out in vagotomized dogs. "Selective" injection of L-3-methoxy-omega-(1-hydroxy-1-phenylisopropylamino) propiophenone hydrochloride (oxyfedrine) into the sinus node artery induced three types of chronotropic response; a pronounced sinus tachycardia, an initial bradycardia followed by sustained tachycarcia, or a definite sinus bradcardia alone. The paradoxical sinus bradycardia induced by oxyfedrine was more pronounced at higher doses of the compound, whereas it was nver produced by the injection of isoproterenol. The oxyfedrine-induced sinus tachycardia, which occurred even in reserpinized preparations, was not suppressed by the treatment with tetrodotoxin, hexamethonium or bretylium, but it was selectively inhibited by propranolol. Atropine, tetrodotoxin or hexamethonium did not prevent the occurrence of sinus bradycardia induced by oxyfedrine, and physostigmine failed to enhance the response. The present study indicates that the oxyfedrine-induced tachycardia is mediated mainly by a direct stimulating action on adrenergic beta-receptors, while the bradycardia appears to be induced by a direct depressant action on the S-A node.     

Stability of oxyfedrine in pharmacological experiments in vitro]

15% of L-3-(beta-hydroxy-alpha-methyl-phenethyl-amino)-3'-methoxy-propiophenone-hydrochloride (oxyfedrine [OF]; ildamen?) are degradated in Krebs-Henseleit solution under conditions which are necessary for recording a complete concentration-effect curve on guinea-pig papillary muscle (total time max. 100 min). Norephedrine and 3-methoxyacrylophenone are qualitatively analysed as products of degradation by thin-layer chromatography (TLC). Secondary reaction products of the primary degradation are not detectable under these conditions. The quantitative analysis of oxyfedrine, norephedrine and 3-methoxyacrylophenone was carried out by spectrophotometry. Comparatively oxyfedrine and norephedrine were analysed by direct quantitative TLC (measuring of reflectance). The same results were obtained, in principle, by both methods. The importance of this relatively slow degradation for pharmacological in vitro experiments on the mode of action of oxyfedrine is pointed out.     

Pharmacologic effects in combined use of oxyfedrine and beta-acetyldiogoxin]

In guinea pigs the toxic effect of beta-acetyldigoxin was not increased by simultaneously administered 3-(beta-hydroxy-alpha-methyl-phenethyl-amino)-3'-methoxy-propiophenone (oxy-fedrine). There was no evidence of a potentiation of the glycoside effect by the combination with oxyfedrine (ildamen-Novodigal). The threshold dose for arrhythmia was increased: typical glycoside tachyarrhythmias only occurred after higher infused doses. In anesthetized dogs with heart failure by overdosed pentobarbital, the therapeutic effects of beta-acetyldigoxin were sustained and enhanced by oxyfedrine.     

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.     

The importance of increased prostaglandins and prostacyclin for the effect of oxyfedrin in isolated guinea pig heart preparations

In isolated perfused heart preparations of guinea pigs coronary dilating and positive inotropic doses of oxyfedrine induce a significant increase of the release of prostaglandin-like substances (PLS) and prostacyclin (PGI2). Indometacin as an inhibitor of prostaglandin biosynthesis (140 mumol/l) enhances after a 10 min lasting perfusion contraction force and coronary flow of the hearts but inhibits PGI2-formation. Under these conditions oxyfedrine loses its positive influence on inotropism, coronary flow and PGI2-efflux. Indometacin (140 mumol/l) also completely abolishes the increase of cardiac performance of isolated auricle preparations by oxyfedrine (50 mumol/l). These findings agree with former results and indicate an involvement of the PLS- and PGI2-biosynthesis in the antianginal efficacy of oxyfedrine.     

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.