放线瑞香宁碱的解热镇痛作用

从青藤科植物黑吹风(Illigera sp)总生物碱中分离出一个单体,经化学鉴定命名为放线瑞香宁碱(actinodapbnine简称Ac)。分子式C_(18)H_(17)NO_4,为10-甲氧基-1,2-(次甲二氧基)-6-去甲阿朴菲-9-醇(图1)。动物实验表明,Ac具有解痉、镇痛、局麻及降低小鼠体温等作用,并证明其镇痛作用系非中枢性。本文进一步研究其镇痛作用和对不同动物正常     

降糖宁胶囊中掺有西药降糖成分的检测

目的检测降糖宁(jiangtangn ing,JTN)胶囊中是否掺有西药降糖成分。方法紫外扫描及HPLC 3D图谱定性,HPLC法定量。结果在降糖宁图谱中发现盐酸苯乙双胍特征图谱。结论降糖宁胶囊中掺有降糖药盐酸苯乙双胍。     

瑞香素对小鼠免疫功能的影响

<正> 瑞香素(Daphnetin,Dap)系瑞香科植物黄瑞香(Daphne giralaii Nitsche)中的有效单体,化学结构为7,8-二羟基香豆素.实验证明Dap有扩张冠状血管,增加冠状血流,改善心肌代谢作用,并有抑制实验性关节炎,兴奋垂体—肾上腺皮质系统,抗血栓形成,抑制血小板聚集和降血脂功能.临床上对冠心病心绞痛,血栓闭塞性脉管炎和风湿及     

瑞香素对血清脂质及脂蛋白胆固醇含量的影响

瑞香素(daphnetin)系瑞香科植物长白瑞香(Daphne koreana Nakai)中的有效单体,化学结构为7,8-二羟基香豆素,并已由长春春城制药厂人工合成。药理实验证明有扩张冠状血管、增加冠脉流量,改善心肌代谢作用,并有抑制实验性“关节炎”及兴奋垂体—肾上     

紫外分光光度法测定盐酸普鲁卡因注射液的含量

目的建立紫外分光度法测定盐酸普鲁卡因注射液含量测定方法.方法采用紫外分光度法测定盐酸普鲁卡因注射液的含量,测定波长为(290±1)nm.结果线性范围为4～12 mg·L-1,盐酸普鲁卡因的平均回收率为99.7%,RSD=0.34%(n=3),r=0.9999(n=5).结论该法简便、快速、准确,可作为盐酸普鲁卡因注射液的含量测定方法.     

雷莫拉宁的研究进展

新型糖肽类抗生素雷莫拉宁(ramoplanin)由游动放线茵(Actinoplanes sp.)发酵液分离获得,其与现有糖肽类抗生素万古霉素和替考拉宁的抑菌机制不同,且对多种耐药致病菌具有很好的抑菌效果,尚未见交叉耐药问题.目前主要开发用于G 菌及其耐药茵引起的皮肤感染及痢疾等胃肠道炎性疾病的治疗.     

基于HPLC多组分定量联合化学计量学及灰色关联度分析的癣宁搽剂质量控制研究

目的 采用高效液相色谱(high performance liquid chromatography, HPLC)法同时检测癣宁搽剂中12个成分含量,并联合化学计量学及灰色关联度分析(grey relational analysis, GRA)对癣宁搽剂质量进行综合评价。方法 以Agilent Extend C₁₈为色谱柱,乙腈-0.1%磷酸(含0.02 mol·L^-1磷酸氢二钠)为流动相,同时测定癣宁搽剂中盐酸黄柏碱、盐酸药根碱、盐酸巴马汀、盐酸小檗碱、白鲜碱、黄柏酮、梣酮、东莨菪碱、莨菪碱、苦参碱、氧化槐果碱和氧化苦参碱含量。采用化学计量学挖掘影响癣宁搽剂产品质量的差异标志物。基于灰色关联度法分析不同批次癣宁搽剂各指标成分数据,以相对关联度为测度,对癣宁搽剂综合质量进行评价。结果 12个成分在各自范围内线性关系良好(r>0.999 0),平均加样回收率(n=9)在96.81%～100.25%之间(RSD<2.0%)。化学计量学分析显示盐酸小檗碱、氧化苦参碱、黄柏酮、盐酸巴马汀和苦参碱是影响癣宁搽剂产品质量的主要潜在标志物。灰色...     

祖师麻基源及化学成分研究概况

目的对中药祖师麻的基源及化学成分进行综述;方法查阅相关文献。结果祖师麻主要来源于瑞香科瑞香属植物黄瑞香(Daphnegiraldii Nitsche)、凹叶瑞香(D.retusa Hemsl)及唐古特瑞香(D.tangutica Maxim)的干燥根皮及茎皮;祖师麻主要含有香豆素类、二萜类、木质素类、黄酮类、蒽醌类等化合物。结论祖师麻药材来源广泛,其中以黄瑞香最为常用;来源不同的祖师麻药材化学成分也有差别。     

系数倍率法测定氯麻滴鼻液中盐酸麻黄碱的含量

<正>氯麻滴鼻液系《中国医院制剂规范》西药制剂(第二版)收载品种,含0.25%氯霉素和1%盐酸麻黄碱,溶液由甘油和蒸馏水组成。其质量控制采用紫外分光光度法中吸收系数法测定氯霉素的含量,中和法测定盐酸麻黄碱的含量[1]。在用氢氧化钠测定盐酸麻黄碱的含量时,操作繁琐,且结果易受空     

宁嗽露中盐酸麻黄碱的含量测定

目的建立高效液相色谱法测定宁嗽露中盐酸麻黄碱的含量。方法采用反相高效液相色谱法,C18色谱柱,流动相为醋酸铵缓冲液-甲醇-乙腈(94:1:5),检测波长为257 nm,流速为1.0 mL.min-1,柱温40℃。结果盐酸麻黄碱浓度在0.058~0.58 mg.mL-1范围内浓度与峰面积呈良好的线性关系(r=0.999 2),该制剂中盐酸麻黄碱的平均回收率为99.12%,RSD为0.92%(n=5)。结论该方法简便、准确、可靠,可用于宁嗽露中盐酸麻黄碱的含量测定。     

The disposition of primaquine in the isolated perfused rat liver. Stereoselective formation of the carboxylic acid metabolite

The disposition of (+) and (-) primaquine (PQ) was studied in the isolated perfused rat liver (IPRL) preparation following a bolus dose (2.0 mg diphosphate salt; N = 6) of each enantiomer. Perfusate plasma concentrations of PQ and the carboxylic acid metabolite (PQm) were determined using previously reported methods. To enable the simultaneous measurement of PQ and PQm in bile a selective and reproducible HPLC assay was developed. Clearance of (-)PQ (8.8 +/- 2.9 ml min-1) was significantly greater than that of (+)PQ (5.5 +/- 1.5 ml min-1) and the apparent volumes of distribution of (-)PQ (606 +/- 182 ml) and (+)PQ (930 +/- 171 ml) were significantly different. Stereoselectivity in the hepatic elimination efficiency was manifest as a significant reduction in half-life (-)PQ 54 +/- 29 min; (+)PQ 123 +/- 33 min) and smaller area under the curve to infinity (-)PQ 254 +/- 96 micrograms ml-1.min, (+)PQ 387 +/- 108 micrograms ml-1.min) for (-)PQ when compared with (+)PQ. A significantly greater peak concentration of PQm was achieved following administration of (-)PQ (0.61 +/- 0.26 micrograms ml-1.min) than (+)PQ (0.19 +/- 0.09 micrograms ml-1). There was no difference between the sum of the areas under the curve to 4 hr for (+) and (-)PQ and the corresponding carboxylic acid metabolite (322 +/- 64 micrograms ml-1 and 317 +/- 75 micrograms ml min-1 respectively). There was no difference in the biliary clearance of (+) and (-)PQ (0.08 +/- 0.02 ml min-1 and 0.14 +/- 0.10 ml min-1 respectively) or the corresponding carboxylic acid metabolites (0.24 +/- 0.13 ml min-1 and 0.29 +/- 0.09 ml min-1). These results strongly suggest stereoselective formation of the carboxylic acid metabolite of primaquine. The significant increase in the volume of distribution of (+)PQ suggests the enantiomer has either an increased affinity for binding sites within the liver and/or erythrocytes or a decreased affinity for circulating perfusate albumin.     

Pharmacokinetics of quinidine and three of its metabolites in man

Disposition parameters of quinidine and three of its metabolism, 3-hydroxy quinidine, quinidine N-oxide, and quinidine 10,11-dihydrodiol, were determined in five normal healthy volunteers after prolonged intravenous infusion and multiple oral doses. The plasma concentrations of individual metabolites after 7 hr of constant quinidine infusion at a plasma quinidine level of 2.9 +/- (SD) 0.3 mg/L were: 3-hydroxy quinidine, 0.32 +/- 0.06 mg/L; quinidine N-oxide, 0.28 +/- 0.03 mg/L; and quinidine 10,11-dihydrodiol, 0.13 +/- 0.04 mg/L. Plasma trough levels after 12 oral doses of quinidine sulfate every 4 hr averaged: quinidine, 2.89 +/- 0.50 mg/L; 3-hydroxy quinidine, 0.83 +/- 0.36 mg/L; quinidine N-oxide, 0.40 +/- 0.13 mg/L; and quinidine 10,11-dihydrodiol, 0.38 +/- 0.08 mg/L. Relatively higher plasma concentrations of 3-hydroxy quinidine metabolite after oral dosing probably reflect first-pass formation of this quinidine metabolite. A two-compartment model for quinidine and a one-compartment model for each of the metabolites described the plasma concentration-time curves for both i.v. infusion and multiple oral doses. Mean (+/- SD) disposition parameters for quinidine from individual fits, after i.v. infusion were as follows: Vl, 0.37 +/- 0.09 L/kg; lambda 1, 0.094 +/- 0.009 min-1; lambda 2, 0.0015 +/- 0.0002 min-1; EX2, 0.013 +/- 0.002 min-1; clearance (ClQ), 3.86 +/- 0.83 ml/min/kg. Both plasma and urinary data were used to determine metabolic disposition parameters. Mean (+/- SD) values for the metabolites after i.v. quinidine infusion were as follows: 3-hydroxy quinidine: formation rate constant kmf, 0.0012 +/- 0.0005 min-1, volume of distribution, Vm, 0.99 +/- 0.47 L/kg; and elimination rate constant, kmu 0.0030 +/- 0.0002 min-1. Quinidine N-oxide: kmf, 0.00012 +/- 0.00003 min-1; Vm, 0.068 +/- 0.020 L/kg; and kmu, 0.0063 +/- 0.0008 min-1. Quinidine 10,11-dihydrodiol: kmf, 0.0003 +/- 0.0001 min-1; Vm, 0.43 +/- 0.29 L/kg; and kmu, 0.0059 +/- 0.0010 min-1. Oral absorption of quinidine was described by a zero order process with a bioavailability of 0.78. Concentration dependent renal elimination of 3-hydroxy quinidine was observed in two out of five subjects studied.     

High clearance of (S)-warfarin in a warfarin-resistant subject.

A 30 year old black male required a 60 mg daily dose of warfarin to elicit a therapeutic anticoagulant response (normal warfarin dose 2.5-10 mg day-1; maximum 15 mg day-1). Hereditary warfarin resistance was suspected after compliance, diet, concurrent medication and any gastrointestinal disorder were eliminated as contributory causes. The disposition of vitamin K and vitamin K epoxide was examined in the propositus, his two sisters and 13 control black male subjects. Each subject was given an i.v. bolus dose (5 mg) of vitamin K prior to and after 2 weeks of warfarin therapy (5 mg day-1). The oral clearances of (S)- and (R)-warfarin were also measured in each subject during the last day of warfarin therapy. The mean (+/- s.d.) systemic clearance of vitamin K was similar in all subjects before (114 +/- 35 ml min-1) and after (112 +/- 40 ml min-1) warfarin therapy. The mean (+/- s.d.) AUC value for vitamin K epoxide was increased by warfarin treatment (6.5 +/- 5.4 micrograms ml-1 min before and 139 +/- 78 micrograms ml-1 min after) in all subjects. In the propositus, the oral clearance of (S)-warfarin (14.5 ml min-1) and the clearance ratio for (S)/(R)warfarin (2.6) differed by more than 7 standard deviations from the control group (4.3 +/- 1.1 ml min-1 and 1.2 +/- 0.2, respectively). In one sister of the propositus, the stereoselective disposition of warfarin was comparable with that of her brother ((S)-warfarin clearance = 16.2 ml min-1; and (S)/(R)-warfarin clearance ratio = 2.7).     

The pharmacokinetics and pharmacodynamics of ketamine in dogs anesthetized with enflurane

The plasma concentration vs. anesthetic effect relationships for ketamine are not well known. It is desirable to establish stable and predictable drug concentrations in plasma (and brain) in order to define such relationships. As a prelude to pharmacodynamic studies, we investigated ketamine pharmacokinetics in eight dogs anesthetized with enflurane and correlated ketamine concentration in plasma (KET) with its ability to reduce the enflurane concentration required for anesthesia (enflurane EC50: MAC--the end-tidal concentration at which half the dogs moved in response to clamping of the tail and half did not move). Four dogs (Group 1) received ketamine 10 mg/kg iv over 30 sec. Blood for determination of KET was collected repeatedly over the 5-h period following injection. Based on the pharmacokinetic parameters determined for Group 1, four dogs in Group 2 received ketamine as a continuous infusion of 300 micrograms.kg-1.min-1 for 5 hr accompanied by an initial loading dose (26 mg/kg administered over 20 min) designed to produce a stable KET of 20 micrograms/ml of plasma. Enflurane MAC and KET were determined regularly during the infusion and for 5 hr after discontinuation of the infusion. There were no significant differences in the following pharmacokinetic parameters determined for Group 1 vs. Group 2: t1/2 beta = 122 +/- 9 vs. 141 +/- 40 min (mean +/- SD) and CL = 18.1 +/- 5.9 vs. 13.9 +/- 2.5 ml.kg-1.min-1, respectively. When administered as a continuous infusion (Group 2), KET remained relatively stable at 22.1 +/- 4.6 micrograms/ml for 5 hr. The degree of MAC reduction remained relatively stable at 73% during the continuous infusion. Finally, the enflurane MAC reduction vs. KET was established over a wide range of plasma concentrations in 4 additional dogs (Group 3). This study determined that the pharmacokinetics of ketamine were consistent under two different experimental conditions and demonstrated the relationship between plasma concentration and anesthetic effect in the dog.     

Plasma histamine and clinical tolerance to infused histamine in normal, atopic and urticarial subjects

Five subjects with a recent history of urticaria (U), five atopic (A) subjects and a non-atopic (NA) control group were given intravenous infusions of histamine starting at 0.05 micrograms/kg/min, increasing by 0.05 micrograms/kg/min every 30 minutes to a maximum of 0.35 micrograms/kg/min. Plasma histamine levels were monitored every 15 minutes. The infusion was stopped when an objective clinical endpoint was reached, involving either evidence of peripheral vasodilatation (rise of skin temperature by at least 1 degree C) or a 20% fall of peak expiratory flow rate. There were no significant differences in resting plasma histamine in the three groups. Those with urticaria reached the clinical endpoint at a lower infusion rate than non-atopic subjects (U 0.22 +/- 0.02 micrograms/kg/min; A 0.26 +/- 0.02 micrograms/kg/min; NA 0.32 +/- 0.2 micrograms/kg/min. p less than 0.008) they also received a lower total histamine dose (U 1.12 +/- 0.33 mg; A 1.42 +/- 0.38 mg, NA 2.2 +/- 0.51 mg, p less than 0.008). Atopic subjects with a history of asthma, eczema or rhinitis also tolerated histamine poorly, some subjects reaching a clinical endpoint while the plasma histamine level was still relatively low (U 1.52 +/- 0.4 ng/ml, A 0.85 +/- 0.19 ng/ml, NA 1.4 +/- 0.44 ng/ml, p = 0.05). After the histamine infusion was stopped, the fall in the blood level of histamine was slower in urticarial subjects than in the other two groups, with a half-life of 6.2 +/- 1.3 min (A 3.0 +/- 1.2 min, NA 4.0 +/- 0.7 min, p less than 0.02). There were thus differences in the metabolism of histamine in our non-atopic urticarial subjects and increased histamine sensitivity in atopic subjects which require further study.     

Diltiazem pharmacokinetics in the rat and relationship between its serum concentration and uterine and cardiovascular effects.

1 The kinetics of diltiazem were investigated in ovariectomized (ovx) non-pregnant and intact late pregnant anaesthetized rats following a bolus i.v. injection (2 mg kg-1) and during a 180 min i.v. infusion (50 micrograms kg-1 min-1 and 100 micrograms kg-1 min-1). Uterine contractions, mean blood pressure and heart rate were measured in the non-pregnant rats. 2 Measurement of serum diltiazem concentrations after bolus i.v. injection in ovx non-pregnant rats showed a biexponential decay with time from which the following parameters were calculated: volume of distribution area (V(area)) - 256 +/- 46 ml; rate constants k12 - 0.46 +/- 0.10 min-1; k21 - 0.09 +/- 0.01 min-1; kel - 0.13 +/- 0.03 min-1; elimination clearance - 3.2 +/- 0.3 ml min-1; distribution t1/2 (t1/2) - 1.4 +/- 0.3 min; elimination t1/2 (t1/2 beta) - 61.2 +/- 13.0 min. In pregnant rats, a biexponential decay was also observed with similar parameters to those in non-pregnant animals except for markedly increased V(area) - 1004 +/- 184 ml; kel - 0.54 +/- 0.16 min-1 and elimination clearance - 14.8 +/- 2.3 ml min-1. 3 Measurement of serum diltiazem concentrations during infusion yielded the following parameters in non-pregnant ovx rats: V(ss)--79 +/- 10 ml; rate constants k12 - 1.02 +/- 0.21 min-1; k21 - 0.03 +/- 0.01 min-1; kel - 0.39 +/- 0.06 min-1; elimination clearance - 7.8 +/- 1.2 ml min-1. In pregnant rats a marked increase was observed in kel - 1.25 +/- 0.38 min-1 and elimination clearance - 36.4 +/- 13.8 ml min-1. 4 An immediate reduction in uterine contractions, mean blood pressure and heart rate was observed after bolus i.v. injection of diltiazem with a return towards control values as serum diltiazem concentrations declined. There were significant correlations between the inhibition of the 3 parameters and the log serum concentrations of diltiazem. Serum concentration-response curves indicated IC50 values of 0.5 microgram ml-1 for inhibition of uterine contractions, 0.7 microgram ml-1 for reduction in blood pressure and 1.2 micrograms ml-1 for reduction in heart rate. There were maintained reductions in the integral of uterine contractions, mean blood pressure and heart rate during infusion. 5 The metabolite desacetyldiltiazem was rarely detected after i.v. bolus injection and was not found in 5/13 rats infused with diltiazem, yet significant inhibition of uterine contractions was observed in all rats. Diltiazem was 3.2 fold more potent than desacetyldiltiazem as an inhibitor of contractions of the rat isolated uterus.(ABSTRACT TRUNCATED AT 400 WORDS)     

Preliminary pharmacokinetic studies of Ukrain in rats

Ukrain (thiophosphoric acid derivative of Chelidonium majus L. alkaloids) was administered to rats i.p. at a dose of 28 mg/kg (equivalent to 0.1 LD50). A high performance liquid chromatography (HPLC) method for rapid determination of Ukrain in plasma has been described. It was found that Ukrain rapidly penetrated into the plasma of the rats and the elimination of the drug from the plasma was slower. The results obtained were as follows: absorption rate constant ka = 0.0432 [min-1]; elimination rate constant K = 0.0113 [min-1]; drug half-life t1/2 = 61.32 min; actual concentration of Ukrain in the plasma C = 33 e-0.0113t - 39 e-0.0432t [microgram/ml]; and delay in drug absorption T0 = 5.23 min.     

Pharmacokinetics of triflusal and its main metabolite in rats and dogs.

The methods for determining plasma concentrations of triflusal (2-acetoxy-4-trifluoromethyl benzoic acid) that have been described, do not distinguish between the drug and its main metabolite HTB (2-hydroxy-4-trifluoromethyl benzoic acid). In the present study, we have developed a new analytical technique based on HPLC that enabled us to carry out a pharmacokinetic study of the drug and its metabolite in animals. An intravenous or oral dose of 50 mg/kg was administered to male Sprague-Dawley rats, and 15 mg/kg was administered to beagle dogs. Plasma levels of triflusal and HTB were determined. In rats, triflusal was quickly eliminated from plasma with a biological half-life (t1/2) of 2.7 min and a clearance (Cl) of 73.4 (ml/kg)/min. The elimination of HTB was much slower with a t1/2 of 21.5 h and a Cl of 5.1 (mg/kg)/h. The maximum concentration (Cmax) of triflusal in rats after an oral administration was 8.1 +/- 2.0 micrograms/ml reached between 2.5 and 10 min. The Cmax of HTB was 237.7 micrograms/ml and was achieved at 0.7 h. The bioavailability of triflusal in rats was only 10.6% while the bioavailability of HTB was more than 100% indicating an important first pass effect. In dogs the t1/2 of triflusal was 14.4 +/- 5.9 min and the Cl was 25.1 +/- 4.7 (ml/kg)/min. HTB was also eliminated very slowly with a t1/2 of 71.1 +/- 12.5 h and a Cl of 2.4 +/- 0.3 (ml/kg)/h. The Cmax of triflusal in dogs was 13.3 +/- 2.9 micrograms/ml and was reached after 19.2 +/- 6.1 min (tmax).(ABSTRACT TRUNCATED AT 250 WORDS)     

Pharmacokinetics and thrombolytic properties of a nonglycosylated mutant of human tissue-type plasminogen activator, lacking the finger and growth factor domains, in dogs with copper coil-induced coronary artery thrombosis

The pharmacokinetics and thrombolytic properties of a variant of human tissue-type plasminogen activator (t-PA), obtained by deletion mutagenesis of the NH2-terminal fibronectin-like finger (F) and epidermal growth factor (E) domains, and substitution of the three known glycosylated Asn residues by Gln (t-PA-delta FE3X), were studied in dogs with a copper coil-induced thrombosis of the left anterior descending coronary artery. Bolus injections were given during 2 min to groups of three dogs. Injection of 0.15 mg/kg resulted in peak antigen levels in plasma of 1.58 +/- 0.72 micrograms/ml (mean +/- SEM) and caused reperfusion within 14 +/- 6 min. With 0.075 mg/kg, corresponding values of 0.81 +/- 0.20 micrograms/ml and 31 +/- 15 min were obtained. A bolus of 0.038 mg/kg yielded plasma peak levels of 0.43 +/- 0.20 micrograms/ml but did not cause coronary recanalization within 3 h. A bolus injection of natural t-PA (Mel-t-PA) at a dose of 0.1 mg/kg in four dogs resulted in plasma peak levels of 0.46 +/- 0.09 micrograms/ml and caused partial coronary artery reperfusion within 3 h in one of four dogs (after 31 min). None of these injections caused a significant decrease of the fibrinogen level. Pharmacokinetic parameters for t-PA-delta FE3X were alpha half-life (t1/2) 14-18 min, beta t1/2 72-125 min, and plasma clearance 21-36 ml/min. For Mel-t-PA, the corresponding values were 3 min, 8 min, and 520 ml/min. We conclude that the variant t-PA-delta FE3X has a markedly longer plasma t1/2 than does Mel-t-PA and, when administered as a bolus injection, a higher thrombolytic efficacy.     

Indecainide: effects on arrhythmias, electrophysiology, and cardiovascular dynamics

The cardiovascular pharmacology of indecainide, a new class I antiarrhythmic agent, was studied in intact animals. Arrhythmias produced by ouabain were converted to sinus rhythm by indecainide (100 micrograms/kg/min, i.v.) at 0.7 +/- 0.1 mg/kg and a corresponding plasma concentration of 1.7 +/- 0.2 micrograms/ml at the time of conversion. Infusion at a slower rate (20 micrograms/kg/min) converted to sinus rhythm at 0.4 +/- 0.1 mg/kg and 0.4 +/- 0.2 micrograms/ml plasma. Arrhythmias produced by prior (24 h) coronary artery occlusion were converted to 50% sinus rhythm by indecainide (100 micrograms/kg/min, i.v.) at 1.3 mg/kg. In conscious dogs, 6 mg/kg indecainide p.o. prolonged the PR and QRS intervals by 31 +/- 5 and 13 +/- 3%, respectively, at a corresponding plasma concentration of 2.8 +/- 0.5 micrograms/ml. His bundle studies revealed that the PR interval prolongation was due to an increase in both A-H and H-V intervals. In anesthetized dogs, indecainide (1-5 mg/kg, i.v.) decreased cardiac contractility, however, this effect was comparable to or less than that produced by other class I agents and was likely due to the Na+-channel-blocking activity of the drug. The autonomic effects of indecainide were slight and no effects were produced on peripheral hemodynamics, the QTc interval, or the central nervous system. It was concluded that indecainide is a potent class I antiarrhythmic agent that would appear to have only minimal propensity for producing adverse side effects in humans.