• Title/Summary/Keyword: anti-arrhythmic agent

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Method Development of Verapamil in Presence of NSAIDs using RP-HPLC Technique

  • Sultana, Najma;Arayne, M. Saeed;Waheed, Abdul
    • Bulletin of the Korean Chemical Society
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    • v.32 no.7
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    • pp.2274-2278
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    • 2011
  • Verapamil is a calcium channel blocker and is classified as a class IV anti-arrhythmic agent. It is used in the control of supra ventricular tachyarrhythmias, and in the management of classical and variant angina pectoris. It is also used in the treatment of hypertension and used as an important therapeutic agent for angina pectoris, ischemic heart disease, hypertension and hypertrophic cardiomyopathy. Verapamil commonly co-administered with NSAIDs (non-steroidal anti-inflammatory drugs) i.e. diclofenac sodium, flurbiprofen, Ibuprofen, mefanamic acid and meloxicam. A simple and rapid RP-HPLC method for simultaneous determination and quantification of verapamil and NSAIDs was developed and validated. The mobile phase constituted of acetonitrile: water (55:45) whose pH was adjusted at 2.7 and pumped at a flow rate of 2.0 mL $min^{-1}$ at 230 nm. The proposed method is simple, precise, accurate, low cost and least time consuming for the simultaneous determination of verapamil and NSAIDs which can be effectively applied for the analysis of human serum.

Encainide, a class Ic anti-arrhythmic agent, blocks voltage-dependent potassium channels in coronary artery smooth muscle cells

  • Hongliang Li;Yue Zhou;Yongqi Yang;Yiwen Zha;Bingqian Ye;Seo-Yeong Mun;Wenwen Zhuang;Jingyan Liang;Won Sun Park
    • The Korean Journal of Physiology and Pharmacology
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    • v.27 no.4
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    • pp.399-406
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    • 2023
  • Voltage-dependent K+ (Kv) channels are widely expressed on vascular smooth muscle cells and regulate vascular tone. Here, we explored the inhibitory effect of encainide, a class Ic anti-arrhythmic agent, on Kv channels of vascular smooth muscle from rabbit coronary arteries. Encainide inhibited Kv channels in a concentration-dependent manner with an IC50 value of 8.91 ± 1.75 μM and Hill coefficient of 0.72 ± 0.06. The application of encainide shifted the activation curve toward a more positive potential without modifying the inactivation curve, suggesting that encainide inhibited Kv channels by altering the gating property of channel activation. The inhibition by encainide was not significantly affected by train pulses (1 and 2 Hz), indicating that the inhibition is not use (state)-dependent. The inhibitory effect of encainide was reduced by pretreatment with the Kv1.5 subtype inhibitor. However, pretreatment with the Kv2.1 subtype inhibitor did not alter the inhibitory effects of encainide on Kv currents. Based on these results, encainide inhibits vascular Kv channels in a concentration-dependent and use (state)-independent manner by altering the voltage sensor of the channels. Furthermore, Kv1.5 is the main Kv subtype involved in the effect of encainide.

A Case of Severe Aconitine Intoxication with Ventricular Tachycardia, Successfully Treated by a Combination of Two Anti-arrhythmic Drugs (두 가지 항부정맥 약제를 병용 투여하여 성공적으로 치료한 심실빈맥이 동반된 부자중독 1례 보고)

  • Ryoo, Seung-Mok;Sohn, Chang-Hwan;Oh, Bum-Jin;Kim, Won;Lim, Kyoung-Soo
    • Journal of The Korean Society of Clinical Toxicology
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    • v.9 no.2
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    • pp.105-108
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    • 2011
  • Aconitine is an anti-inflammatory agent with therapeutic uses in oriental medicine as an analgesic and for treatment of stroke. Because of its sodium channel effect, aconitine can promote undesirable, wide complex tachyarrhythmia. If tachycardia develops during use of aconitine, class Ia and class III anti arrhythmic drugs can be utilized for treatment. However there are no single anti-arrhythmia agents which are uniformly effective. We report a case, characterized by wide complex tachyarrhythmia and severe hypotension, which was successfully treated by simultaneous injections of amiodarone and lidocaine. A 59-year-old woman exhibiting clinical signs of drowsiness as a result of ingesting 6 g of aconitine, was admitted to the emergency department. Initially, wide complex tachyarrhythmia (ventricular tachycardia and pulse rate of 180 beats/min) and severe hypotension (blood pressure of 53/26 mmHg) was observed. After simultaneous injection of amiodarone and lidocaine, the patient's rhythm pattern changed to an accelerated junctional rhythm with ventricular premature complex. Two hours later, the patient's heart pattern became a sinus rhythm. As demonstrated by this case, simultaneous injections of amiodarone and lidocaine can be useful in treating ventricular arrhythmia induced by aconitine.

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Atrial Flutter with Poor Ventricular Response in a Bull Terrier Dog (불테리어종 개에서 발생한 미약한 심실반응이 있는 심방조동)

  • Lee, Joon-Seok;Han, Suk-Hee;Hyun, Chang-Baig
    • Journal of Veterinary Clinics
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    • v.27 no.4
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    • pp.435-439
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    • 2010
  • A six-year-old intact female Bull Terrier dog (weighing 17 kg) was referred to the Veterinary Teaching Hospital with exercise intolerance and occasional syncope as the primary complaint. Diagnostic studies revealed a rare case of atrial flutter with complete heart block and aberrant ventricular activation from the ectopic focus, possibly due to idiopathic dilated cardiomyopathy. Although the dog was responded with cardiac medication for right-sided heart failure and anti-arrhythmic agent (dofetilide), the dog died suddenly of cardiac arrest after 11 months of treatment.

The Effect of Lidocaine and Procainamide on the Hepatic Aldehyde Oxidase Activity (알데히드 옥시다제의 활성에 미치는 리도카인 및 프로카인아미드의 영향)

  • Huh, Keun;Kim, Jin-Sook;Jin, Da-Qing;Ha, Eun-Pil;Lee, Sang-Il;Yong, Chul-Soon
    • YAKHAK HOEJI
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    • v.43 no.6
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    • pp.756-761
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    • 1999
  • Lipid peroxidation mediated by hydroxyl radicals which are generated during myocardial ischermia has suggested as a possible mechanism of ischemic myocardial damage. Recently, it has been reported that anti-arrhythmic action of lidocaine, a local anesthetic, is attributed to its "membrane-stabilizing" properties through scavenging free radicals, thus, inhibiting lipid peroxidation. Aldehyde oxidase and xanthine oxidase which catalyze the oxidation of many purine, pyrimidine and pteridine derivatives are known as free radical generating systems. In this experiment, we studied the effect of lidocaine and procainamide on the hepatic aldehyde and xanthine oxidase activity and antioxidative activities. It was found that lidocaine and procainamide inhibited both NADPH-dependent and independent lipid peroxidation. Both of tested compounds were found to be ineffective in inhibiting xanthine oxidase. Lidocaine and procainamide, however, inhibited aldehyde oxidase activity in vitro as well as in vivo. Based on the above results, lidocaine and procainamide could be employed as a therapeutic agent for aldehyde oxidaserelated disease.d disease.

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