胺碘酮加小剂量地高辛转复房颤32例报告

目的　观察可达龙 (胺碘酮 )加小剂量地高辛对部分经冠脉造影确诊的高血压性心脏病 (高心病 )与冠心病患者心房颤动 (房颤 )转复窦性心律的可能与安全性。方法　符合入选条件、住院连服 2周可达龙 (0 .2g,3/d)未复律的高心病、冠心病并房颤患者 32例 ,加服地高辛 0 .1 2 5g ,2 /d ,2周后为观察终点 ,判断其房颤转复成功率与用药安全性 ;并随访半年 ,观察房颤复发率。结果　 32例中转复窦性心律 2 3例 ,转复率 71 .9% ,平均转复时间 (7± 2 )d ,无一例出现药物副作用 ;随访半年 ,复发 6例 ,复发率占复律者的 2 6 .1 %。结论　可达龙加小剂量地高辛对高心病、冠心病患者的房颤转复窦性心律 ,具有疗效较高 ,安全性与依从性好等优点 ,但仍有一定的复发率。     

Amiodarone-induced experimental acute neuropathy in rats.

Amiodarone was injected endoneurially at increasing doses into the exposed tibial nerve of rats to study its electrophysiologic and pathologic effects on peripheral nerve fibers. Forty-five male Wistar rats were used, and each of the following concentrations was injected into 15 nerves: 25 micrograms/mL, 50 micrograms/mL, and 100 micrograms/mL. Microinjection of a 25 micrograms/mL concentration of amiodarone resulted in a subacute, incomplete conduction block evident at day 3 postinjection. This conduction block remained stable until day 10 and recovery was complete at day 35. Microinjection of a 50 micrograms/mL concentration of amiodarone produced a faster evolving conduction block, and significant axon degeneration (approximately 40% of fibers). Injection of a 100 micrograms/mL concentration resulted in severe acute motor axon degeneration followed by complete but delayed regeneration. Results of morphological studies closely correlated with electrophysiological findings. Amiodarone thus seems to have a direct toxic effect on axons at high concentrations in the peripheral nerve, and we suggest that different pathological changes described in human amiodarone neuropathy could be related to different concentrations of the drug in the nerve, perhaps due to variability of blood-nerve barrier efficacy.     

Amiodarone pharmacokinetics. I. Acute dose-dependent disposition studies in rats

Single intravenous bolus doses of amiodarone hydrochloride of 30, 60, 90 and 120 mg/kg were administered to male Sprague-Dawley rats to determine the effects of dose on amiodarone pharmacokinetics. Serial blood samples and total urine were collected over 48 hr and assayed for amiodarone and desethylamiodarone by HPLC. The blood amiodarone concentration-time curves for the four doses were best described by a triexponential equation with terminal half-lives (t _1/2 ) ranging from 17 to 20 hr. Over the dose range studied, no changes in , t _1/2 , or central compartment volume (Vc=1.2–1.4 L/kg) were observed. On the other hand, reductions in amiodarone clearance (CL and steady-state volume of distribution (V _ss of 44% (17.7 to 10.0 ml/min per kg) and 50% (16.4 to 8.2 L/kg), respectively, were noted as the dose of amiodarone increased. The conversion of amiodarone to desethylamiodarone (fm was dose-independent and amounted to approximately 10% of each amiodarone dose. No amiodarone or desethylamiodarone was detected in the urine of any of the treated animals. The blood-to-plasma concentration ratio of amiodarone was concentration-independent and therefore did not account for the dose-dependent changes in V_ss and CL observed. The data suggested that the dose-dependent changes noted were due to an alteration in the volume (s) of the peripheral tissue compartment(s).Supported by a Grant-in-Aid from the American Heart Association, Nebraska Affiliate.     

胺碘酮抑制缺血浦肯野纤维起搏离子流

目的观察正常及模拟“缺血”时胺碘酮对绵羊心室浦肯野纤维起搏离子流（Ｉｆ）的影响。方法双微电极电压钳制术,使膜电位过度极化以激活Ｉｆ。结果胺碘酮１×１０－５ｍｏｌ／Ｌ在正常台氏液中显著降低浦肯野纤维Ｉｆ幅值;模拟“缺血”也使Ｉｆ幅值降低,在此基础上,胺碘酮使Ｉｆ幅值进一步减小,加剧了“缺血”对Ｉｆ离子流的抑制作用。结论提示胺碘酮能抑制心肌缺血时心室正常自律性活动。     

胺碘酮对兔缺血再灌注纤溶活性、内皮血管活性物质的影响

目的探讨兔缺血再灌注纤溶活性、内皮血管活性物质的变化及胺碘酮的影响。方法新西兰大白兔60只,随机分为5组,每组12只,Ⅰ组:假手术组,Ⅱ组:急性心肌梗死(acutemyocardialinfarction,AMI)组,Ⅲ组:缺血再灌注(ischemicreperfusion,IR)组,Ⅳ组:IR+利多卡因组,Ⅴ组:IR+胺碘酮组;各组(除Ⅰ组外)分别结扎冠状动脉左室支中点,缺血60min,再灌注240min(Ⅰ,Ⅱ组不进行再灌注),分别取结扎前、再灌注前、再灌注240min血测定内皮素(endochelin,ET)、一氧化氮(nitricoxideNO)浓度和组织型纤溶酶原激活剂(tissuetypeplasminogenactivator,tPA)、纤溶酶原激活剂抑制物(plasminogenactivatorinhibitorPAI)活性。结果冠状动脉结扎后,血浆ET,NO浓度和PAI活性显著高于结扎前(P<0.01),tPA活性显著低于结扎前(P<0.01),再灌注后,血浆ET,NO浓度和PAI活性进一步升高,tPA活性进一步下降,与再灌注前对比均有显著性差异(P<0.01)。再灌注后,与IR组对比,胺碘酮能显著降低血PAI活性和ET浓度(P<0.01);利多卡因组无显著变化。结论胺碘酮可抑制缺血再灌注过程中PAI活性、抑制内皮细胞释放ET的有益作用。     

胺碘酮治疗开胸手术后心律失常

目的 评价静脉注射胺碘酮对非心脏开胸手术后心律失常的治疗效果及安全性。方法 46例开胸手术后发生室上性心动过速24例、频发室性早搏15例、心房颤动7例。用胺碘酮150mg缓慢静脉注射后，效果不佳者重复上述剂量。结果 快速室上性与室性心律失常者治疗总有效率分别为91．66％(22／24)和86．67％(13／15)，心房颤动者达100％(7／7)。结论 胺碘酮对胸部手术后心律失常具有良好的安全性。     

Thyroid Hormones and Cardiovascular Function and Diseases

Thyroid hormone (TH) receptors are present in the myocardium and vascular tissue, and minor alterations in TH concentration can affect cardiovascular (CV) physiology. The potential mechanisms that link CV disease with thyroid dysfunction are endothelial dysfunction, changes in blood pressure, myocardial systolic and diastolic dysfunction, and dyslipidemia. In addition, cardiac disease itself may lead to alterations in TH concentrations (notably, low triiodothyronine syndrome) that are associated with higher morbidity and mortality. Experimental data and small clinical trials have suggested a beneficial role of TH in ameliorating CV disease. The aim of this review is to provide clinicians dealing with CV conditions with an overview of the current knowledge of TH perturbations in CV disease.     

心律平与胺碘酮治疗心律失常疗效比较的Meta分析

目的 评价文献中运用心律平与胺碘酮治疗心律失常的疗效.方法 运用计算机检索Pubmed、EMbase、Cochrane图书馆、中国生物医学文献数据库中关于心律平和胺碘酮在治疗心律失常疗效的随机对照试验,将检索时限定为2000年1月～2014年7月.对检索到的论文进行客观质量评价,应用Cochrane协作网提供的Rev Man 5.3软件进行Meta分析.结果 通过药物静脉注射给药,2组心律失常总有效率差异有统计学意义(OR=1.68,95％ CI:1.25 ～2.26,P＜0.0001);药物口服给药,2组心律失常总有效率差异有统计学意义(OR=1.49,95％ CI:1.09 ～ 2.03,P=0.010);2组不良反应发生率比较差异无统计学意义(OR=0.85,95％ CI:0.62 ～ 1.16,P＞0.05).结论 胺碘酮组治疗心率失常的疗效优于心律平,但对于药物的不良反应率并不增加.