钙镁合剂干预奥沙利铂所致周围神经毒性疗效及安全性的荟萃分析

目的荟萃分析钙镁合剂对奥沙利铂所致周围神经毒性(OIPN)的干预作用。方法计算机检索PubMed、ScienceDirect、VIP、CNKI以及万方数据库,检索时间从建库至2016年8月,纳入钙镁合剂干预OIPN的随机对照试验(RCTs),并进行质量评价和资料提取,采用RevMan5.3软件进行荟萃分析。结果共纳入24个RCT,1961例患者。荟萃分析结果表明:钙镁合剂与空白对照组在OIPN总发生率〔RR=0.64,95%CI(0.53,0.77),P<0.00001〕、严重OIPN发生率〔RR=0.66,95%CI(0.58,0.75),P<0.00001〕以及急性OIPN发生率〔RR=0.73,95%CI(0.63,0.84),P<0.00001〕方面均有统计学差异,但在客观缓解率和疾病控制率方面无差异。亚组分析表明,OIPN总发生率及严重OIPN总发生率在奥沙利铂的中、低剂量组有统计学差异,而在高剂量组无差异。结论钙镁合剂能有效干预OIPN的发生,且不影响化疗疗效,安全性较好。     

音乐疗法对维持性血透患者的心理干预观察

目的:探讨音乐疗法对维持性血透患者的心理影响。方法:将80例血透患者随机分成音乐组和对照组,每组40例。观察音乐对血液透析患者的心率(HR)、呼吸频率(RR)、血压(BP)及焦虑程度的影响。音乐组透析过程中进行音乐疗法,对照组按常规进行透析;透析前后分别记录2组患者的HR、RR、BP以及精神状态和焦虑程度。结果:与对照组相比,音乐组HR和RR下降更快(P<0.01),焦虑程度减轻。音乐可以显著降低患者的HR、RR、收缩压、舒张压(P<0.05)。同时,音乐可以改善血透患者的心理状态,保持心态平衡。结论:音乐可以明显改善维持性血液透析患者的心理状态,减轻焦虑程度。因此建议把音乐干预作为常规透析治疗的辅助措施之一。     

谷胱甘肽预防奥沙利铂致周围神经毒性疗效的系统评价

目的:系统评价谷胱甘肽(GSH)预防奥沙利铂致周围神经毒性(OIPN)的疗效与安全性,为临床提供循证参考。方法:全面检索Pub Med、EMBase、Cochrane图书馆、中国期刊全文数据库、万方数据库和中文科技期刊数据库中收录的GSH对比安慰剂/无任何措施(统称安慰剂组)或其他药物预防OIPN疗效的随机对照试验(RCT)。提取资料并用改良的Jadad量表进行质量评价后,采用Rev Man 5.3统计软件进行Meta分析。结果:共纳入18项RCT,合计1 200例患者。Meta分析结果显示,GSH组患者奥沙利铂致慢性周围神经毒性(OICPN)总发生率[RR=0.71,95%CI(0.59,0.87),P<0.001]、严重OICPN发生率[RR=0.50,95%CI(0.42,0.60),P<0.001]显著低于安慰剂组,差异均有统计学意义,但两组患者奥沙利铂致急性周围神经毒性(OIAPN)发生率比较差异无统计学意义[RR=0.89,95%CI(0.72,1.09),P=0.25];GSH组患者严重OICPN发生率显著高于甲钴胺组,差异有统计学意义[RR=2.06,95%CI(1.07,3.99),P=0.03];GSH组与钙镁合剂组患者OICPN总发生率[RR=1.38,95%CI(0.83,2.31),P=0.21]与严重OICPN发生率[RR=1.91,95%CI(0.85,4.30),P=0.12]比较差异均无统计学意义。结论:GSH可以有效预防OICPN的发生,预防效果与钙镁合剂相当,但在预防严重OICPN方面疗效劣于甲钴胺。     

妊娠中晚期孕妇体重对妊娠结局的影响

目的探讨妊娠中晚期孕妇体重增加不足或过多对妊娠结局的影响。方法收集在本院产前门诊建卡并住院分娩的1751名单胎健康初产妇的病例资料,分析孕期体重增加对分娩小于(或大于)孕龄儿、剖宫产、妊娠期高血压疾病、妊娠期糖尿病等的影响,计算相对危险度(RR)和95%可信区间(95%CI)。结果孕中期孕妇体重增加不足与小于孕龄儿相关(RR=1.8,95%CI 1.4~2.4),而体重增加过多与大于孕龄儿相关(RR=2.1,95%CI 1.5~2.9),且有更高的剖宫产率(RR=2.6,95%CI 1.6~2.9)及不良妊娠结局;孕晚期体重增加不足与不良妊娠结局无明显相关性。结论孕中期是控制孕妇体重增加的关键时期,而孕晚期适当减少体重增长,不增加不良妊娠结局风险。     

社区护理干预对老年糖尿病患者治疗效果影响的Meta分析

目的评价社区护理干预对老年糖尿病治疗效果的影响。方法计算机检索PubMed、EMbase中国生物医学文献数据库(CBM)、万方数据库和中国期刊全文数据库,纳入老年糖尿病社区护理干预的随机对照实验,由2人独立进行数据提取和文献评价。采用RevMan5.0软件进行分析。结果共纳入6个RCT。Meta分析结果显示在血糖控制率[RR=4.07,95%CI(3.08,5.38),P<0.00001]、疾病知识掌握情况[RR=4.43,95%CI(3.26,6.03),P<0.00001]、遵医嘱率[RR=1.72,95%CI(1.31,2.24),P<0.0001]方面均具有统计学意义。结论 Meta分析显示社区护理干预对老年糖尿病的疗效优于传统护理方法。     

心房颤动患者动态心电图的RR间期表现分析

目的回顾性分析心房颤动（房颤）者动态心电图的RR间期表现,包括特点、分布、影响因素等内容,为房颤治疗提供重要参考。方法对该院2010年1月-2013年12月接受动态心电图的60例房颤患者的心电图临床资料进行回顾性分析,对动态心电图RR间期最值（最长、最短）、发生时间、不同时间段（1.5秒、3.0秒为分界点）内的心率、最高/低心率等进行统计分析。结果 RR间期小于1.5秒16例（26.67%）;RR间期大于2秒35例（58.33%）;RR间期大于3秒5例（8.33%）。结论房颤患者RR长间期较常见,分布呈昼夜节律性,且RR长间期不受心脏大小、心功能等影响。     

干扰素β治疗复发缓解型多发性硬化疗效分析及安全性评价

目的评价干扰素(IFN)β与安慰剂对照治疗复发缓解型多发性硬化(RRMS)的有效性及安全性。方法采用Cochrane系统评价的方法,搜集Cochrane图书馆、Medline、EMbase、中国生物医学文献数据库及中文全文期刊数据库(CNKI)关于IFN-β与安慰剂对照治疗RRMS的随机对照试验,根据文献质量评价标准纳入研究文献,采用RevMan4.2.10统计软件进行Meta分析。结果纳入IFN-β与安慰剂对照治疗RRMS的4项随机对照试验,共计1117例患者,文献质量评分A级3项,B级1项,Meta分析结果显示,IFN-β治疗RRMS复发的RR值为0.82,P<0.01;使RRMS转化为慢性持续进展型MS发生的RR值为0.70,P=0.001。流感样症状发生的RR值为1.70,P=0.001;发热发生的RR值为1.92,P<0.01;肌痛发生的RR值为1.88,P=0.04;寒战发生的RR值为2.32,P=0.001;白细胞减少发生的RR值为4.51,P=0.001;转氨酶升高发生的RR值为3.62,P=0.0002;IFN-β治疗组均高于安慰剂治疗组。而发生恶心及腹泻(RR值为1.51)、抑郁(RR值为0.96)、疲乏(RR值为1.27)、注射部位异常反应(RR值为2.40)、头痛(RR值为1.19)的不良反应两组间差异无统计学意义(P>0.05)。结论IFN-β治疗可减少RRMS的复发及延缓RRMS转化为慢性持续进展的发生;不良反应以干扰素β治疗组较常见。     

不同的脱钙液在骨组织制片中的比较应用

目的比较不同的脱钙液对骨组织的脱钙能力的差异,探讨其对HE染色的影响。方法选取50例手术切除的新鲜骨标本,运用4种常用的脱钙液(14%硝酸、10%盐酸、20%甲盐酸和EDTA脱钙液)进行脱钙,比较其脱钙效果和对HE染色的影响。结果不同的脱钙液对骨组织的脱钙能力、HE染色效果影响有显著区别。结论 14%硝酸脱钙能力最强,用时间最短,染色的效果最差;10%盐酸对骨组织的损伤小,HE染色的效果最好,但用时较长;20%甲盐酸脱钙能力和HE染色效果都介于10%盐酸和EDTA脱钙液之间;EDTA脱钙液脱钙用时最长,对骨组织的损伤最小。     

脑卒中复发影响因素的Cox回归分析

目的 探讨脑卒中复发的主要影响因素.方法 2 065例脑卒中新发病例为研究人群,随访患者的复发情况,调查影响复发的各种因素.随访时间为3年.应用Cox比例风险回归模型对影响脑卒中复发的各种因素进行单因素和多因素分析.结果 截至随访终点,受访病例共1 881例,失访病例184例.复发病例327例（17.38%）,6个月内复发45例（13.76%）,6个月至1年复发68例（20.80%）,1～2年复发97例（29.66%）,～3年复发117例（35.78%）.单因素Cox回归分析：高龄（RR=1.48）、吸烟（RR=1.35）、脂肪摄入（RR=1.83）、高血压史（RR：2.54）、糖尿病史（RR=1.72）、高脂血症（RR=1.83）、脑卒中家族史（RR=2.62）、抑郁（RR=1.84）、生活事件（RR=2.53）、纤维蛋白原（RR=1.75）、颈动脉斑块（RR=2.68）为脑卒中复发的危险因素;女性（RR=0.64）、运动（RR=0.33）、社会支持（RR=0.36）为脑卒中复发的保护因素.多因素Cox回归分析表明：高血压史（RR=1.86）、高脂血症（RR=1.95）、脑卒中家族史（RR=2.62）、生活事件（RR=2.38）、颈动脉斑块（RR=2.77）是引起脑卒中复发的危险因素;运动（RR=0.35）、社会支持（RR=0.32）是脑卒中复发的保护因素.结论 对脑卒中患者的高血压史、高脂血症、脑卒中家族史的预防、多参加体育运动、增强对生活事件的应对能力,有助于脑卒中复发的预防.     

水杨酸镁对胎鼠脑细胞内钙的影响

目的　观察水杨酸镁对脑细胞内钙的影响 ,探讨其中枢神经系统的钙拮抗作用。方法　应用新一代钙离子指示剂Fura 2 /AM技术 ,用双波长荧光分光光度计测定细胞内钙浓度。结果　在不同外钙条件下 (外钙 0 ,0 0 1,0 1,1 0 ,1 3mmol·L-1)细胞内静息钙浓度分别 41± 5 ,5 9± 6 ,84 7± 2 5 ,10 4± 7,(12 6± 5 )nmol·L-1(各组n =8)。水杨酸镁0 2mmol·L-1对静息细胞内钙无显著影响 (P >0 0 5 )。但水杨酸镁 (0 0 5～ 0 4mmol·L-1)可以剂量依赖性抑制高钾及L 谷氨酸诱发的细胞内钙增高。其IC50 分别为 0 32 3mmol·L-1(95 %CI为 0 12 2～ 0 85 4mmol·L-1)和 0 12 4mmol·L-1(95 %CI为 0 0 73～ 0 2 10mmol·L-1)。结论　水杨酸镁通过抑制电压依从性及受体操纵型的钙通道 ,对中枢神经系统具有较强的钙拮抗作用。     

大黄素对豚鼠单个心室肌细胞胞浆游离钙浓度及L-型钙电流的影响

目的研究大黄素(emodin)对豚鼠心室肌细胞钙信号的影响。方法酶解法分离豚鼠单个心室肌细胞,应用激光扫描共聚焦显微镜联合全细胞膜片钳技术测量豚鼠心室肌细胞钙信号的变化。结果在静息状态下,1～100 μmol·L^-1大黄素对［Ca²⁺］i均无影响;对60 mmol·L^-1 KCl诱导的外钙内流引起的胞浆钙升高有不同的影响,1 μmol·L^-1表现为促进作用;10 μmol·L^-1无作用;100 μmol·L^-1则表现为抑制作用。膜片钳研究结果表明,1 μmol·L^-1大黄素可明显促进L-型钙电流,10 μmol·L^-1对L-型钙电流无影响;100 μmol·L^-1明显抑制L-型钙电流。结论大黄素对心肌细胞内钙及L-型钙电流具有双向调节作用。     

Effects of the calcium sensitizer [+]-EMD 60263 and its enantiomer [-]-EMD 60264 on cardiac ionic currents of guinea pig and rat ventricular myocytes

The thiadiazinone enantiomers [+]-EMD 60263 and [-]-EMD 60264 ((+)-5-(1-(alpha-ethylimino-3,4-dimethoxybenzyl)-1,2,3,4-tetrah ydroquinoline-6-yl)-6-methyl-3,6-dihydro-2H-1,3,4-thiadiazine-2 -on) exhibit distinct stereoselectivity for Ca2+-sensitizing action ([+]-enantiomer) and phosphodiesterase inhibition ([-]-enantiomer). However, in isolated guinea pig papillary muscle, both compounds cause an action-potential prolongation that has been related to a nonselective depression of the delayed rectifier potassium current. Because [-]-EMD 60264 did not increase force of contraction despite phosphodiesterase inhibition, we postulated that one or several additional actions may oppose the anticipated positive inotropic effect. Therefore we investigated whether other membrane currents were also affected in voltage-clamped ventricular cardiomyocytes. Both [+]-EMD 60263 and [-]-EMD 60264 reduced sodium current as well as L-type calcium current in guinea pig ventricular myocytes, but steady-state inactivation or conductance curves of I(Na) and I(Ca) were not shifted along the voltage axis. Inward rectifier and transient outward current were studied in rat myocytes, but neither current was affected. We conclude that the positive inotropic action of [+]-EMD 60263 can be explained by prevalence of the Ca2+-sensitizing effect over its inhibitory actions on Na+ and Ca2+ current, whereas the negative inotropic effect of [-]-EMD 60264 may be caused by inhibition of I(Ca) predominating over PDE inhibition.     

毒毛旋花子苷元对豚鼠心室肌细胞内钙浓度的影响

观察毒毛旋花子苷元(strophanthidin, Str)对分离豚鼠心室肌细胞内游离钙浓度(［Ca²⁺］_i)的影响。酶解分离豚鼠心室肌细胞, 用Fluo 3-AM负载, 激光共聚焦显微镜法测定单个豚鼠心室肌细胞［Ca²⁺］_i的荧光密度。Str可浓度依赖性地升高［Ca²⁺］_i, Str (10 μmol·L^-1)在［Ca²⁺］_i升高达峰值时, 可使细胞挛缩, 而Str (1和10 nmol·L^-1)对细胞形态无影响。TTX、 尼索地平或升高细胞外钙可影响Str (1和100 nmol·L^-1)对［Ca²⁺］_i的升高作用,而对Str (10 μmol·L^-1)无明显影响。在外液中加入ryanodine或去除细胞外钙, 则3个检测浓度的Str升高［Ca²⁺］_i作用均被明显抑制。在无K⁺、 无Na⁺液中, 10 μmol·L^-1 Str升高［Ca²⁺］_i的作用减弱, 而Str (1和100 nmol·L^-1)升高［Ca²⁺］_i的作用无明显影响。加入TTX、 尼索地平或增加细胞外的钙离子浓度, 则3个检测浓度Str的作用均受到影响。提示低浓度Str对［Ca²⁺］_i的升高作用与抑制Na⁺、K⁺-ATP酶活性无关, 而与促进L-型钙通道和TTX敏感性钠通道的“slip-mode”钙电导有关; 高浓度Str升高［Ca²⁺］_i的作用则是抑制Na⁺、K⁺-ATP酶的结果。此外, Str对［Ca²⁺］_i的升高作用还与直接作用于ryanodine受体促进内钙释放有关。     

BK channel activation by NS-1619 is partially mediated by intracellular Ca2+ release in smooth muscle cells of porcine coronary artery

1. Effects of NS-1619, an opener of large conductance Ca2+-activated K+ (BK) channel, on intracellular Ca2+ concentration ([Ca2+]i) and membrane potential were examined in single myocytes freshly isolated from porcine coronary artery. 2. Under current clamp mode, the application of 1-30 microM NS-1619 hyperpolarized the membrane in concentration-dependent manner. The NS-1619-induced hyperpolarization was abolished by the presence of 100 nM iberiotoxin. 3. Application of 1-10 microM NS-1619 hyperpolarized the membrane by approximately 6 mV or less but did not change significantly the [Ca2+]i. When membrane hyperpolarization of 12 mV or so was caused by 30 microM NS-1619, [Ca2+]i was unexpectedly increased by approximately 200 nM. This increase in [Ca2+]i and the concomitant outward current activation were also observed under voltage-clamp at holding potential of -40 mV. 4. The increase in [Ca2+]i by 30 microM NS-1619 occurred mainly in peripheral regions than in the centre of the myocytes. The removal of extracellular Ca2+ affected neither the membrane hyperpolarization nor the increase in [Ca2+]i. 5. In the presence of 10 mM caffeine and 10 microM ryanodine, the increase in [Ca2+]i by 30 microM NS-1619 was not observed and the membrane hyperpolarization was reduced to approximately 67% of the control. 6. These results indicate that the opening of BK channels by NS-1619 at 30 microM, which is the most frequently used concentration of this agent, is partly due to Ca2+ release from caffeine/ryanodine-sensitive intracellular storage sites but is mainly due to the direct activation of the channels.     

Inotropic effects and mechanisms of matrine, a main alkaloid from Sophora flavescens AIT

It has been well documented that matrine, a tetracyclo-quinolizindine alkaloid, possessed a positive inotropic effect. However, the underlying mechanisms at the cellular and ion channel levels have not been completely clarified. Therefore, the present study was designed to identify the cellular target and the mechanisms of inotropic effect of matrine. Guinea pig papillary muscles were used to study the contractile force of the heart and ventricular myocytes were used to study L-type calcium channel (ICa-L) and intracellular calcium concentration ([Ca2+]i). In electrically driven papillary muscles, matrine enhanced the contractile force in a dose-dependent manner and the positive inotropic effect was not inhibited by alpha- and beta-adrenergic receptor antagonists. In ventricular myocytes, matrine also increased ICa-L in a dose-dependent manner and shifted the inactivation curve toward right. Matrine markedly enhanced the KCl-induced elevations of [Ca2+]i. In a conclusion, ICa-L might be a main target of matrine. Matrine enhanced [Ca2+]i by stimulating ICa-L and exerted positive inotropic effects on electrically driven guinea pig papillary muscles.     

Increasing Intracellular calcium of guinea pig ventricular myocytes induced by platelet activating factor through IP3 pathway

We used Fluo-3/AM to examine the effect of platelet-activating factor on the intracellular Ca2+([Ca2+]i) levels in isolated myocytes of guinea pig ventricle. Myocytes were isolated with Langendorff perfusion technique and were challenged with platelet-activating factor. Addition of platelet-activating factor (1 pM to 10 nM) significantly increased the [Ca2+]i in the presence and absence of extracellular Ca2+. The notion that increases in intracellular Ca2+ induced by platelet-activating factor is the result of stimulation of intracellular Ca2+ pool rather than increasing Ca2+ influx was further supported by the whole cell patch-clamp experiments in which the platelet-activating factor did not alter the activity of L-type of Ca2+ channels (I(Ca-L)). Treatment of myocytes with ryanodine failed to abolish the stimulatory effect of platelet-activating factor on [Ca2+]i. In contrast, inhibition of IP3-sensitive Ca2+ release pool with 2-aminoethoxydiphenyl borate (2-APB) blocked the effect of platelet-activating factor. We conclude that the platelet-activating factor-induced increase in intracellular Ca2+ is mediated by stimulation of IP3 receptor but not by stimulation of I(Ca-L) and ryanodine-sensitive receptor.     

苯丙-甲硫-精-苯丙氨酸多肽对豚鼠心室肌细胞Na~+/Ca~(2+)交换尾电流的影响

目的　研究苯丙 -甲硫 -精 -苯丙氨酸 (FMRFa)多肽对心肌细胞膜钙瞬变触发的 Na+ / Ca2 + 交换尾电流的影响。方法　采用蛋白酶 E急性分离的豚鼠心室肌细胞。利用全细胞膜片钳技术观察 FMRFa多肽对心肌细胞膜 Na+ / Ca2 + 交换尾电流的作用。结果　 FMRFa多肽 1、5、10、2 0μm可分别抑制 Na+ / Ca2 + 交换尾电流(13± 3) % ,(2 5± 7) % ,(73± 9) %和 (110± 10 ) %。结论　 FMRFa多肽可剂量依赖性地抑制豚鼠心室肌细胞膜钙瞬变触发的 Na+ / Ca2 +交换尾电流     

Effects of pyruvate on intracellular Ca2+ regulation in cardiac myocytes from normal and diabetic rats

1. Pyruvate has been shown to enhance the contractile performance of cardiac muscle when provided as an alternative substrate to glucose. The aims of the present study were to determine whether the inotropic effects of pyruvate are due to increased mobilization of intracellular Ca2+ ([Ca2+]i) and to compare the effects of pyruvate on [Ca2+]i levels in myocytes from normal and diabetic animals. 2. Fura-2 was used to monitor [Ca2+]i in ventricular myocytes isolated from control and streptozotocin-treated male Wistar rats. The experiments were performed at 25 degrees C, with an extracellular [Ca2+] of 1.5 mmol/L and either 10 mmol/L glucose or 10 mmol/L pyruvate as the substrate. 3. In myocytes from both control and diabetic rats, increasing the stimulus frequency from 0.33 to 2.0 Hz resulted in significant increases in resting and peak [Ca2+]i as well as in the amplitude of the [Ca2+]i transient, irrespective of substrate. Compared with glucose, pyruvate significantly increased resting and peak [Ca2+]i and the amplitude of the [Ca2+]i transient at each stimulus frequency in myocytes from both control and diabetic animals. However, the extent of potentiation of the [Ca2+]i transient amplitude produced by pyruvate was significantly less in myocytes from the diabetic rats. 4. The rate of restitution of the [Ca2+]i transient was used as an index of the rate of Ca2+ cycling by the sarcoplasmic reticulum (SR). Pyruvate enhanced the rate of restitution in control but not diabetic rat cells. 5. The time course of decay of the [Ca2+]i transient was analysed as a measure of the rate of removal of Ca2+ from the cytosol. Pyruvate tended to increase the rate of decay in cells from control but not diabetic animals. The rate of decay was slower in cells from diabetic animals compared with controls. 6. The data reveal that pyruvate increases SR Ca2+ cycling, leading to greater Ca2+ release and an increase in the amplitude of the [Ca2+]i transient. Therefore, it seems highly likely that increased [Ca2+]i mobilization is responsible for the previously reported positive inotropic actions of pyruvate. These effects of pyruvate are attenuated in diabetic rat cells, which may reflect an impaired capacity of mitochondria in diabetic hearts to oxidize pyruvate, thus limiting potential energetic benefits.     

Effects of beauvericin on the metabolic state and ionic homeostasis of ventricular myocytes of the guinea pig

Beauvericin, a cyclic hexadepsipeptide with antibiotic properties, has been shown to reduce contraction force and to affect action potential parameters of guinea pig papillary muscles. Its potential to form cation-selective channels in mammalian membranes has been demonstrated. Patch clamp and fluorescence imaging techniques were used to investigate its effects in enzymatically isolated ventricular myocytes. Application of 10 microM beauvericin caused a large [Ca2+]i increase in Fura 2AM-loaded cardiomyocytes leading to cell shortening. The effect could be partially inhibited by ryanodine pretreatment and was largely dependent on external Ca2+ and blocked by 5 mM Ni2+. Beauvericin initiated a progressive increase in [Mg2+]i, the time course of which developed similarly upon increasing the external chemical gradient of Mg2+ 10-fold, to produce an ionophoric challenge. Monitoring of pH(i) with BCECF showed that beauvericin caused cytosolic acidification. Confocal microscopy revealed mitochondrial depolarization in TMRM-loaded cardiomyocytes, which resembled the effect of classical mitochondrial uncouplers. However, the NADH autofluorescence signal followed a biphasic pattern, in contrast to the NADH response to the uncouplers FCCP and the K+-ionophore valinomycin. These results suggest that beauvericin, possibly via its ionophoric properties, acts as an atypical mitochondrial uncoupler, greatly disturbs the physiological ionic balance and pH, challenges cellular metabolism, and causes ATP depletion.     

甲基莲心碱对心肌细胞I_(Na)、I_(Ca-L)及稳态外向K~+电流的影响

目的　为证明甲基莲心碱（ Ｎｅｆｅｒｉｎｅ, Ｎｅｆ） 对单个心肌细胞离子通道电流的影响及抗心律失常作用的离子通道机制。方法　采用全细胞记录膜片钳技术,记录了 Ｎｅｆ 对培养大鼠心室肌细胞钠电流（ Ｉ Ｎａ） 及豚鼠心室肌细胞动作电位、 Ｉ Ｎａ 、 Ｌ 型钙电流（ Ｉ Ｃａ Ｌ） 及稳态外向 Ｋ＋ 电流的影响。结果　 Ｎｅｆ ３０ ,１００ μｍｏｌ· Ｌ－ １ 明显抑制培养大鼠心室肌细胞 Ｉ Ｎａ ,分别从对照水平的（３４ ±０７） ｎ Ａ 降至（２１ ±０５） 和（０４ ±０２） ｎ Ａ。 Ｎｅｆ １０ μｍｏｌ· Ｌ－ １ 可降低豚鼠心室肌细胞动作电位振幅、静息电位,延长动作电位时程。 Ｎｅｆ １０ ,３０ μｍｏｌ· Ｌ－ １ 分别使豚鼠心室肌细胞 Ｉ Ｎａ 及 Ｉ Ｃａ Ｌ从给药前的（７９ ±２１） ｎ Ａ 和（６８９ ±２４３） ｐ Ａ 降至（４０ ±１４） 、（１３ ±０６） ｎ Ａ和（３７４ ±１７２） 、（１０９ ±６７） ｐ Ａ。 Ｎｅｆ １０ μｍｏｌ· Ｌ－ １ 还抑制 Ｉ Ｎａ 、稳态外向 Ｋ＋ 电流和 Ｉ Ｃａ Ｌ的 Ｉ Ｖ 曲线并使后者的峰值电流电位略右移。结论　 Ｎｅｆ 有钠、 Ｌ 型钙通道阻滞作用并抑制稳态外向 Ｋ＋ 电流,这些可解释