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单相动作电位

单相动作电位的相关文献在1989年到2020年内共计184篇,主要集中在内科学、基础医学、药学 等领域,其中期刊论文175篇、会议论文5篇、专利文献40474篇;相关期刊85种,包括四川生理科学杂志、中国心血管杂志、中国心脏起搏与心电生理杂志等; 相关会议5种,包括全国第四次麻醉药理学学术会议暨2013年贵州省麻醉学术年会、第四届心房颤动国际论坛、第七次全国中西医结合心血管病学术研讨会等;单相动作电位的相关文献由446位作者贡献,包括高鸿、冯志强、刘艳秋等。

单相动作电位—发文量

期刊论文>

论文:175 占比:0.43%

会议论文>

论文:5 占比:0.01%

专利文献>

论文:40474 占比:99.56%

总计:40654篇

单相动作电位—发文趋势图

单相动作电位

-研究学者

  • 高鸿
  • 冯志强
  • 刘艳秋
  • 张存泰
  • 陆再英
  • 张凯强
  • 李泱
  • 曾晓荣
  • 李惠
  • 王腾
  • 期刊论文
  • 会议论文
  • 专利文献

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    • 牛欢; 陈曼丽; 董博; 何智余; 杨波
    • 摘要: 目的研究Urocortin-I通过激活蛋白激酶B(Akt)/糖原合成酶激酶3β(GSK-3β)通路,对缺血再灌注(I/R)心肌单相动作电位及氧化炎症反应的作用。方法制备离体心肌Langendorff灌注模型,并分为对照组、I/R组、Urocortin-I组、Urocortin-I+LY组。对照组进行常规灌流;I/R组给予常规预处理、Urocortin-I组给予Urocortin-I预处理、Urocortin-I+LY组给予Urocortin-I+LY294002预处理后,均进行缺血再灌注处理。比较4组间心肌酶、心肌梗死面积、单相动作电位、炎症因子、氧化应激产物、Akt/GSK-3β通路分子的差异。结果与对照组比较,I/R组乳酸脱氢酶(LDH)、磷酸肌酸激酶同工酶(CK-MB)、肿瘤坏死因子α(TNF-α)、白细胞介素6(IL-6)、细胞间黏附分子1(ICAM-1)、活性氧簇(ROS)、丙二醛(MDA)的含量及心肌梗死面积明显增加,APA、APD50、APD90的水平及p-Akt、p-GSK-3β的含量明显减少(P<0.05)。与I/R组比较,Urocortin-I组LDH、CK-MB、TNF-α、IL-6、ICAM-1、ROS、MDA的含量及心肌梗死面积明显减少,APA、APD50、APD90的水平及p-Akt、p-GSK-3β的含量明显增加(P<0.05)。与Urocortin-I组比较,Urocortin-I+LY组LDH、CK-MB、TNF-α、IL-6、ICAM-1、ROS、MDA的含量及心肌梗死面积明显增加,APA、APD50、APD90的水平及p-Akt、p-GSK-3β的含量明显减少(P<0.05)。结论Urocortin-I通过激活Akt/GSK-3β通路改善I/R心肌的单相动作电位及氧化炎症反应。
    • 王贵龙; 高鸿; 王子君; 易菁; 李伟超; 刘艳秋
    • 摘要: 目的 观察不同浓度七氟醚对大鼠离体心脏缺血-再灌注时心肌单相动作电位(MAP)的影响.方法 健康成年雄性 SD大鼠 32 只,体重 280~320 g,成功制备 langendorff离体心脏灌注模型,K-H 液平衡灌注 1 5 min后,随机分为四组,每组 8 只:缺血-再灌注组(IR组):K-H 液继续灌注 15 min后停止,注射Thomas液(4°C,20 ml/kg)使心脏停搏60 min,心脏周围用低温(4°C) Thomas液保护,30 min时半量复灌Thomas液(4°C,10 ml/kg),60 min时再灌注K-H 液 30 min;0.5 MAC七氟醚组(Sev0.5 组):K-H 液为含饱和 0.5 MAC七氟醚液体,余同 IR 组;1.0 MAC 七氟醚组(Sev1.0 组):K-H 液为含饱和 1.0 MAC 七氟醚液体,余同 IR 组;2.0 MAC 七氟醚组(Sev2.0 组):K-H 液为含饱和2.0 MAC七氟醚液体,余同IR组.记录平衡灌注1 5 min(T0)、继续灌注 15 min(T1)、再灌注 15 min(T2)、再灌注 30 min(T3)的 HR 及左心室前壁外膜层、中层和内膜层心肌 MAP,计算MAP复极50%及90%的时程(MAPD50、MAPD90).并记录心律失常发生情况.结果 与T0和T1时比较,T2、T3时IR组、Sev1.0 组、Sev2.0 组 HR明显减慢(P<0.05);与IR组比较,T2、T3时Sev0.5 组、Sev1.0 组HR明显增快,Sev2.0 组HR明显减慢(P<0.05).与IR组比较,T3时 Sev0.5 组 MAPD50,Sev0.5 组、Sev1.0 组、Sev2.0 组 MAPD90明显缩短(P<0.05).心脏复跳时 IR组有 6 例,Sev0.5 组有 1 例,Sev1.0 组有 2 例,Sev2.0 组有 1 例发生心律失常,与 IR组比较,Sev0.5 组、Sev1.0 组和 Sev2.0 组心律失常发生率明显降低(P<0.05).结论 不同浓度七氟醚均可缩短缺血-再灌注心肌单相动作电位 MAPD90,且这一作用在 0.5~2.0 MAC 的七氟醚浓度范围内无剂量依赖性,这可能是其减少缺血-再灌注心律失常发生风险的机制.%Objective To study the effects of different concentrations of sevoflurane on monophasic action potentials (MAPs)of three-layer myocardium of ischemia reperfusion in isolated rat hearts.Methods Thirty-two healthy SD male rats,weighing 280-320 g,were randomly divided into four groups after successful preparation of langendorff isolated heart perfusion model and 1 5 min perfusion and balance of K-H fluid.In the ischemia-reperfusion group(group IR),K-H fluid perfusion was stopped and balanced for 15 min and cardiac arrest was induced for 60 min with the injection of Thomas solution (4°C,20 ml/kg)while the heart was protected by the low temperature Thomas so-lution (4°C)around it.Reperfusion of Thomas solution (4°C,10 ml/kg)was performed for 30 min and the heart was resuscitated by the perfusion of K-H fluid for 60 min.In the 0.5 MAC sevoflurane group (group Sev0.5 ),K-H fluid contained 0.5 MAC sevoflurane and other procedures were the same as in group IR.1.0 MAC sevoflurane group (group Sev1.0 ),K-H fluid contained 1.0 MAC sevoflurane and other procedures were the same as in group IR.2.0 MAC sevoflurane group (group Sev2.0),K-H fluid contained 2.0 MAC sevoflurane and other procedures were same as in group IR. HR,MAPs including time course (MAPD50,MAPD90)and MAP amplitude of endocardium,mid-layer myodardium and epicardium was recorded at the time of continuous balance perfusion for 1 5 min (T0),continuous perfusion for 15 min (T1),reperfusion for 15 min (T2)and 30 min (T3). Results Compared with T0and T1,HR was slower at T2and T3(P<0.05);Compared with group IR at T2and T3,HR in group Sev0.5 and group Sev1.0 was higher,that in group Sev2.0 was slower P<0.05);At T2,arrhythmia was observed in 6 rats in group IR,while arrhythmia was observed in 1 rats in group Sev0.5 ,and arrhythmia was observed in 2 rats in group Sev1.0 and arrhythmia was observed in 1 rats in group Sev2.0;Compared with group IR at T3,MAPD50in group Sev0.5 was shorter in three sites(P<0.05);Compared with group IR at T3,MAPD90in other three groups was shorter.Conclusion Different concentrations of sevoflurane can shorten MAPD90of MAPs,and the effects don't depend on the concertrations of sevoflurane when it changes from 0.5 MAC to 2.0 MAC;which may be the mechanism of decreased arrhythmias risk caused by sevoflurane.
    • 李伟超; 高巨; 高鸿; 佘玉琦; 王子君; 刘艳秋
    • 摘要: Objective To investigate the electrophysiological protective effect of HTK solution containing sevoflurane on rat cardiac transplantation. Methods Twenty-four male Sprague-Dawley rats were divided into the control group,sevoflurane group and Heptanol group. Rat hearts in 3 groups were stored in HTK solution,containing sevoflurane and sevoflurane+heptanol HTK solution for 6 h. Heart resuscitation time,the duration of arrhythmia and monophasic action potential(MAP)and heart rate(HR)at different time points were recorded.Monophasic action potential duration of repolarization at 50% and 90%(MAPD50 and MAPD90),monophasic action potential amplitude(MAPA)and maximal velocity(Vmax)were analyzed. Results The isolated rat hearts in each group can be successfully restored to the spontaneous heart beat. Compared with group C ,heart resuscitation time in group S and group H was significantly shortened,heart rate(HR)was significantly decreased at T1,MAPD50 and MAPD90 in heart intima and epicardium were shortened at T1 ~ T2,the incidence of ventricular fibrillation and reperfusion arrhythmia Scores were reduced,with the shorter duration of ventricular fibrillation(P0.05).结论 含七氟醚HTK液和含庚醇HTK液在电生理方面有相似作用,都可抑制延长的单相动作电位(MAP),减轻心律失常.含七氟醚HTK液的电生理保护作用可能与缝隙连接抑制相关.
    • 佘玉琦; 高鸿; 张凯强; 李惠; 刘艳秋; 王冬婷
    • 摘要: Objective To evaluate efficacy of rotigaptide ZP123 on prevention of negative chronotropic effect caused by dexmedetomidine lengthening repolarization duration of the isolated rat hearts.Methods Eighteen healthy adult SD rats of either gender,weighing (300±30) g,were prepared isolated heart perfusion model by Langendorff.After 15 min perfusion and balance of K-H fluid,the isolated hearts were randomly divided into 3 groups (n=6 each): The hearts were continuously pefused for 30 min with 37°C K-H solution in control group (group C),with dexmedetomidine 50 ng/ml in dexmedetomidine group (group D),or with rotigaptide 80 nmol/L combined with dexmedetomidine 50 ng/ml in rotigaptide combined with dexmedetomidine group (group ZD).In the whole Langendorff-perfused hearts,at the end of balanced infusion for 15 min (T0) and at 15(T1),30(T2) min of continued perfusion with K-H solution,the monophasic action potential (MAP) and heart rate (HR) were recorded from left anterior free wall,MAP duration at 50% repolarization (MAPD50) and at 90% repolarization (MAPD90),monophasic action potential amplitude (MAPA) and maximal velocity (Vmax) were calculated.Results Compared with T0,HR in group D was significantly declined at T1,T2;MAPD90 and MAPD50 in group D were significantly increased at T1,T2 (P<0.05).Compared with groups C and ZD,HR in group D was significantly declined at T1,T2;MAPD90 and MAPD50 in group D were significantly increased at T1,T2 (P<0.05).There was no significant difference in MAPA and Vmax between the three groups.Conclusion Rotigaptide antagonizes negative chronotropic effect induced by dexmedetomidine through shortening monophasic action potential duration in the myocardium of left ventricle of the isolated rat hearts.%目的 探讨缝隙连接改造剂ZP123对右美托咪定诱发鼠离体心脏复极时程延长所致的负性变频效应.方法 健康成年SD大鼠18只,雌雄不拘,体重(300±30)g,制备Langendorff离体心脏灌注模型,K-H液平衡灌注15 min后,随机分为三组,每组6只:空白对照组(C组)继续灌注37°C K-H液30 min;右美托咪定组(D组)灌注含50 ng/ml右美托咪定的K-H液30 min,右美托咪定+ZP123组(ZD组)灌注含50 ng/ml右美托咪定+80 nmol/L ZP123的K-H液30 min.于平衡灌注15 min(To)、继续灌注15 min(T1)、30 min(T2)时记录HR和左心室心肌单相动作电位(MAP),计算MAP复极50%、90%的时程(MAPD50、MAPD90)、单相动电位振幅(MAPA)和最大去极化速度(Vmax).结果 与T0时比较,T1、T2时D组HR明显减慢(P<0.05),T1、T2时D组HR明显慢于C组和ZD组(P<0.05).与T0时比较,T1、T2时D组心肌MAPD50、MAPD90明显延长(P<0.05);T1、T2时D组心肌MAPD50、MAPD90明显长于C组和ZD组(P<0.05).三组心肌内外两层膜MAPA和Vmax组间组内差异均无统计学意义.结论 缝隙连接改造剂ZP123通过缩短心肌单相动作电位复极的时程从而拮抗右美托咪定诱发的鼠离体心脏的负性变频效应.
    • 陈宇; 赵新华; 尹德录
    • 摘要: Objective To investigate the feasibility of recording the endocardial monophasic action potentials (MAP) with a platinum-electrode ablation catheter.Methods Multipoint endocardium monophasic action potentials(MAP) were recorded in twenty patients preformed catheter ablation of tachycardia.According to their different recording methods,the twenty patients were divided into two groups:the platinum-electrode group and the Ag AgCl-electrode group.The amplitudes(AMP),MAP duration at 90% repolarization(APD90),the activation time (AT) and the repolarization time(RT) during sinus rhythm were recorded at every recorded site.Results In the recorded sites of right ventricular apex and right vèntricular outflow tract,the Ag-AgCl-electrode group and the platinum-electrode group recorded 48 and 46 MAPs separately.Of all the MAPs in the platinum-electrode group,only 3 MAPs had baseline disturbances 10% of the plateau amplitudes of the MAPs,at the same time,the plateau amplitudes of the MAPs were >10 mV in 33 of the all 46 MAPs in that group,which met the needs of stable MAP signals.Compared to the Ag-AgCl-electrode group,the AMP,APD90,AT,RT in the platinum-electrode group were not distinctly different (P > 0.05).Conclusions Our study suggested that it is possible to recording monophasic action potentials with a platinum-electrode ablation catheter instead of Ag-AgCl-electrodes.%目的 探讨使用用于射频消融的普通铂电极记录心内膜单相动作电位(MAP)的可行性.方法 20例阵发性室上性心动过速行导管消融的患者分两组,分别使用铂电极和银-氯化银(Ag-AgCl)电极在右室心尖部及右室流出道进行MAP标测,测量各标测点MAP的振幅(AMP)、动作电位复极达90%的时程(APD90)、激动时间(AT)和复极时间(RT),比较两组间各指标的差异.结果 在右室心尖部和右室流出道Ag-AgCl电极组和铂电极组分别测得48和46个标测点,其中铂电极组仅有3个标测点基线干扰较大,并且该组振幅大于10 mV的标测点共有33个,基本满足稳定的MAP信号的要求.与Ag-AgCl电极组相比,铂电极组测得的MAP的AMP、APD90、AT、RT值均没有显著差异(P均>0.05).结论 在临床研究中使用铂电极代替Ag-AgCl接触电极作为同时记录MAP和射频消融的两用电极具有可行性.
    • 姜婵; 王晞; 刘自强; 饶盼盼; 黄从新
    • 摘要: 目的 利用光遗传学技术是否能有效实施光照夺获心脏,实现心脏光起搏,探讨光照强度对心脏夺获率的影响.方法 取15只C57雌性小鼠,随机分成3组:正常组6只,空载病毒组6只,ChR2组3只(A、B、C小鼠),经颈静脉给三组小鼠分别注射100μl生理盐水,100μl pAOV-CAG-mcherry,100μlpAOV-CAG-hChR2(H134R)-mcherry.8周后,进行离体心脏Langendorff离体灌流,并给予473 nm的蓝光光照刺激,观察小鼠的心律是否能被光刺激夺获,并比较不同功率下的光刺激对心脏夺获率的影响,观察光刺激和电刺激产生的单相动作电位(MAP)之间是否存在差异.结果 ChR2组小鼠的心脏节律能被光照夺获,一定范围内夺获率与功率成正相关关系,且17.3 mW的光照基本能满足光照夺获心律所需功率的大小,正常组和空载病毒组小鼠心脏的节律均不能被光照夺获.ChR2组A、B、C3只小鼠光照夺获心律所需的功率大小差别较大,B小鼠心脏更容易被光夺获,可能与心脏ChR2表达量有关.光刺激与电刺激产生的MAP存在差异,光刺激产生的MAP的达峰时间比电刺激短,且动作电位的复极时程达10%,30%,50%,70%的值小于电刺激.结论 利用光遗传学技术实现心脏光起搏技术可行.光敏蛋白ChR2成功表达在靶器官上是光遗传学关键的一步,光刺激心脏的夺获率不仅与光照功率的大小有关,可能还与心脏表达ChR2的量相关.%Objective To investigate the possibility of capturing the rhythms of heart and achieving optical pacing by optogenetics and compare the effectiveness of illumination with different parameters.Method Fifteen C57 mice were randomly divided into three groups,the normal group (n =6),the no-load virus group (n =6),and the ChR2 group (n=3;A,B,C mice).Three groups of mice were separately injected 100 μl normal saline,100 μl pAOV-CAG-mcherry and 100 μl pAOV-CAG-hChR2(H134R)-mcherry into jugular vein.After eight weeks,the isolated heart was stimulated by 430nm blue light with different illumination intensities closed to the surface of heart in Langendorff apparatus.We observed whether the rhythm of heart can be captured by light stimulation with different illumination power and compare the difference of monophasic action potential(MAP) induced by light stimula tion and electric stimulation.Result The rhythm of the heart expressing ChR2 was easier to be controlled by the blue light pulse with higher power,and the light with the power of 17.3 mW was sufficient to pacing the heart.However the normal group and the no-load virus group cannot be captured by light.The result showed that the illumination power required for optogenetics pacing of the heart was obviously dissimilar,and B was easier to be paced which may related to the expression of ChR2.The record of MAP showed that the time to peak and the action potential duration APD 10,30,50,70 produced by light pulse was shorter than electric stimulation.Conclusion Optical pacing of the heart by optogenetics is feasible,and it is associated with not only illumination power but also the expression of light-sensitive protein.
    • 刘盈盈; 李勤
    • 摘要: 目的:研究心肌缺血-再灌注所致单相动作电位振幅(MAPA)改变与心肌损伤程度的相关性.方法:选择新西兰家兔作为实验动物并随机分为对照组和缺血再灌注组(I/R组),建立心肌缺血再灌注损伤模型后分离心脏并在Langendorff灌流系统内测定心肌内膜层、中膜层、外膜层的MAPA;另取血清标本及心肌组织,测定心肌损伤分子的含量.结果:I/R组动物心肌内膜层、中膜层、外膜层的MA-PA水平均显著高低于对照组;I/R组动物血清中CK-MB、cTnI、cTnT、MDA的含量以及心肌组织中Bax、Caspase-3、Caspase-9的mRNA表达量均显著高于对照组且与心肌内膜层、中膜层、外膜层的MAPA水平呈负相关,血清中SOD、GSH-Px、HO-1的含量以及心肌组织中Bcl-2、Bcl-xL的mRNA表达量显著低于对照组且与心肌内膜层、中膜层、外膜层的MAPA水平呈正相关.结论:心肌缺血-再灌注会引起MAPA降低且与心肌氧化应激损伤及凋亡密切相关.%Objective:To study the correlation between myocardial ischemia - reperfusion-induced monophasic action potential amplitude (MAPA)change and myocardial damage.Methods:New Zealand rabbits were selected as experimental ani-mals and randomly divided into control group and ischemia-reperfusion group (I/R group),myocardial ischemia-reperfusion injury models were established,then the heart was separated and the MAPA of myocardial intima layer,media layer and outer layer were determined in Langendorff perfusion system;serum samples and myocardial tissue were collected to determine the contents of myocardial injury molecules.Results:MAPA levels of myocardial intima layer,media layer and outer layer of I/R group were significantly lower than those of control group;CK-MB,cTnI,cTnT and MDA contents in serum as well as Bax, Caspase-3 and Caspase-9 mRNA expression in myocardial tissue of I/R group were significantly higher than those of control group and negatively correlated with MAPA levels of myocardial intima layer,media layer and outer layer while SOD,GSH-Px and HO-1 contents in serum as well as Bcl-2 and Bcl-xL mRNA expression in myocardial tissue were significantly lower than those of control group and positively correlated with MAPA levels of myocardial intima layer,media layer and outer layer.Con-clusion:Myocardial ischemia-reperfusion can induce the decrease of MAPA and is closely related to myocardial oxidative stress injury and apoptosis.
    • 杨淑红; 曹红; 胡河; 陈玉婷; 徐辉文
    • 摘要: Objective:To investigate effects of valeriana officinalis L extract (VOL)on correlated electrophys-iological parameters of ventricular arrhythmias induced by congestive heart failure (CHF)in rabbits.Method:The male New Zealand rabbits (n=30)were divide into control,CHF and CHF+VOL (VOL)groups.The CHF mod-els were induced by injection isoproterenol (0.3mg/Kg/d for 3 weeks),and control rabbits were injected 0.9%NaCl with same ways.The VOL group rabbits were injected 50mg/L VOL.The main cardioelectrophysiological pa-rameters such as RMP,APA,Maxdv/dt and APD10-90 ,as well as basic cycle length (BCL),rate and time of induced arrhythmias by recording monophasic action potential (MAP)with Burst-pacing in rabbits in vivo with 50mg/L VOL administration.The L-type calcium current (ICa-L )was recorded via whole-cell patch clamp technique in enzy-matically dissociated single rabbit ventricular myocytes.Results:Compared with control group,RMP,APA and Maxdv/dt were significantly lowered,as well as APD10-90 were notably lingered in CHF rabbit (P of all <0.01,re-spectively).Compared with CHF group,VOL could significantlyincrease RMP,APA and Vmax ,as well shorten APD10-90 inVOL group in vivo (P of all <0.01,respectively).Compared with control group,BCL and persistence time inducing ventricular arrhythmias were significantly lengthened,and occurrence of ventricular arrhythmias were obviously increased in CHF group (P of all <0.01,respectively).However,VOL could obviously shorten BCL and persistence time of ventricular arrhythmias,and decrease rate of inducibility of ventricular arrhythmias with burst-pacing in VOL group in vivo (P of all <0.01,respectively).VOL could markedly increase the current densi-ty of ICa-L ,and alter down of current-voltage (I-V)relationship curve in different command potential in CHF ventric-ular myocytes.When command potential was +20mV,the current densities of ICa-L were significantly increased from (7.14±0.33)pA/pF in CHF group to (10.86±0.50)pA/pF in VOL group(P<0.01)with VOL administration. Conclusion:VOL could significantly decrease the vulnerability and susceptibility of ventricular arrhythmias induced by CHF,which was contributed to anti-ventricular arrhythmias induced by CHF.It is suggested that the mecha-nisms might attribute to that VOL could markedly increase ICa-L in CHF rabbits.%目的:观察缬草提取物(VOL)对慢性心力衰竭(CHF)致室性心律失常兔电生理指标的影响。方法:雄性新西兰大耳白兔30只,随机平分为三组:正常对照组(Control 组)、CHF 模型组(CHF 组)和 CHF+VOL 组(VOL组)。CHF模型组经耳缘静脉推注异丙肾上腺素(0.3mg/kg/天,连续注射3周)诱导;Control组平行推注等体积生理盐水;VOL组对CHF兔持续静脉滴注浓度为50mg/L的 VOL。记录各组在体心脏左心室单相动作电位(MAP)主要参数静息膜电位(RMP)、动作电位幅度(APA)、动作电位最大上升速率(Maxdv/dt )和动作电位复极化恢复时程(APD10-90);观察各组室性心律失常诱发周长(BCL)、诱发率和心律失常持续时间;分离单个心室肌细胞后,全细胞膜片钳技术记录心室肌细胞 L-型钙电流(ICa-L )及电流-电压(I-V)曲线。结果:与 Control 组比较,CHF 组RMP、APA、Maxdv/dt均明显降低,APD10、APD20、APD50和 APD90均显著延长(P 均<0.01);与 CHF组比较,VOL组RMP、APA、Maxdv/dt均明显增加,各 APD时程均显著缩短(P<0.01)。CHF组诱发室性心律失常 BCL、心律失常诱发率和持续时间均大于Control组(P<0.01);VOL组BCL、心律失常诱发率和持续时间均小于 CHF组(P<0.01)。当钳制电位为+20mV时,与 Control 组比较,CHF组心室肌细胞 ICa-L电流密度由(-12.13±0.99pA/pF)下降为(-7.14±0.33pA/pF)(P<0.01);VOL组则较 CHF组 ICa-L电流密度明显上升(-10.86±0.50pA/pF)(P<0.01),VOL组 ICa-L的 I-V曲线较CHF组明显下移,接近 Control 组。结论:VOL 能显著降低 CHF心室肌电生理易损性和室性心律失常易感性,拮抗CHF室性心律失常;其机制可能与 VOL可增加心室肌细胞 ICa-L有关。
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