阿尔及利亚求购制药原料

阿尔及利亚求购制药原料阿尔及利亚一公司求购制药原料（ＰＲＯＤＵＩＴＳＰＡＲＡＰＨＡＲＭＡＴＩＱＵＥＳ）。公司名称：ＣＯＮＤＩＰＨＡＲＭ联系人：ＭＲ．Ｙ．ＫＥＴＦＩ地址：１２９，ＲＵＥＤＩＤＯＵＣＨＥＭＯＵＲＡＤ，１６０００ＡＬＧＥＲＡＬＧＥＲＩＥ电话...     

生物心脏瓣膜钙化前后的应力分析

生物心脏瓣膜钙化前后的应力分析李珏匡震邦（西安交通大学，西安７１００４９）刘维永（西京医院，西安７１００３２）ＳＴＲＥＳＳＡＮＡＬＹＳＩＳＯＦＮＯＲＭＡＬＡＮＤＣＡＬＣＩＦＩＥＤＢＩＯＰＲＯＳＴＨＥＴＩＣＨＥＡＲＴＶＡＬＶＥＳＬｉＪｕｅ，ＫｕａｎｇＺ...     

对两种第三代丙肝试剂检测的不同功能区抗体组份研究

目的　比较第二代和第三代丙肝试剂对丙肝不同功能区抗体的检出能力。方法　用两种第二代抗 Ｈ Ｃ Ｖ Ｅ Ｉ Ａ 试剂（ Ｋ２ 中国制造, Ａ２ 美国制造） 及两种第三代主流试剂（ Ａ３ 德国制造, Ｏ３ 美国制造） 对１２１ 份来源于全国各地的供血员血样进行了检测。结果　该１２１ 份样品经 Ｒ Ｉ Ｂ Ａ Ｈ Ｃ Ｖ３ ．０ 试剂及 Ｐ Ｃ Ｒ 方法确证, 其中４３ 份为阳性样品,７８ 份为阴性样品。两种第二代试剂 Ｋ２ , Ａ２阳性检出符合率为３６／４３ 和３７／４３ , 两种第三代试剂 Ａ３ , Ｏ３ 阳性检出符合率分别为４０／４３ 和３９／４３ 。在４３ 份阳性样品中,２０ 份既含有抗 Ｈ Ｃ Ｖ 核心抗体, 也含有抗 Ｈ Ｃ Ｖ Ｎ Ｓ３ 抗体,用 Ｋ２ , Ａ２ , Ａ３ , Ｏ３ 四种试剂分别检出１８ 、１８ 、１９ 和２０ 份。１４ 份含有抗 Ｈ Ｃ Ｖ Ｎ Ｓ３ 抗体而不含有抗 Ｈ Ｃ Ｖ 核心抗体的样品中,用两种第二代试剂（ Ｋ２ , Ａ２） 分别检出９ 份和１０ 份, 而用两种第三代试剂（ Ａ３ , Ｏ３） 则全部检出。与此相反,９ 份含有抗 Ｈ Ｃ Ｖ 核心抗体而不含抗 Ｈ Ｃ Ｖ Ｎ Ｓ３ 抗体的样品, 用两种第二代试剂（ Ｋ２ , Ａ２）均可检出, 而用两种第三代试剂（ Ａ３ , Ｏ３） 却     

长期糖尿病大鼠心脏β肾上腺素受体及其亚型的改变

目的：观察长期糖尿病大鼠心脏β肾上腺素受体（β－ＡＲ）及其亚型的改变。方法：链脲佐菌素（ＳＴＺ）诱导糖尿病大鼠动物模型,用放射配体结合实验和离体左心房收缩功能实验。结果：糖尿病大鼠心脏β－ＡＲ的最大结合容量下降３４％（Ｐ＜００５）,ＫＤ值不变。ＣＧＰ２０７１２Ａ竞争抑制曲线两位点分析显示β１－和β２－ＡＲ之间比例未发生改变。糖尿病组异丙肾上腺素（ｉｓｏｐｒｏｔｅｒｅｎｏｌ,ＩＳＯ）激动β－ＡＲ介导的最大收缩反应（Ｒｍａｘ）较对照组下降６４％（Ｐ＜００５）,ｐＤ２值显著增大（Ｐ＜００５）,ＣＧＰ２０７１２Ａ阻断β１－ＡＲ后,β２－ＡＲ介导心肌的Ｒｍａｘ不变,而ｐＤ２值显著高于对照组（Ｐ＜００５）;ＩＣＩ１１８５５１阻断β２－ＡＲ后,β１－ＡＲ介导心肌的Ｒｍａｘ显著低于对照组（Ｐ＜００５）,ｐＤ２值与对照组相比无显著差异。结论：长期糖尿病大鼠心脏β－ＡＲ总数明显下调,且β１－和β２－ＡＲ下调的程度相同;β－ＡＲ对ＩＳＯ敏感性的增加,主要是由β２－ＡＲ的改变引起,β－ＡＲ介导的最大收缩反应的降低,是由β１－ＡＲ的改变引起。     

低密度脂蛋白诱导肾小管上皮细胞增殖的信号通路

为观察低密度脂蛋白（ＬＤＬ）对肾上管上皮细胞的影响及涉及的相关信号传导机制，以人近曲行小管上皮细胞系（ＨＫ－２）为对象，采用３Ｈ－ＴｄＲ掺入与细胞计数测定增殖；特异性底物磷酸化法测定细胞外信号调节激酶（Ｅｎｇ）活性；凝胶迁移率法检测转录活化因于（ＡＰ－１）ＤＮＡ结合活性。发现ＬＤＬ１００～５００ｕｇ／ｍＬ刺激ＨＫ－２细胞７２ｈ可促进其增殖：加入ＬＤＬ２５０ｕｇ／ｍＬ后２～６０ｍｉｎ内可使该细胞ＥＲＫ活性明显增加，１０ｍｉｎ时达高峰；不同剂量（５０～５００ｕｇ／ｍＬ）刺激时，ＥＲＫ活性分别较对照组增加１．５６～２．１９倍。ＬＤＬ促使核内转录因子ＡＰ－１结合活性增加。ＥＩＵＬ特异性阻断剂ＰＤ（５０ｕｍｏｌ／Ｌ）可以分别阻断ＬＤＬ刺激的ＨＫ－２细胞ＥＲＫ活性和ＤＮＡ合成。ＲＭＡ阻断ＰＫＣ信号途径后，ＬＤＬ对于ＥＲＫ的活化效应明显减弱。     

生长激素诱导心肌细胞外信号调节酶激活及其上游调控

目的和方法：用生长激素（ＧＨ）刺激培养的新生大鼠心肌细胞,用含ＭＢＰ凝胶分离法测定细胞外信号调节酶（ＥＲＫｓ）活性,用Ｗｈａｔｍａｎ Ｐａｐｅｒ Ｆｉｌｔｅｒ法测定Ｒａｆ－１活性,观察ＧＨ是否激活心肌细胞Ｒａｆ－１－ＥＲＫ级联反应。观察负显突变Ｒａｓ质粒（Ｄ．Ｎ．Ｒａｓ）与ＨＡ－ＥＲＫ２质粒复合转染或有关抑制剂对ＧＨ诱导ＥＲＫ激活的影响。结果：ＧＨ以时间和浓度依赖性方式激活心肌细胞ＥＲＫ１和ＥＲＫ     

太原地区妊娠期感染TORCH的母婴传播及围产儿结局

目的：探讨妊娠妇女ＴＯＲＣＨ感染的母婴间传播及其围产儿不良结局。方法：收集８８６例孕妇的静脉血及其新生儿脐血,用ＥＬＩＳＡ法检测血清ＴＯＲＣＨ－ＩｇＭ抗体和ＨＢｓＡｇ及梅毒血清抗体。结果：孕妇血ＴＯＸ（弓形体）、ＲＶ（风疹病毒）、ＣＭＶ（巨细胞病毒）、ＨＳＶ－２（单纯疱疹病毒２型）ＩｇＭ抗体和ＨＢｓＡｇ,梅毒血清抗体的阳性率分别为０．２％、０．３％、１．７％、１．０％、０．７％、０．１％。２９例孕     

类风湿关节炎患者外周血及滑膜液Ⅹ型胶原反应性B细胞检测及其特异性分析

目的：探讨类风湿关节炎（ＲＡ）患者体内是否存在抗Ⅹ型胶原Ｂ细胞反应。方法：以ＥＬ４ＯＵｒＢＵｒ／ｒＩＬ２／ＰＭＡ作为刺激系统,通过酶联斑点技术检测抗Ⅹ型胶原免疫球蛋白分泌Ｂ细胞（ａｎｔｉＨＣⅩＩＳＣ）频率。结果：２８例ＲＡ患者滑膜中１１例出现ａｎｔｉＨＣⅩＩＳＣ,而对照组骨性关节炎（ＯＡ）患者滑膜液中则未检测到ａｎｔｉＨＣⅩＩＳＣ。ＲＡ患者外周血及滑膜液ＣＤ１９＋及ＣＤ２０＋细胞百分率于刺激前后无明显变化,但ＣＤ５＋Ｂ细胞百分率却明显增加,外周血刺激前后分别为１７．０±６．０,２７．０±９．０,滑膜液分别为８．０±３．２,１６．０±６．０。结论：（１）ＲＡ患者体内存在抗Ⅹ型胶原Ｂ细胞反应,（２）ＣＤ４＋ＥＬ４ＯＵｒＢＵｒ／ｒＩＬ２／ＰＭＡ是激活ＣＤ５＋自身抗体产生Ｂ细胞的有效方法。     

类风湿关节炎患者外周血及滑膜液X型胶原反应性

目的：探讨类风湿关节炎（ＲＡ）患者体内是否存在抗Ｘ型胶原Ｂ细胞反应。方法：以ＥＬ－４ ＯＵ^rＢＵ^r／ｒＩＬ－２／ＰＭＡ作为刺激系统,通过酶联斑点技术检测抗Ｘ型胶原免疫球蛋白分泌Ｂ细胞（ａｎｔｉ－ＨＣＸ ＩＳＣ）频率。结果：２８例ＲＡ患者滑漠中１１例出现ａｎｔｉ－ＨＣＸ ＩＳＣ,而对照组骨性关节炎（ＯＡ）患者滑膜液中则未检测到ａｎｔｉ－ＨＣＸ ＩＳＣ。ＲＡ患者外周血主滑漠液ＣＤ１９^ 及ＣＤ２０^ 细胞     

DEFINITION AND MECHANISM RESEARCH OF NK CELLS AC-TIVATION THROUGH THE CD45 PATHWAY

为鉴定介导ＮＫ细胞激活的表面分子及其作用机制，本研究用一系列粘附分子单抗及配体体外刺激ＮＫ细胞，定量检测ＮＫ细胞ＩＦＮ－γ的分泌；检测了ＮＫ细胞经ＩＬ－２诱导后其异构体的变化及其不同异构体单抗对ＮＫ细胞的刺激作用；以ＣＤ２２α、ＣＤ２２β基因导入Ｂ７８Ｈ１细胞后观察转染细胞对ＮＫ细胞的粘附和刺激效应。结果表明：ＩｇＧ２ａ和ＩｇＧ１亚类ＣＤ４５单抗及其Ｆ（ａｂ）２均可独立刺激ＮＫ细胞释放ＩＦＮ－γ；ＮＫ细胞经ＩＬ－２培养诱导后其表面ＣＤ４５分子异构体的表达呈ＲＯ逐渐增加，而ＲＡ逐渐减少的特征；ＣＤ４５ＲＯ单抗可刺激ＮＫ细胞释放ＩＦＮ－γ；ＣＤ２２α、ＣＤ２２β转染细胞可粘附，但不能刺激ＮＫ细胞激活。结果提示：ＮＫ细胞可经ＣＤ４５ＲＯ途径激活并释放ＩＦＮ－γ，该途径与ＣＤ１６分子无关，ＣＤ４５分子的特异性配体并非既往所报道的ＣＤ２２，尚待进一步鉴定     

KV2.1 K+ channels underlie major voltage-gated K+ outward current in H9c2 myoblasts

The H9c2 clonal cell line derived from embryonic rat ventricle is an in vitro model system for cardiac and skeletal myocytes. We used the whole-cell patch clamp technique to characterize the electrophysiological and pharmacological properties of an outward K+ current (IK(V)) and determined its molecular correlate in H9c2 myoblasts. IK(V) was activated by threshold depolarization to -30 mV, and its current amplitude and rate of activation increased with further depolarizations. IK(V) inactivated slowly with a time constant of 1-2 s, and the V(0.5) for steady-state inactivation was -37.9 +/- 4.6 mV (n = 10). Tetraethylammonium and quinidine suppressed IK(V) with IC(50)'s of 3.7 mM and 11.6 microM, respectively. Using RT-PCR analysis we found that the K(V )2.1 gene is the most abundantly expressed among genes for K(V)1.2, 1.4, 1.5, 2.1, 4.2, and 4.3, and by Western blotting we confirmed the synthesis of the K(V)2.1 alpha-subunit protein. We conclude that IK(V), the predominant voltage-gated outward current in H9c2 myoblasts, flows through the channels comprised of the K(V)2.1-subunit gene product.     

胡椒碱减轻H2O2 引起的兔心房肌细胞内向整流钾电流及超速激活延迟整流钾电流的异常改变

目的: 研究胡椒碱对H₂O₂引起的兔单个心房肌细胞内向整流钾电流(I_K1)及超速激活的延迟整流钾电流(I_KUr)异常的影响。方法: 采用全细胞膜片钳技术分析50 μmol/L H₂O₂对兔单个心房肌细胞I_K1和I_KUr的影响,并研究预先应用7 μmol/L胡椒碱对其的保护作用。结果: 7 μmol/L胡椒碱对正常兔心房肌细胞I_K1和I_KUr及其通道动力学无显著影响。在50 μmol/L H₂O₂作用下,兔心房肌细胞I_K1峰值由(-148.2±16.7)pA/pF降低至(-64.2±9.8)pA/pF (P<0.05),电流-电压曲线上移;而I_KUr峰值由(16.0±2.1)pA/pF降低至(6.1±1.4)pA/pF (P<0.05),电流-电压曲线下移,通道稳态激活曲线右移,通道稳态失活曲线左移及恢复时间减慢,而且存在频率依赖性特征。预先给予7 μmol/L胡椒碱,明显减轻H₂O₂对I_K1和I_KUr的抑制作用(P<0.01),并可减少H₂O₂对超速激活延迟整流钾通道动力学的异常影响。结论: 胡椒碱可减轻氧化应激对心房肌细胞I_K1和I_KUr的影响。     

An investigation of the role played by the E-4031-sensitive (rapid delayed rectifier) potassium current in isolated rabbit atrioventricular nodal and ventricular myocytes

The aim of this study was to measure and compare the profile of rapid delayed rectifier potassium current (IKr) elicited by action potential (AP) waveforms applied to isolated rabbit atrioventricular nodal (AVN) and ventricular myocytes. All measurements were made using whole-cell patch-clamp recordings at 37 degrees C. In AVN myocytes, IKr during voltage steps and slow ramp depolarisations showed "inward rectification" (characteristic for this channel) at positive potentials. The E-4031-sensitive current showed half-maximal activation at -10.8 +/- 0.86 mV, with a slope factor for the activation relation of 6.5 +/- 0.77 mV (n = 7). During AVN APs, IKr rapidly reached a peak after the AP upstroke and remained at similar amplitude until late in AP repolarisation. At the maximum diastolic potential following the AVN AP, a component of IKr remained which decayed during the pacemaker depolarisation, consistent with a role for the current in generating AVN pacemaker activity. In ventricular myocytes IKr was small at the beginning of the AP, and increased slowly during the AP plateau. Measurement of Ba-sensitive-inward rectifier K current (IK1) in ventricular myocytes revealed that IK1 rapidly increased during the final AP repolarisation phase, whilst IKr declined. It is concluded that IKr may participate in both AP repolarisation and the pacemaker depolarisation in AVN cells, whilst in ventricular myocytes, IKr and IK1 participate in controlling early and final AP repolarisation respectively.     

正常大鼠心室肌细胞钠、钙和钾离子流记录和特点

目的研究正常Sprague—Dawley大鼠外膜、中膜和内膜心室肌细胞钠离子电流（INa）、L-型钙离子电流（ICa-L）、瞬时外向钾离子电流（I60）、延迟整流性钾离子电流（IK）、内向整流性钾离子电流（IK1）的特点。方法采用酶消化法获得大鼠外膜、中膜和内膜心室肌细胞,以全细胞膜片钳技术记录心室肌细胞INa、ICa-L、Ito、IK和IK1。结果外膜至内膜心室肌细胞Ito电流密度逐渐减小,而外膜至内膜心室肌细胞INa、ICa-L、IK和IK1的电流密度无差异（P〉0．05）。结论大鼠心室肌细胞Ito存在分层差别,INa、ICa-L、IK和IK1不存在分层差别。     

Inhibition of cardiac delayed rectifier K+ currents by an antisense oligodeoxynucleotide against IsK (minK) and over-expression of IsK mutant D77N in neonatal mouse hearts

The IsK (minK or KCNE1) protein is known to co-assemble with the KvLQT1 (KCNQ1) protein to form a channel underlying the slowly activating delayed rectifier K+ current (IKs). Controversy remains as to whether the IsK protein assembles with ERG (the ether-a-go-go-related gene) products to form or modulate the channel-underlying the rapidly activating delayed rectifier K+ current (IKr). We investigated the effects of antisense oligodeoxynucleotides (AS-ODN) against IsK and its mutant D77N [which underlies a form of long QT syndrome (LQT5) in humans] on the delayed rectifier K+ current (IK) of neonatal mouse ventricular myocytes in primary culture. Patch-clamp experiments on these cells showed that IK consists of IKs and IKr. IK was not recorded from ventricular cells transfected with AS-ODN, while it was recorded from cells transfected with the corresponding sense oligodeoxynucleotides (S-ODN). IK was not recorded from cells transfected with the D77N mutant, and the action potential duration was much longer than in cells transfected with wild-type IsK. Furthermore, HERG could not induce currents in COS-1 cells co-expressed with the D77N mutant and HERG (the human form of ERG). These results indicate that the IsK protein associates with both KvLQT1 and ERG products to modulate IKr and IKs in cardiac myocytes.     

Zacopride增强心肌内向整流钾电流(I_(K1))发挥抗心律失常效应

目的:探讨zacopride对乌头碱、氯化钡药物性心律失常模型的影响和增强心肌内向整流钾电流(IK1)与其抗心律失常的关系。方法:应用全细胞膜片钳技术观测zacopride对大鼠心室肌细胞膜主要离子流及静息膜电位(RMP)、动作电位(AP)和乌头碱所致延迟后除极(DAD)及触发活动(TA)的影响。并观察zacopride对乌头碱(30μg/kg,iv)和氯化钡(4 mg/kg,iv)2种药物性心律失常的影响。结果:0.1-10.0μmol/L zacopride可浓度依赖性激活大鼠心室肌IK1(P0.01),而对INa、Ito、ICa-L等影响动作电位的主要离子流均无显著影响(P0.05);使心室肌细胞膜超极化,动作电位时程(APD)缩短。1.0μmol/L为其最大效应浓度,使IK1内向电流部分(-100mV)增大33.8%,外向电流部分(-60 mV)增大32.4%;RMP由(-81.3±0.9)mV增大至(-87.5±1.7)mV,APD90由(32.48±2.70)ms缩短至(25.61±3.97)ms(P0.01),并有效消除乌头碱所致延迟后除极(DAD)和触发活动(TA)。对于乌头碱、氯化钡所致心律失常,15μg/kg zacopride可使2种心律失常持续时间分别由(57.58±3.21)min、(49.31±2.46)min缩短至(38.25±2.59)min和(30.94±1.73)min(P0.01)。结论:Zacopride对乌头碱、氯化钡药物性心律失常的抑制作用是由其激活心肌细胞IK1进而增大静息膜电位介导的。增强心室肌IK1可能成为抗心律失常的新机制。     

心房颤动患者内向整流性钾电流及Kir2.1 mRNA表达水平的研究

目的：研究心房颤动(房颤，AF)患者心房肌细胞内向整流性钾电流(Ik1)密度及Kir2.1(编码Ik1)mRNA表达水平，初步探讨慢性AF患者心房肌电生理重构机制。方法： 胶原酶Ⅱ两步酶解法分离心房肌细胞，膜片钳全细胞记录法记录离子电流；半定量逆转录聚合酶链反应方法检测心房组织Kir2.1 mRNA表达水平。结果： (1)AF患者心房肌细胞Ik1在超极化状态显著高于窦性心律(SR)组，在膜电位-120 mV时AF组Ik1增加34.04%(P＜0.05)，在-30 mV-+10 mV时其外向电流成分显著增加；(2)以GAPDH为内参标基因，AF组和SR组心房肌Kir2.1 mRNA相对表达量无显著差异(P＜0.05)。结论： AF患者右心房肌细胞Ik1密度在超极化状态显著增加是其电生理重构的重要离子基础之一；AF患者心房肌Kir2.1 mRNA表达水平无显著改变，推测Ik1重构为转录后调节。     

Enhancement of ATP-sensitive potassium current in cat ventricular myocytes by beta-adrenoreceptor stimulation.

1. To address the questions of whether beta-adrenoreceptor stimulation can augment ATP-sensitive potassium current (IK(ATP)), and what the mechanism of such an effect might be, action potentials and whole-cell ionic currents were recorded from adult cat cardiac ventricular myocytes using a conventional whole-cell patch technique. 2. An outwardly directed, ohmic, non-inactivating, glyburide (10 microM)-sensitive current reversing near the reversal potential for potassium (EK) developed slowly (10-25 min) in cells dialysed with an ATP-free pipette (intracellular) solution. During this time, action potential duration markedly decreased while the resting membrane potential hyperpolarized closer to EK. Extended (> 30 min) periods of internal dialysis with ATP-free solution eventually resulted in run-down of the outward current. 3. Externally applied isoprenaline (1 microM) caused a rapidly developing (< or = 60 s), sustained enhancement of a glyburide (10 microM)-sensitive IK(ATP) in cells internally dialysed with ATP-free solution. IK(ATP) remained elevated even after the isoprenaline was removed, and subsequent applications of the beta-agonist failed to increase IK(ATP) further. Half-maximal isoprenaline stimulation of IK(ATP) occurred at a concentration of approximate of 1.5 nM. 4. Pretreatment with propranolol (1 microM) prevented the enhancement of IK(ATP) by a beta-agonist. 5. Isoprenaline-induced IK(ATP) could be blocked by either internal application of GDP-beta-S (2-5 mM) or pretreatment with cholera toxin (1-10 microgram ml-1, > 18 h). Pretreatment with pertussis toxin (1-2 microgram ml-1, > 18 h) did not attenuate the isoprenaline response, whereas internally applied GTP-gamma-S (100 microM) or F- (20 mM) caused IK(ATP) to increase rapidly in the absence of the beta-agonist. 6. Although externally applied forskolin (10 microM) also stimulated IK(ATP), neither 1,9-dideoxyforskolin (10 microM) nor 8-(4-chlorophenylthio)-cAMP (200 microM) had any effect on the current. Internal application of the adenylate cyclase inhibitor 2'-deoxyadenosine-3'-monophosphate (100 microM) resulted in a reduction in the response to isoprenaline, while internal application of a protein kinase A inhibitor (PKI5-24, 22.5 microM) did not attenuate the response to the beta-agonist. 7. IK(ATP) developed slowly during internal dialysis with ATP-free solution.(ABSTRACT TRUNCATED AT 400 WORDS)     

Ascending aortic stenosis selectively increases action potential-induced Ca2+ influx in epicardial myocytes of the rat left ventricle

A decrease of the transient outward potassium current (Ito) has been observed in cardiac hypertrophy and contributes to the altered shape of the action potential (AP) of hypertrophied ventricular myocytes. Since the shape and duration of the ventricular AP are important determinants of the Ca2+ influx during the AP (QCa), we investigated the effect of ascending aortic stenosis (AS) on QCa in endo- and epicardial myocytes of the left ventricular free wall using the AP voltage-clamp technique. In sham-operated animals, QCa was significantly larger in endocardial compared to epicardial myocytes (803 +/- 65 fC pF(-1), n = 27 vs. 167 +/- 32 fC pF(-1), n = 38, P < 0.001). Ascending aortic stenosis significantly increased QCa in epicardial myocytes (368 +/- 54 fC pF(-1), n = 42, P < 0.05), but did not alter QCa in endocardial myocytes (696 +/- 65 fC pF(-1), n = 26). Peak and current-voltage relation of the AP-induced Ca2+ current were unaffected by AS. However, the time course of the current-voltage relation was significantly prolonged in epicardial myocytes of AS animals. Model calculations revealed that the increase in QCa can be ascribed to a prolonged opening of the activation gate, whereas an increase in inactivation prevents an excessive increase in QCa. In conclusion, AS significantly increased AP-induced Ca2+ influx in epicardial but not in endocardial myocytes of the rat left ventricle.     

四逆汤对过氧化氢所致心肌细胞L型钙电流异常的作用

目的探讨四逆汤对氧自由基所致心肌细胞L型钙电流异常的作用。方法用急性酶解法获得单个大鼠心室肌细胞,用标准的全细胞膜片钳技术记录钙通道电流,首先观察5mmol/LH2O2对心肌细胞ICa,L的改变,然后观察预先用四逆汤含药血清孵育30min后5mmol/LH2O2对心肌细胞ICa,L的影响。结果在H2O2作用下,大鼠心室肌细胞ICa,L电流密度增加,电流-电压曲线显著下移,稳态失活曲线明显左移。四逆汤含药血清对离子电流无直接影响,但可以减轻H2O2所引起的稳态失活曲线的异常改变。结论四逆汤可减轻H2O2对心肌细胞钙通道的损伤作用。