特异性抗原诱发致敏豚鼠心室乳头肌早期后除极和触发活动的…

采用微电极细胞内记录和电子计算机实时采样技术,研究了特异性抗原对致敏豚鼠心室乳头肌动作电位的影响。特异性抗原激发后,致敏心肌动作电位发生了下列改变：２ｍｉｎ左右ＡＰＤ５０、ＡＰＤ９０明显延长;５ｍｉｎ后,ＡＰＤ５０、ＡＰＤ９０、３期时程明显缩短;２０ｍｉｎ以后,上述改变逐渐恢复。心性过敏反应可诱发早期后除极（发生率５５％）和触发活动,形成快速自发动作电位（发生率５０％）,早期后除极在低频驱动时易于     

特异性抗原诱发致敏豚鼠心室乳头肌早期后除极和触发活动的研究

采用微电极细胞内记录和电子计算机实时采样技术,研究了特异性抗原（卵白蛋白０．２５μｍｏｌ／Ｌ）对致敏豚鼠心室乳头肌动作电位的影响。特异性抗原激发后,致敏心肌动作电位发生了下列改变：２ｍｉｎ左右ＡＰＤ＿（５０）、ＡＰＤ＿（９０）明显延长;５ｍｉｎ后,ＡＰＤ＿（５０）、ＡＰＤ＿（９０）、３期时程明显缩短;２０ｍｉｎ以后,上述改变逐渐恢复。心性过敏反应可诱发早期后除极（发生率５５％）和触发活动,形成快速自发动作电位（发生率４０％）,早期后除极在低频驱动（０．２－１．０Ｈｚ）时易于发生,且在２ｍｉｎ左右多见。结果提示,心性过敏反应诱发的动作电位时程的变化、早期后除极和触发活动,可能和超敏反应时发生的快速自律型心律失常有关。     

缺血对心室浦肯野纤维跨膜电位和起搏离子流的影响

采用细胞内微电极和双微电极电压箝制术观察缺血对绵羊心室浦肯野纤维跨膜电位和起搏离子流（Ｉｆ）的影响。结果：模拟缺血液灌流３０ｍｉｎ,浦肯野纤维最大舒张电位（ＭＤＰ）、动作电位幅度（ＡＰＡ）明显减少;动作电位时程ＡＰＤ５０,ＡＰＤ９０明显缩短（ｎ＝１５Ｐ＜０．０１）;起搏离子流（Ｉｆ）,幅度降低,激活曲线向超极化方向移位,最大激活时间及半最大激活时间延长（ｎ＝１３Ｐ＜０．００１）。上述结果表明：心肌缺血时,心室浦肯野细胞跨膜电位及正常起搏活动不是增强,而是减弱。提示缺血性室性心律失常不是由于正常心室自律活动异常增强引起     

降钙素基因相关肽的心肌电生理作用

应用浮置微电极技术,记录和观察降钙素基因相关肽（ＣＧＲＰ）对家兔正常及缺血心肌电生理反应的影响。实验表明,ＣＧＲＰ能够显著增加心室肌细胞静息电位,提高动作电位幅度。心肌缺血后,ＣＧＲＰ除有上述作用外,尚能明显延长复极化至３０％和５０％（ＡＰＤ＿(３０),ＡＰＤ＿(５０)）的时程,而缩短复极化至１００％（ＡＰＤ＿(１００)）的时程,从而逆转了心肌缺血的ＡＰＤ异常变化。结果表明,ＣＧＲＰ对心肌电活动具有调节作用,对缺血心肌的电生理具有稳定和保护作用。     

抗心律失常药UK－68798对家兔心脏房室结区不同细胞的电生理作用

在离体家兔ＡＶＮ区标本上,用微电极技术研究了Ⅲ类抗心律失常新药ＵＫ－６８７９８对ＡＮ,Ｎ,ＮＨ,Ｈ４种细胞的电生理效应。浓度５×１０－９至５×１０－６ｍｏｌ／Ｌ的ＵＫ－６８７９８对４种细胞的动作电位幅值（ＡＰＡ）、静息膜电位（ＲＰ）皆无影响。对ＡＶＮ的自搏率有剂量依赖性减慢作用,但不改变Ａ－Ｈ传导时间。在５×１０－８－５×１０－６ｍｏｌ／Ｌ剂量范围,此药使动作电位时程（ＡＰＤ５０）和（ＡＰＤ９０）发生剂量依赖性延长。４种细胞中以Ｎ细胞的ＡＰＤ５０和ＡＰＤ９０延长百分率最高。各种细胞ＡＰＤ９０延长百分率的排列次序为Ｎ＜ＡＮ＜Ｈ＜ＮＨ,当浓度为５×１０－６ｍｏｌ／Ｌ时的延长百分率分别为９５±２６％（Ｎ）,７５±２２％（ＡＮ）,６３±２６％（Ｈ）,４６±２６％（ＮＨ）。在ＵＫ－６８７９８的作用下,４种细胞的有效不应期（ＥＲＰ）也发生剂量依赖性延长,但不存在像ＡＰＤ延长百分率那样的差别。此外,４种细胞ＥＲＰ所相当的复极化膜电位未受药物影响,从而避免了由于兴奋性恢复的不均一性,使ＡＶＮ区成为折返性心律失常的发源地．     

组胺对培养新生大鼠心肌细胞自发性搏动及动作电位的影响

以培养大鼠乳鼠心肌细胞为模型,观察组胺对培养心肌细胞自发性搏动频率及动作电位的影响。结果表明：组胺０．１－１０ｕｍｏｌ／Ｌ可以引起剂量依赖性的心肌细胞搏动频率的增快,而且这种效应呈时间依赖性。组胺１０ｕｍｏｌ／Ｌ可以使心肌细胞动作电位的幅度（ＡＰＡ）,最大上升速率（Ｖｍａｘ）及超射（ＯＳ）明显增加,动作电位持续时间（ＡＰＤ５０和ＡＰＤ９０）明显延长,窦性周长（ＳＣＬ）明显缩短。以上结果提示,组胺致     

豚鼠主动脉前庭自发性慢反应电位去极离子流的初步分析

为研究主动脉前庭自发慢反应电位的去极离充性质,利用豚鼠的离体以及心脏,常规玻璃微电极细胞内记录方法和离子通道组断剂,观测最大舒张电位（ＭＤＰ）、０相除极幅度（ＡＰＡ）、０相最大除极速度（Ｖｍａｘ）、４个自动除极速度（ＶＤＤ）、复极５０％（ＡＰＤ５０）和９０％（ＡＰＤ９０）的时间以及自发放电频率（ＲＰＦ）。结果发现：⑴０．５μｍｏｌ／Ｌ尼索地平（Ｎｉｓ）可使该慢电位的ＡＰＡ、Ｖｍａｘ、ＶＤＤ明显减小     

东亚钳蝎蝎毒成分BmK—9及其次级提取物对心肌细胞电活动的影响

培养小鼠的心肌细胞,用微电极胞内引导快反应心肌细胞动作电位。以五项除极化参数ＡＰＡ,ＯＳ,ＭＤＰ,ＴＰ,Ｖｍａｘ和波宽参数ＡＰＤ５０为指标,发现东亚钳蝎蝎毒三级提取物ＢｍＫ－９－（３）、ＢｍＫ－９－（４）、ＢｍＫ－９－（５）３μｇ／ｍｌ使除极有关参数全部减小,而不影响动作电位波宽。表明它们可能是蝎毒中单纯阻滞钠通道的活性成分。     

T—2毒素对心肌细胞电生理特性的影响及硒的保护作用

本实验在培养的Ｗｉｓｔａｒ大鼠乳鼠心肌细胞上观察了Ｔ－２毒素对膜电位活动的影响及硒的保护作用。结果表明,Ｔ－２毒素（０．１,０．５,５．０ｍｇ／Ｌ）使心肌细胞动作电位幅值（ＡＰＡ）、超射（ＯＳ）、阈电位（ＴＰ）、最大舒张电位（ＭＤＰ）及最大除极速率（Ｖｍａｘ）显著降低。使复极化时程（ＡＰＤ１０、ＡＰＤ５０、ＡＰＫ９０）延长;动作电位发放频率（ＡＰＦ）受到明显抑制。提示Ｔ－２毒素能抑制Ｃａ＾２＋、Ｋ     

内皮素和ATP敏感性钾通道介导缺氧所致家兔窦房结起搏细胞的电生理效应

用细胞内微电极技术研究了ＡＴＰ－敏感性钾（Ｋ_（ＡＴＰ））通道和内皮素（ｅｎｄｏｔｈｅｌｉｎ,ＥＴ）在缺氧所致窦房结起搏细胞负性频率中的作用,主要结果如下：（１）缺氧引起窦房结起搏细胞的ＲＰＦ降低和ＡＰＤ缩短,这一效应随时间延长而加重。（２）Ｋ_（ＡＴＰ）通道开放剂ｃｒｏｍａｋａｌｉｍ浓度依赖性地对窦房结起搏细胞有负性频率作用,且明显缩短ＡＰＤ_（５０）。该通道的阻断剂格列苯脲能部分阻断缺氧对起搏细胞的上述效应,表明缺氧效应中有Ｋ_（ＡＴＰ）通道的参与。（３）ＥＴ－１可显著加重缺氧所致的ＲＰＦ降低,使起搏细胞停跳时间前移;而以ＥＴ_Ａ受体阻断剂ＢＱ－１２３预处理窦房结标本后,则能有效地缓解缺氧对起搏细胞的效应,提示内源性ＥＴ－１的释放在缺氧效应中的作用。上述结果表明,缺氧所致起搏细胞的负性频率作用和ＡＰＤ缩短,与Ｋ_（ＡＴＰ）通道的激活和内源性ＥＴ－１的释放有关。     

Correlation of repolarization of ventricular monophasic action potential with ECG in the murine heart

Transgenic mice have become important experimental models in the investigation of mechanisms causing cardiac arrhythmias because of the ability to create strains with alterations in repolarizing membrane currents. It is important to relate alterations in membrane currents in cells to their phenotypic expression on the electrocardiogram (ECG). The murine ECG, however, has unusual characteristics that make interpretation of the phenotypic expression of changes in ventricular repolarization uncertain. The major deflection representing the QRS (referred to as "a") is often followed by a secondary slower deflection ("b") and sometimes a subtle third deflection ("c"). To determine whether the second or third deflections or both represent ventricular repolarization, we recorded the ventricular monophasic action potential (MAP) in open-chest mice and correlated repolarization with the ECG. There was no significant correlation by linear regression, between action potential duration to 50% or 90% repolarization (APD(50) or APD(90)), respectively, of the MAP and either the interval from onset of Q to onset of b (Qb interval) or onset of c (Qc interval). Administration of 4-aminopyridine (4-AP) significantly prolonged APD(50) and APD(90) and the Qb interval, indicating that this deflection on the ECG represents part of ventricular repolarization. After 4-AP, the c wave disappeared, also suggesting that it represents a component of ventricular repolarization. Although it appears that both the b and c waves that follow the Q wave on the ECG represent ventricular repolarization, neither correlates exactly with APD(90) of the MAP. Therefore, an accurate measurement of complete repolarization of the murine ventricle cannot be obtained from the surface ECG.     

神经递质对豚鼠左心室流出道自律细胞电活动的影响

为研究左心室流出道慢反应自律细胞的神经支配和受体分布,本实验采用标准玻璃微电极细胞内记录技术,分别观测了肾上腺素能和胆碱能受体激动剂及相应的受体拮抗剂对离体豚鼠左心室流出道组织自发慢反应电位的影响。观测指标有：最大舒张电位（maximal diastolic potential,MDP）、动作电位幅度（amplitude of action potential,APA）、0相最大去极速度（maximal rate of depolarization,Vmax）、4相自动去极速度（velocity of diastolic depolarization,VDD）、复极50％时间（50％of duration of action potential,APD50）和90％时间（90％ of duration of action potential,APD50）以及自发放电频率（rate of pacemaker firing,RPF）。结果表明：（1）100μmol／L异丙肾上腺素（isoprenaline,Iso）可使RPF和VDD显著加快（P〈0．01）,MDP绝对值和APA显著增大（P〈0．05,P〈0．01）,Vmax加快（P〈0．05）,APD50缩短（P〈0．01）,这些变化均可被5μmol／L心得安拮抗;（2）100μmol／L肾上腺素（epinephrine,E）可使RPF和VDD加快（P＜0．01,P〈0．05）,APA显著增大（P〈0．001）,Vmax加快（P〈0．05）,APD50和APD90缩短（P＜0．05）;（3）100μmol／L去甲肾上腺素（norepinephrine,NE）可使VDD和RPF加快（P＜0．05）,APA显著增大（P〈0．05）,Vmax明显加快（P〈0．05）,APD50缩短（P〈0．05）,这些变化可被100μmol／L酚妥拉明拮抗;（4）10μmol／L ACh可使VDD和RPF减慢（P〈0．05）,APA显著减小（P〈0．01）,APD50缩短（P〈0．05）;ACh对APD50的缩短效应可被10μmol／L阿托品拮抗（P〈0．05）。结果提示：左心室流出道自律细胞膜上可能存在α-肾上腺素能受体（α-adrenergic receptor,α-AR、β-肾上腺素能受体（β-adrenergic receptor,β-AR）以及M型胆碱能受体（muscarinic receptor,MR）,其自律性电活动可能也接受心交感神经和心迷走神经调控。     

迷走神经对家兔在体心脏心室肌细胞跨膜电位的影响

本研究观察了电刺激迷走神经对家兔在体心脏心室肌细胞跨膜电位的作用及钾通道阻滞剂氯化四乙基铵对这一作用的影响。结果表明,在自然心率条件下,迷走神经刺激可使静息电位(RP)、动作电位振幅(APA)和0相最大上升速率(dv/dt)_(max)增加,动作电位时程(APD)缩短。冠脉注射氯化四乙基铵使心室肌细胞复极过程明显延长,迷走神经刺激不再引起 RP、APA 增大,动作电位时程不再缩短,(dv/dt)_(max)反而减小。这些结果提示,迷走神经刺激对正常心室肌细胞跨膜电位的影响可能是通过外向 K~ 流增加引起的。     

在生理温度下降钙素基因相关肽对豚鼠心房肌复极过程的影响

实验应用常规微电极方法研究了在生理温度下 (36 5± 0 5℃ )降钙素基因相关肽 (calcitoningene relatedpeptide ,CGRP)对豚鼠心房肌细胞复极过程的影响及其与钾电流的关系。结果表明 :(1)CGRP(16nmol/L)可拮抗由钾通道阻断剂BaCl2 、4 AP引起的动作电位时间延长。 (2 )CGRP(16nmol/L)能够增加细胞外高钾 (18 5mmol/L)条件下心房肌慢反应动作电位的APA和Vmax,并缩短传导时间。 (3)CGRP(16nmol/L)能减弱甚至消除因并用CsCl (5mmol/L)和无钾灌流液诱发的触发活动。 (4)CGRP对动作电位复极过程的作用因温度条件而异。在生理温度下 ,CGRP(5、16和 5 0nmol/L)能够使动作电位平台抬高 ,缩短动作电位复极化 2 0 %、5 0 %和 90 %时程。其中 ,对动作电位复极化 2 0 %、5 0 %时程的作用呈剂量依赖性。而在室温下 (2 5 5± 2 1℃ ) ,CGRP使动作电位复极化 2 0 %、5 0 %和90 %时程延长。上述结果提示 ,CGRP对心房肌细胞具有多重电生理效应 ,其中生理温度下CGRP对钾电流的促进作用在动作电位的改变中占重要地位 ,今后有必要进一步研究CGRP对各种钾通道的作用     

白藜芦醇甙对大鼠心室乳头状肌动作电位的影响及其离子机制(英文)

有研究表明白藜芦醇甙(polydatin)具有抗缺血性心律失常作用,但其电生理学机制尚未明了。本研究旨在应用细胞内记录和全细胞膜片钳方法,探讨白藜芦醇甙对大鼠心室乳头状肌动作电位的影响及其离子机制。结果显示:(1)白藜芦醇甙(50和100μmol/L)可剂量依赖性地缩短正常乳头状肌动作电位复极化50%时间(APD50)和90%时间(APD90)(P<0.01)。白藜芦醇甙对正常乳头状肌静息电位(resting potential,RP)、动作电位幅值(amplitude of action potential,APA)、超射值(overshoot,OS)和0期最大上升速度(Vmax)无影响(P>0.05)。(2)对部分去极化的乳头状肌,白藜芦醇甙(50μmol/L)不但缩短APD50和APD90,而且还降低动作电位OS、APA和Vmax(P<0.05)。(3)ATP敏感钾通道阻断剂格列本脲(10μmol/L)可部分阻断白藜芦醇甙(50μmol/L)的电生理效应。(4)一氧化氮合酶抑制剂L-NAME(1 mmol/L)对白藜芦醇甙的上述效应无影响。(5)白藜芦醇甙(25、50、75、100μmol/L)可浓度依...     

酒石酸锑钠对家兔心肌细胞电生理特性的影响

家兔20只均分成两组:一组为正常家兔,另一组为酒石酸锑钠(SAT)急性中毒的家兔。分别取出窦房结-心房肌标本。用浮置式微电极引导动作电位,观察SAT对两组标本的影响。SAT在两组标本上均能导致如下改变:起搏细胞动作电位幅值、0相平均去极速率和舒张期去极速率增加,动作电位时程(APD_(25)、APD_(50)、APD_(90))缩短;心房肌细胞动作电位幅值增加,动作电位时程(APD_(25)、APD_(50)、APD_(90))延长;心房肌收缩幅值增加,收缩时程延长,心率增加。还观察到各种类型的心律失常:早搏、逸搏、阵发性心动过速和心动过缓、早发性后除极和迟发性后除极。SAT的上述作用可能与细胞内Ca~(2 )增高有关。我们也观察到:锑剂急性中毒组家兔的上述变化值均小于正常家兔的对应值,我们推测可能与锑剂静脉注射对在体心肌的抑制作用有关。     

Effects of quinidine and lidocaine on action potential and membrane currents of frog ventricles

The effects of quinidine and lidocaine on frog ventricle were studied by using a single sucrose gap voltage clamp technique. In Ca2+-Ringer, quinidine (80 microM) caused slight prolongation of action potential duration (APD50) and significant inhibition of twitch tension. Lidocaine (40 microM) shortened APD50 without significant effect on twitch tension. In tetrodotoxin (TTX)-treated preparations, quinidine caused significant prolongation of APD50 from 529 +/- 19 msec to 597 +/- 11 msec, (n = 9) and inhibition of twitch tension, but lidocaine did not affect APD50 and twitch tension. Under voltage clamp condition, quinidine reduced peak inward current in the absence of TTX, but enhanced peak inward current in the presence of TTX. The steady state outward current was increased by quinidine. Lidocaine didn't affect peak inward current in the absence or in the presence of TTX. Membrane current through the inward rectifier (IK1) was slightly increased by lidocaine, but significantly inhibited by quinidine. The enhancement of peak inward current by quinidine was retarded or reversed in preparation bathed with Sr2+-Ringer. When Ni2+ was added to a preparation bathed in Ca2+-Ringer, an inhibition of calcium inward current and action potential plateau was observed. The spike amplitude of the action potential was, however, unaffected by Ni2+. In this Ni2+-treated preparation, lidocaine (20 microM) caused significant shortening of APD50 without significant effect on action potential amplitude. The shortening of APD50 was associated with a slight increase of steady state outward current. The increase of steady state outward current by lidocaine was absent in the TTX-treated preparation.(ABSTRACT TRUNCATED AT 250 WORDS)     

The effect of NADP+ on cardiomyocyte electrophysiological properties of C57BL/6 and mdx mice

We have studied the influence of NADP⁺ on routine electrocardiography (ECG) in 6-month-old C57BL/6 and mdx mice. The animals were anesthetized by ether before ECG recording. ECG registration was carried out at a speed of 100 mm/s. The first ECG recording was made before intraperitoneal NADP⁺ injection in a dose of 13 or 80 mg/kg. The second ECG recording was made 10 min after NADP⁺ injection. Anesthesia was then terminated. The mice were occasionally anesthetized 45–60 min later, and the third ECG was recorded 1 h after injection of NADP⁺. ECG recording was carried out at a speed of 100 mm/s in standard leads I, II, and III and unipolar leads AvR, AvL, and AvF. Values of standard ECG characteristics, such as the P wave and the intervals PQ, QT, RR, and the QRS complex, were measured in milliseconds in standard lead II. We did not observe any differences between ECG magnitudes of 2- to 3-month-old C57BL/6 and mdx mice during trial experiments. Mice of both strains had a sinus rhythm in their heart rate. The QRS complex in mdx mice had a tendency to be larger than in C57BL/6 mice. Heart rates fluctuated between 722 ± 22 and 681 ± 21 beats per minute. The effect of NADP⁺ was studied in 6-month-old male mice. The increase in the RR interval and the decline in heart rate from 697 ± 21 to 461 ± 23 and 491 ± 28 beats per min for C57BL/6 mice (p < 0.01) and from 722 ± 28 beats per minute to 454 ± 31 beats per min for mdx mice were registered 10 min after NADP⁺ injection at a dose of 80 mg/kg. The increase in the RR interval can be explained by an increase in the QT interval. A statistically significant reduction in the QT interval leading to a diminished RR interval was observed in mdx mice 1 h after NADP⁺ injection. NADP⁺ at a dose of 13 mg/kg did not significantly change the ECG properties in mdx mice. ECG of mdx mice was characterized by negative repolarization of the T wave in 37% of all leads. The amount of leads with negative T-wave repolarization decreased up to 3% 1 h after NADP⁺ injection in dose of 80 mg/kg. The results have shown that cytomembranes of ventricular cardiac myocytes and the degree of oxidative stress are the main targets of the action of NADP⁺ in C57BL/6 and mdx mouse hearts.     

抗心律失常药对豚鼠左心室流出道自律细胞电活动的影响

目的:研究抗心律失常药对豚鼠左心室流出道自律细胞电活动的影响。方法:采用标准玻璃微电极细胞内记录技术,记录并分析了四类抗心律失常药及腺苷对离体豚鼠左心室流出道自发慢反应电位的效应。结果:ⅠA类抗心律失常药1μmol/L奎尼丁可使左心室流出道自发慢反应电位的放电频率(RPF)和4相自动去极速度(VDD)减慢(P0.05),动作电位幅度(APA)降低(P0.05),0相最大去极速度(Vmax)减慢(P0.05),复极50%(APD50)和90%时间(APD90)延长(P0.05);ⅠB类抗心律失常药1μmol/L利多卡因灌流标本后,RPF和VDD减慢(P0.05),最大复极电位(MDP)绝对值和APA减小(P0.05),Vmax减慢(P0.05),APD50和APD90缩短(P0.05);ⅠC类抗心律失常药0.5μmol/L普罗帕酮可使RPF(P0.01)和VDD(P0.05)减慢,APA降低(P0.05),Vmax减慢(P0.01),APD50(P0.01)和APD90(P0.05)延长;Ⅱ类抗心律失常药5μmol/L普萘洛尔可使RPF和VDD减慢(P0.01),MDP绝对值和APA减小(P0.01),Vmax减慢(P0.05),APD50和APD90延长(P0.01);Ⅲ类抗心律失常药1μmol/L胺碘酮可使RPF和VDD减慢(P0.01),APA降低(P0.01),Vmax减慢(P0.05),APD50(P0.01)和APD90(P0.05)延长;Ⅳ类抗心律失常药1μmol/L维拉帕米可使RPF和VDD减慢(P0.01),MDP绝对值和APA减小(P0.05),Vmax减慢(P0.05),APD50和APD90延长(P0.05);50μmol/L腺苷可使RPF和VDD减慢(P0.05),APA降低(P0.05),Vmax减慢(P0.01),APD50和APD90缩短(P0.05)。结论:抗心律失常药均可显著降低左心室流出道组织的自律性,通过改变APD50和APD90影响有效不应期而起到抗心律失常作用。