Activation of the right atrioventricular valve in the avian heart

Using intramural needle electrode, in situ determinations have been made of the moment of activation of the right muscular atrioventricular valve during electrical systole of the heart. In the hen, Gallus domesticus, the electrical activation of the valve was observed 8.8 +/- 1.4 ms (mean QRS duration 25 ms) whereas in the pigeon Columba livia--5 +/- 1 ms (QRS duration 17 ms) after the beginning of ventricular depolarization, i.e. during excitation of the main bulk of the myocardium of the free wall of the right ventricle.     

去甲肾上腺素引起蟾蜍背根神经节神经细胞膜电位变化的离子机制

本文应用细胞内记录方法,对去甲肾上腺素(NA)引起蟾蜍背根神经节(DRG)神经细胞膜电位去极化或超极化反应时的膜电导及翻转电位值进行了测量,并观察了钾和钙离子通道阻断剂灌流DRG对NA引起膜电位反应的影响。当NA引起去极化反应时,15个细胞的膜电导减小32.6％。少数细胞膜电导开始增加,继而减小(n=4)。NA超极化反应时膜电导增加13.2％(n=8)。NA去极化反应的翻转电位值为-88.5±0.9mV((?)±SE,n=4),NA超极化反应在膜电位处于-89至-92mV时消失。 钾通道阻断剂四乙铵可使NA去极化幅值增加73.7±11.9％((?)±SE,n=7),并使NA超极化幅值减小40.5％(n=4)。细胞内注入氯化铯使苯肾上腺素去极化幅值增加34.5％(n=4)。钙通道阻断剂氯化锰使NA去极化及超极化反应分别减小50.5±9.9％((?)±SE,n=10)和89.5±4.9％((?)±SE,n=7)。结果提示,NA引起DRG神经细胞膜电位的去极化或超极化反应,可能与膜的钾及钙通道活动的改变有关。     

乙酰胆碱对豚鼠心房肌和心室肌的动作电位和收缩力的不同作用

实验采用标准玻璃微电极细胞内记录技术记录心肌细胞动作电位（action potential,AP）、肌力换能器记录心肌收缩力（force contraction,Fc）,研究乙酰胆碱（acetylcholine,ACh）对离体豚鼠心房肌、心室肌的作用。结果表明,10μmol/L ACh可缩短心房肌、心室肌动作电位的时程（action potential duration,APD）。心房肌APD在给药前后分别为208.57±36.05ms及101.78±14.41ms（n=6,P<0.01）,心室肌APD在给药前后分别为286.73±36.11ms及265.16±30.06 ms（n=6,P<0.01）。心房肌动作电位的幅度（action potential amplitude,APA）也降低,给药前后分别为88.00±9.35 mV及62.62±20.50 mV（n=6,P<0.01）,而心室肌APA无明显变化。ACh还降低心房肌、心室肌的收缩力,心房肌、心室肌Fc的抑制率分别为100％（n=6,P<0.01）和37.57±2.58％（n=6,P<0.01）。ACh对心房肌、心室肌APD和Fc的抑制作用在一定范围内（1nmol/L～100μmol/L）随ACh浓度的增高而增强。用Scott法求出ACh对心房肌、心室肌APD缩短作用的KD值,分别为0.275和0.575μmol/L,对Fc抑制作用的KD值分别为0.135和0.676μmol/L。各浓度下ACh对心房肌效应与心室肌效应作组间t检验,从10nmol/L到0.1mmol/L均有显著的统计学差异。此外,10μmol/L阿托品及20mmol/L     

Sustained release of calcium elicited by membrane depolarization in ryanodine-injected mouse skeletal muscle fibers

The effect of micromolar intracellular levels of ryanodine was tested on the myoplasmic free calcium concentration ([Ca(2+)](i)) measured from a portion of isolated mouse skeletal muscle fibers voltage-clamped at -80 mV. When ryanodine-injected fibers were transiently depolarized to 0 mV, the early decay phase of [Ca(2+)](i) upon membrane repolarization was followed by a steady elevated [Ca(2+)](i) level. This effect could be qualitatively well simulated, assuming that ryanodine binds to release channels that open during depolarization and that ryanodine-bound channels do not close upon repolarization. The amplitude of the postpulse [Ca(2+)](i) elevation depended on the duration of the depolarization, being hardly detectable for pulses shorter than 100 ms, and very prominent for duration pulses of seconds. Within a series of consecutive pulses of the same duration, the effect of ryanodine produced a staircase increase in resting [Ca(2+)](i), the slope of which was approximately twice larger for depolarizations to 0 or +10 mV than to -30 or -20 mV. Overall results are consistent with the "open-locked" state because of ryanodine binding to calcium release channels that open during depolarization. Within the voltage-sensitive range of calcium release, increasing either the amplitude or the duration of the depolarization seems to enhance the fraction of release channels accessible to ryanodine.     

乙酰胆碱对蟾蜍背根神经节神经元膜电位的影响及离子机制

在离体灌流的蟾蜍背根神经节(DRG)标本上,用微电极进行胞内记录。在73个神经元中,依神经纤维的传导速度将神经元分为 A 型及 C 型,其中 A 型细胞67个,C 型6个,静息膜电位为-67.5±1.3mV((?)±SE)。当加4×10~(-4)—6×10~(-4)mol/L 乙酰胆碱(ACh),可观察到如下四种膜电位变化:1.超极化:幅值9.1±3.0mV((?)±SE,n=23);(2)去极化:幅值12.9±2.2mV((?)+SE,n=20);(3)双相反应(n=24):先超极化,后去极化,超极化幅值8.0±2.4mV((?)+SE),去极化幅值10.9±3.1mV((?)±SE);(4)无反应(n=6)。用阿托品(1.3×10~(-5)mol/L,n=23),或同时应用筒箭毒与六甲双铵(浓度均为1.4×10~(-5)mol/L,n=8)灌流,能分别阻断 ACh 引起的膜的超极化或去极化。ACh 引起超极化反应时膜电导平均增加13.8%,翻转电位值大约-96mV。四乙铵(TEA,20mmol/L)能使 ACh 的去极化幅值增加48.2±3.2%((?)±SE,n=6),超极化幅值减小79.4±4.3%((?)±SE,n=8)。MnCl_2(4mmol/L)使 ACh 的去极化及超极化幅值分别减小54.2±7.2%((?)±SE,n=5)及69.2±6.4%((?)±SE,n=14)。以上结果提示:ACh 引起的 DRG 神经细胞膜去极化反应由 N 型乙酰胆碱受体介导,而超极化反应由 Μ 型乙酰胆碱受体介导,前者可能包含了多种离子电导的改变,后者则可能与钾电导增加有关。     

Properties of aconitine-modified sodium channels in single cells of mouse ventricular myocardium

Effects of the plant alkaloid Aconitine on the kinetics of sodium channels were studied in enzymatically isolated single cells of the mouse ventricular myocardium. Aconitine (1 mumol/l) induced a prolongation of the 90% repolarization of action potentials from 52.4 +/- 3.7 ms to 217.0 +/- 12.5 ms. Delayed terminal repolarization and oscillatory afterpotentials preceded spontaneous activity with high frequencies. Peak sodium currents were diminished from 28.0 +/- 9.0 to 14.0 +/- 6.0 nA. The reversal potential of the sodium current was shifted from 16.0 +/- 11.0 to -8.0 +/- 6.0 mV (52.5 mmol/l extracellular sodium concentration) suggesting a decreased selectivity of the Aconitine-modified Na channels. The m-affinity-curves were shifted 31 mV towards more negative potentials at a constant slope. The h affinity-curves were shifted in the same direction by 13 mV. The slope parameter of the h affinity-voltage relationship was enlarged from 9.1 +/- 2.2 mV to 15.6 +/- 4.4 mV. Shifts in m affinity and h affinity resulted in an increased "window". The alkaloid modified channels inactivated extremely slowly at potentials negative to -40 mV, but showed a fast and complete inactivation at potentials positive to -40 mV.     

Basic electrophysiological parameters and frequency sensitivity of the ventricular myocardium of human embryos

The basic electrophysiological manifestations of the ventricular myocardium of twelve 7- to 12-week human embryos were measured with a glass electrode and a programmed stimulation technique. The resting membrane potential value was 79.37 +/- 0.34 mV and the overshoot 32.7 +/- 0.57 mV; the action potential (AP) duration at 1 Hz stimulation frequency was 120.0 +/- 5.7 ms at AP plateau phase levels and 258 +/- 17 ms at the level corresponding to 95% repolarization. The duration of the AP was a function of the stimulation frequency. i.e. it altered in correlation to the stimulation programme fully developed frequency sensitivity). In stimulation with different frequencies the duration of the steady state AP was in an inverse relation to the stimulation frequency, the maximum changes being found in the terminal repolarization zone. An interpolated extrasystole mainly affected the duration of the plateau phase.     

Termination of atrial flutter by directed transesophageal atrial pacing during transesophageal echocardiography.

INTRODUCTION: The purpose of this study was to evaluate termination of atrial flutter (AFL) by directed rapid transesophageal atrial pacing (TAP) with and without simultaneous transesophageal echocardiography (TEE) performed using a novel TEE tube electrode. MATERIALS AND METHODS, AND RESULTS: A total of 16 AFL patients (age 63+/-12 years; 13 males) with mean AFL cycle length of 224+/-24 ms (n=12) and mean ventricular cycle length of 448+/-47 ms (n=12) were analyzed using either an esophageal TO electrode (n=10) or a novel TEE tube electrode consisting of a tube with four hemispherical electrodes that is pulled over the echo probe (n=6). AFL could be terminated by directed rapid TAP using an esophageal TO electrode, leading to induction of atrial fibrillation (AF) (n=6), induction of AF and spontaneous conversion to sinus rhythm (SR) (n=3), and with conversion to SR (n=1). AFL could also be terminated by directed rapid TAP using the TEE tube electrode, with induction of AF (n=3) or induction of AF and spontaneous conversion to SR (n=3). CONCLUSION: AFL can be terminated by directed rapid TAP with hemispherical electrodes with and without simultaneous TEE. TAP with the directed TEE tube electrode is a safe, simple, and useful method for terminating AFL.     

血小板活化因子对豚鼠心室肌细胞动作电位和钾通道的影响

应用全细胞膜片钳技术研究了血小板活化因子(platelet activatingfactor,PAF)对豚鼠心室肌细胞动作电位和钾电流的影响.结果发现,当电极内液ATP浓度为5 mmol/L(模拟正常条件)时,1 μmol/L PAF使APD90由对照的225.8±23.3 ms延长至352.8±29.8ms(n=5,P＜0.05);使IK尾电流在指令电压 30 mV由对照的173.5±16.7 pA降至152.1±11.5 pA(P＜0.05,n=4);使Ikl在指令电压为-120 mV时由对照组的-6.1±1.3 nA降至-5.6±1.1 nA(P＜0.05,n=5);但PAF在生理膜电位范围(-90mV～ 20mV)对IK1没有影响.当电极内液ATP浓度为0mmol/L时,IK·ATP开放(模拟缺血条件),1 μmol/LPAF却显著缩短APD90,由对照的153±24.6 ms缩短至88.2±19.4 ms(n=5,P＜0.01).而用1 μmol/L格列本脲(IK·ATP的特异阻断剂)预处理后,恢复了PAF可显著延长动作电位时程的作用.结果提示,PAF可能扩大缺血心肌和正常心肌细胞动作电位时程的不均一性,是缺血/再灌注性心律失常发生的重要原因.     

Ventricular automaticity induced by bromobenzoyl-methyladamantylamine (BMA) in different membrane potential ranges in guinea pig heart

The electrophysiological effects of bromobenzoyl - methyladamantylamine ( BMA ) were investigated in isolated electrically driven right ventricular papillary muscles of guinea pigs using conventional glass-microelectrode technique. BMA markedly increased the action potential duration, depolarized the membrane, reduced the maximum rate of depolarization (Vmax) and induced pacemaker-like action potentials. In ventricular myocardium depolarized partially (up to --40 mV) by incubation with 26 mM K+-Krebs solution, BMA induced slow action potentials. In these preparations, BMA was also able to evoke automaticity. Since the pacemaker activity occurring in the voltage range of --90 mV to --60 mV has been attributed to the deactivation of a pacemaker K+ current labelled IK2, and that occurring in the plateau range (from --40 mV to +10 mV) has been attributed to the deactivation of an outward plateau K+ current labelled IX1 , it can be concluded that BMA may inhibit both IK2 and IX1 currents.