氯胺酮对离体大鼠心室肌细胞瞬时外向钾电流的影响

目的研究氯胺酮对大鼠心室肌细胞瞬时外向钾电流(Ito)的影响。方法酶解法分离大鼠心室肌细胞,采用全细胞膜片钳技术记录Ito,观察50μmol/L氯胺酮对Ito电流-电压曲线以及不同浓度氯胺酮对Ito的影响,并研究氯胺酮对Ito通道动力学的影响。结果钳制电压-40mV,刺激电压 70mV条件下,临床相关浓度的氯胺酮50μmol/L使Ito的电流峰值降低23·4%(P<0·01),冲洗后,Ito能够完全恢复。5、10、50、100、500、1000、5000μmol/L的氯胺酮抑制Ito呈浓度依赖性,电流抑制率分别为(13·8±9·7)%、(17·5±6·7)%、(23·4±8·8)%、(31·5±6·7)%、(63·3±5·5)%、(79·7±2·7)%、(88·9±4·4)%,其半数有效浓度(IC50)为299μmol/L。100μmol/L的氯胺酮对激活曲线没有影响;使Ito的失活曲线明显右移,半数失活电压(V1/2)在给药前后数值分别为(-28·27±0·20)mV和(-25·34±0·27)mV(P<0·01),斜率因子(k)值分别为(3·23±0·46)mV和(3·40±0·55)mV(P>0·05)。结论氯胺酮可明显阻滞大鼠心室肌的Ito,这是氯胺酮延长大鼠心室肌动作电位的机理之一,同时氯胺酮使Ito的失活曲线右移。     

The Effects of Na~+/Ca~(2+) exchange (NCX) on the Repolarization of Canine Ventricular Myocyte-Potential Arrhythmogenic Effect of NCX during a Mis-matched Repolarization and Relaxation Xiamen Zhongshan Hospital, Xiamen Medical College, Xiamen University

The Effects of Na~+/Ca~(2+) exchange (NCX) on the Repolarization of Canine Ventricular Myocyte-Potential Arrhythmogenic Effect of NCX during a Mis-matched Repolarization and Relaxation Xiamen Zhongshan Hospital, Xiamen Medical College, Xiamen University@巩燕$Visiting scholar of cardiac arrhythmia research institute,university hospital of Oklahoma!U.S.A @王焱 @BELA Szabo$Basic cardiac research laboratory,cardiac arrhythmia research institute,university hospital of Oklahoma!…     

解耦联蛋白在心肌中的表达与心力衰竭

位于心肌线粒体内膜上的解耦联蛋白 (UCPs) ,作为质子通道驱散氧化呼吸时形成的H 梯度 ,使产能转化为产热 ,从而增加呼吸 ,阻止ATP形成 ,并抑制活性氧族的产生 ,最终阻止了心肌细胞的程序性死亡。脂肪酸、寒冷、甲状腺激素、肾上腺素等能调控UCPs的浓度和活性。UCPs在心力衰竭中的作用仍然不清楚 ,有待进一步研究     

哺乳期营养对室间隔心肌细胞发育的影响——游离心肌细胞的形态测量

在心肌细胞分化性生长时期,改变新生鼠的哺乳期营养条件对这些鼠的空间隔心肌细胞将会产生暂时性作用和持久性影响。哺乳期高营养的暂时性作用是增加空间隔心肌细胞的大小和数量;而低营养的暂时性作用则是减慢室间隔心肌细胞的生长。哺乳期高营养的持久性作用是限制室间隔心肌细胞的过度肥大;而低营养则促进成熟鼠的室间隔心肌细胞的过度肥大。     

壳聚糖对豚鼠单一心室肌细胞延迟外向钾电流的作用

研究壳聚糖对豚鼠单一心室肌细胞延迟外向钾电流（Ｉｋ）的作用，从离子通道角度初步春作用机理。应用膜片钳全细胞记录方式，设保持电位为－４０ｍＶ，指令电位为－６０￣＋７０ｍＶ，步阶脉冲１０ｍＶ，刺激频率１Ｈｚ，波宽３００ｍｓ，刺激间隔６ｓ的方波钳制方案。结果表明壳聚糖能抑制Ｉｋ，并具有浓度依赖关系，能抑制豚鼠单一心室肌细胞延迟外向Ｋ＾＋电流。     

Multiple effects of caffeine on calcium current in rat ventricular myocytes

Caffeine exerts a number of different effects on L-type calcium current in rat ventricular myocytes. These include: (1) a slowing of inactivation that is comparable to, but not additive to, that produced by prior treatment of the cells with ryanodine (a selective sarcoplasmic reticulum Ca²⁺ releaser) or high concentrations of intracellular 1,2-bis[2-aminophenoxy]ethane-N,N,N,N-tetraacetic acid (BAPTA) (a fast Ca²⁺ chelator), (2) a stimulation of peak I _Ca that is comparable to, but not additive to that produced by prior treatment with isobutylmethylxanthine (a selective phosphodiesterase inhibitor), and (3) a dose-dependent decrease of peak I _Ca that is not prevented by pretreatment with any of these agents. None of the caffeine actions could be mimicked or prevented by administration of 8-phenyltheophylline, a specific adenosine receptor antagonist. We conclude that only the slowing of I _Ca inactivation is due to caffeine's ability to deplete the sarcoplasmic reticulum of calcium. The stimulatory effect of caffeine on peak I _Ca is probably due to phosphodiesterase inhibition, while caffeine's inhibitory effect on I _Ca is independent of these processes and could be a direct effect on the channel. The multiplicity of caffeine actions independent of its effects on the sarcoplasmic reticulum lead to the conclusion that ryanodine, though slower acting and essentially irreversible, is a more selective agent than caffeine for probing sarcoplasmic reticulum function and its effects on other processes.The experimental part of this work was published during the postdoctoral stay of I. Zahradník in the Department of Physiology and Biophysics, The University of Texas Medical Branch, Galveston, TX 77555, USA     

法乐四联症心肌纤维结构变化与心功能关系研究

目的　探讨法乐四联症心肌纤维肥大的程度对心功能与术后恢复的影响。方法　对 80例法乐四联症患者右室流出道心肌组织切片改变观察及心肌纤维直径测定 ,结合临床术前彩超测定心功能参数以及右心导管测定参数进行分析。结果　心肌纤维肥大程度与心功能指标有一定的关系。一部分四联症病例心肌纤维发生增生肥大 ,肥大的程度对射血分数无影响 (P >0 0 5 ) ,但与心肌每搏量和年龄有十分显著的相关关系 (P <0 0 1) ,并对术后恢复有一定的影响。结论　法乐四联症心肌纤维形态改变随年龄增长而加重 ,提示在条件允许的情况下 ,应尽早手术为宜     

Serum contains a potent factor that decreases β-adrenergic receptor-stimulated L-type Ca2+ current in cardiac myocytes

L-type Ca²⁺ current (I _Ca) was measured in cultured atrial myocytes from hearts of adult guinea-pigs using whole-cell voltage clamp. Potentiation of I _Ca induced by -adrenergic stimulation (isoprenaline 2· 10^–7 M) could be completely antagonized by diluted sera (1100 v/v). Half-maximal inhibition of -receptorstimulated I _Ca occurred at about 11000. Basal I _Ca was not affected by serum. Atropine in a concentration (10^–6M) that completely antagonized the anti-adrenergic effect of acetylcholine (ACh, 2·10^–6 M) did not interfere with the effect of serum. In cells dialysed with cyclic adenosine monophosphate (cAMP)-containing (10^–4 M) pipette solution, potentiated I _Ca was insensitive to both ACh and serum. Preincubation of the myocytes with pertussis toxin almost completely abolished the anti-adrenergic effects of both ACh and serum. The potency of serum was not reduced by dialysis. It is concluded that serum contains a factor which, like ACh, inhibits -receptor-stimulated adenylyl cyclase via G_iprotein.A preliminary report of this work has appeared in abstract form [11]     

The catalytic subunit of cyclic AMP-dependent protein kinase directly inhibits sodium channel activities in guinea-pig ventricular myocytes

We investigated the effects of the purified catalytic subunit (C subunit) of the cAMP-dependent protein kinase (A-kinase) on the cardiac Na⁺ channel currents. Single Na⁺ channel currents in guinea-pig ventricular myocytes were recorded using the patch clamp technique of the inside-out configuration. Application of C subunit decreased the peak average current and slowed the current decay, effects which were caused by decrease in the open probability of Na⁺ channels and increase in the first latency, whereas the unitary current amplitude and mean open times were not affected. We conclude that the cardiac Na⁺ channel is directly modulated by phosphorylation process through A-kinase.     

VEGF真核表达载体的构建及在内皮与心肌细胞内的表达

目的：探讨外源性人VEGF165基因在内皮细胞与心肌细胞内表达的可行性。方法：构建了(vaseular endothelium growth factor,VEGF)与增强型绿色荧光蛋白(enhanced green fluorescent protein，EGFP)基因其表达载体pIRES2—FGFP—VEGF165，以脂质体法转染内皮细胞和心肌细胞，采用荧光显做镜检测内皮细胞与心肌细胞中EGFP的表达，同时利用免疫组织化学方法检测VEGF的表达。结果：成功地构建了真核表达载体pIRES2—EGFP—hVEGF165，采用脂质体法转染内皮细胞与心肌细胞后，经荧光显微镜观察，可见细胞内有EGFP的表达，同时经免疫组化证实有VEGF的表达。结论：采用脂质体法可以成功地将外源性VEGF165基因转染到内皮细胞与心肌细胞中，并进行表达。本研究为今后利用VEGF基因治疗心肌缺血等疾病提供了实验基础。