压力负荷性心衰小鼠左心室跨壁L-型钙电流的变化

为了观察正常和心衰时心内膜下和心外膜下心肌细胞L-型钙电流(ICa-L)的差别,我们采用主动脉弓狭窄的方法建立小鼠压力超负荷性心衰模型,采用全细胞膜片钳技术记录了正常、主动脉狭窄(band)及假手术对照(sham)组动物左心室游离壁内、外膜下心肌细胞的动作电位时程(action potential duration,APD)和ICa-L。结果显示:(1)与sham组同龄的正常小鼠左心室心内膜下细胞动作电位复极达90％的时程(APD90)为(38．2±6．44)ms,较心外膜下细胞的APD90(15.67±5.31)ms明显延长,二者的比值约为2．5:1;内膜下细胞和外膜下细胞ICa-L密度没有差异,峰电流密度分别为(-2.7±0.49)pA/pF和(-2.54±0．53)pA/pF;(2)Band组内、外膜下细胞的动作电位复极达50％的时程(APD50)、APD90均较sham组显著延长,尤以内膜下细胞延长突出,分别较sham组延长了400％和360％,内、外膜下细胞APD90的比值约为4.2:1;(3)与sham组相比, band组内膜下细胞ICa-L密度显著减小,在+10 mV～+40 mV的4个电压下分别降低了20．2％、21．4％、21.6％和25.7％(P< 0．01),但其激活电位、峰电位和翻转电位没有改变;band组外膜下细胞的ICa-L密度与同期sham组相比无明显变化;band组钙通道激活、失活及复活的动力学特征与sham组相比没有改变。以上结果提示,生理状态下小鼠左心室内、外膜下细胞ICa-L密度不存在明显差别,提示ICa-L与APD跨壁异质性的产生无关;心衰时左心室内、外膜下细胞APD明显延长,以内膜下细胞延长尤为突出,内膜下细胞ICa-L密度明显减少,而外膜下细胞ICa-L密度无明显改变,这种ICa-L的非同步变化在心衰时可能起到对抗APD延长、减少复极离散度的有益作用。     

兔前腔静脉心肌细胞动作电位和非特异性阳离子通道电流特性的研究

作为阵发性房颤的另外一个重要异位兴奋灶的起源部位,与右心房相比,上腔静脉有着独特的电生理学特性．本实验中,通过对兔的前腔静脉观察发现,在不同刺激频率下,前腔静脉心肌细胞APD90明显大于右心房;右心房和前腔静脉心肌细胞均可出现传导阻滞;少数前腔静脉心肌细胞可出现类似起搏细胞的慢反应动作电位与早期后去极化（EAD）．进一步对去极化的电流进行分析时,实验证明,兔右心房和前腔静脉心肌细胞均存在一种特殊的离子通道电流：非特异性阳离子通道电流（nonselective cation current,NNs）;前腔静脉的,NNs峰值电流密度小于右心房;去除细胞外二价阳离子和葡萄糖的灌流液可激动这种INs;在右心房心肌细胞上阻断INs,动作电位时程明显增大;在前腔静脉心肌细胞上激动INs,动作电位时程缩短．结果表明,前腔静脉心肌细胞具有异位激动能力及传导阻滞的条件;兔右心房和前腔静脉心肌细胞的动作电位时程的大小存在显著差异,部分由于氐。在二者之间分布的差异所致;INs的激动剂或阻滞剂可以影响兔右心房或前腔静脉心肌细胞动作电位时程,从而可能影响前腔静脉出现早后去极化和电传导阻滞的发生．兔心房上的INs与TRPC3通道非常近似,它在阵发性心房颤动机制中可能起到一定的作用．     

慢性低氧对豚鼠右室心肌细胞钙、钾电流的影响

采用全细胞膜片箝技术,分别记录并比较正常对照组与慢性低氧组豚鼠单个右室心肌细胞的膜电容、L型钙电流和延迟整流钾电流峰值和电流-电压关系曲线,以探讨慢性低氧对豚鼠右室心肌细胞L型钙电流和延迟整流钾电流的影响。结果表明,上述两组细胞膜电容分别为（155±13．2）pF、（179±14,8）pF,低氧组显著大于正常对照组（P＜0．01）;L型钙电流峰值分别为（1．07±0．21）nA和（0．99±0．17）nA,两组之间无显著差异;在-20mV至＋20mV,慢性低氧组L型钙电流密度较正常对照组显著下降（P＜0．05）。在＋月mV至＋60mV之间,慢性低氧组豚鼠右室心肌细胞延迟整流钾电流幅度均小于正常对照组;在-20mV至＋60mV之间,慢性低氧组豚鼠右室心肌细胞延迟整流钾电流密度明显低于正常对照组。可见慢性低氧能使豚鼠右室心肌细胞膜电容增加,L型钙电流幅度不变,但L型钙电流密度下降;同时慢性低氧降低豚鼠右室心肌细胞延迟整流钾电流幅度和密度。     

心室不同部位起搏对正常犬和扩张型心肌病心力衰竭犬模型在体心肌跨室壁复极离散的影响

实验以正常犬和扩张型心肌病心力衰竭犬(dilated cardiomyopathy congestive heart failure,DCM-CHF)模型为对象、以心肌跨室壁复极离散的相关参数为指标,研究左心室心外膜起搏、双心室起搏(模拟临床上心室再同步治疗的方法)后的心肌电生理特性变化。实验以快速右心室起搏的方法制备DCM-CHF犬模型;正常犬和DCM-CHF犬均经射频消融希氏束制备三度房室传导阻滞模型;采用同步记录犬体表心电图和内膜下、中层、外膜下三层心肌单相动作电位(monophasic action potentials,MAP)的方法,测定不同部位起搏时的QT间期、Tpeak-Tend(Tp-Te)间期和三层心肌的单相动作电位时程(MAP duration,MAPD)、跨室壁复极离散度(transmural dispersion of repolaization,TDR)。结果显示:在正常犬,左室心外膜与双心室起搏后三层心肌的MAPD均延长,同时TDR增大(左室心外膜起搏47.16 ms、双心室起搏37.54 ms、右室心内膜起搏26.75 ms,P<0.001),体表心电图Tp-Te间期的变化与之平行;在DCM-CHF犬较正常犬已表现出中层心肌MAPD延长(276.30 ms vs 257.35 ms,P<0.0001)和TDR(33.8 ms vs 27.58 ms,P=0.002)增大的基础上,左室心外膜参与起搏后仍进一步使三层心肌的MAPD延长和TDR增大。研究结果提示,左室心外膜起搏和双心室起搏后使内膜下、中层     

兔LQT2模型心室肌复极化的性别差异

本研究旨在探讨长QT综合征（long QT syndromes,LQTS）室性心律失常发生的性别差异及其电生理机制,初步观察了不同性别兔LQT2模型左心事原已存在的电生理异质性和心事复极动力学的特征。实验分为3组,上下常组以标准台氏液灌流;LQT2模型组给予含100gmol／L dl-sotalol的台式液灌流;LQT2模型＋低钾组给了含3．0mmol／LKCl、100μmol／L dl-sotalol的台式液灌流。采用冠状动脉旋支灌注兔左室心肌楔形组织块标本,应用浮置玻璃微电极记录技术进行记录。给予基础刺激周长（basic cycle length,BCL）为500、l000和2000ms的S1刺激,同步记录心事肌内膜侧、外膜侧细胞动作电位,并记录跨壁心电图：在BCL为500和1000ms时加用S2程序刺激以记录动作电位时程（action potential duration,APD）恢复曲线。研究发现：在不同刺激频率时,3组实验雌兔心肌细胞的跨壁复极化离散（transmural dispersion of repolarization,TDR）、APD恢复曲线斜率均大于雄兔,有显著性差异（P〈0．05）,并呈频率依赖性;LQT2模型组及LQT2模型＋低钾组雌雄兔TDR、APD恢复曲线斜率较正常组明显增人（P〈0．01）。BCL为1000ms时,LQT2模型组雌兔7例中1例发生尖端扭转性窀性心动过速（torsade de pointes,TdP）;LQT2模型＋低钾组雌兔7例中5例诱发TdP,雄兔7例中2例诱发TdP,有显著性差异（P〈0．05）。结果提示：LQT2模型心肌原已存在的电生理异质性和动态异质性均有明显的性别差异,并≯频率依赖性。存LQT2模型中,TDR以及APD恢复曲线斜率的增大可能是雌性动物较雄性更易发生尖端扭转性心律失常的原因。     

花药壁及其中绒毡层的结构与功能

花药壁及其中绒毡层的结构与功能牛佳田（黑龙江省佳木斯师范专科学校１５４００７）被子植物的花药壁是指雄蕊花药中药室外面由抱子体性质的几层细胞所组成的壁结构。分化至完全的花药壁从外至内依次是表皮、药室内壁（成熟后分成纤维层和唇细胞）、中层、绒毡层。花药壁...     

CRT_D介导室性心动过速的研究进展

心室再同步心脏转复除颤器（CRT）可有效改善心力衰竭（CHF）患者的运动耐量和生活质量,预防猝死,提高生存率,但_DCHFCRTD植入后由于心室激动顺序的改变,使QT间期延长、跨室壁复极离散度（TDR）增加,潜在致室性心律失常风险;且CHF患者通常存在心肌解剖改变,传导的不均一性,也为折返性心动过速的发生提供了维持的机制;而多次电击也可导致肌钙蛋白升高,引起心肌损伤,局部心肌复极离散度增加（DRVR）和QT间期延长,以及电除颤后心肌纤维化和急性细胞损伤,反复室速、室颤也会引起进行性左心功能不全、心肌细胞凋亡、恶化心律失常基质和增加心律失常易感性。CRT_D潜在致室性心律失常作用逐渐引起人们的重视,本文就近年来CRTD致室性心律失常的电生理机制与临床防治对策等做一综述。     

七叶树小孢子发生及雄配子体发育研究

用石蜡切片法观察了七叶树花药的发育过程.结果表明:(1)雄蕊花药四室,花药壁完全分化时,从外到内依次是表皮、药室内壁、中层和绒毡层,花药壁发育为基本型.表皮细胞1层,发育过程中始终存在;药室内壁在花药成熟时形成带状纤维层加厚;幼小花药壁的中层3~4层细胞,在花药发育成熟时退化消失;绒毡层1层细胞,发育类型为分泌型,小孢子母细胞减数分裂时绒毡层开始退化解体,花药成熟完全消失,仅剩1层绒毡层膜.每一花药中有多列雄性孢原细胞,发生于幼小花药表皮下方;(2)小孢子母细胞减数分裂为同时型,四分体多呈正四面体排列;减数分裂过程中,小孢子母细胞外方被胼胝质壁所包被,小孢子形成后胼胝质壁逐渐消失.成熟花粉二细胞型,外形呈圆三角状,具三孔沟.     

严重烫伤延长大鼠心室肌细胞动作电位时程的机制

严重烫伤引起心肌细胞动作电位时程（action potential duration,APD）延长,通过加重烫伤心肌细胞钙紊乱和诱发室性心律失常,促进烫伤心功能障碍的发生,但APD延长的机制尚不清楚。通过制作约40％体表面积（total body surface area,TBSA）Ⅲ度烫伤大鼠模型,在伤后12h大鼠心功能明显减弱时分离其心肌细胞,采用膜片钳技术观察心肌细胞APD以及动作电位复极化相关的重要离子通道电流,包括瞬间外向钾电流（transient outward K^＋ current,Ito）,L-型钙电流（L-type Ca^2＋ current,ICa-L）和内向整流钾电流（inward rectifier K^＋ current,IK1）。结果显示,烫伤后12h单个心肌细胞APD明显延长,APD50和APD90在烫伤组分别为（46．02±3．78）ms、（123．24±12．48）ms（n=19）,明显长于对照组的（23．28±4．85）ms、（72．12±3．57）ms（n=17）（P〈0．01）。烫伤引起,Ito电流密度降低,＋60 mV下烫伤组的电流密度（20．39±1．98）pA／pF（n=25）明显低于对照组的（34．15±3．78）pA／pF（n=20,P〈0．01）;烫伤组在-120至-80mV电压刺激下所产生的IK1电流密度显著低于对照组：而两组之间ICa-L电流密度、电压依赖性的激活和失活无显著性差异。结果提示,烫伤引起心肌细胞APD延长的机制与瞬间外向钾通道和内向整流钾通道功能下调有关。     

HOE642对减轻缺氧／复氧致未成熟兔心肌细胞内钙超载的作用

目的观察Na+/H+交换抑制剂HOE642（Cariporide）对缺氧／再复氧前后未成熟兔心肌细胞内游离钙离子浓度(［Ca2+］i）的影响,探讨HOE642对未成熟心肌保护机制。方法6枚新西兰幼兔心脏,用酶解法分离成单个未成熟兔心肌细胞悬液,每份细胞悬液均随机分为基础组、对照组和实验组,基础组未经缺氧直接测量细胞内Ca2+及心肌酶含量（CK、LDH）,而后两组均经受缺氧60min,再复氧30min后测量,其中实验组于缺氧时加入HOE642（1μmol／L）。用Flou-3／AM标记,激光扫描共聚焦显微镜测定单个未成熟免心肌细胞内游离钙浓度。另测定三组心肌细胞悬液中心肌酶含量（CK、LDH）。结果缺氧／再复氧后对照组未成熟兔心肌细胞内［Ca2+］i（2814±236/1375±102）及心肌酶漏出量明显高于缺氧前基础值(P＜0.01);再复氧后HOE642处理组心肌细胞内［Ca2+］i较缺氧前基础值增加不显著（1446±128/1375±102,P>0.05);而较未用药对照组明显减少（1446±128／2814±236,P<0.01）。而HOE642处理组细胞悬液心肌酶漏出量较基础值有所增加,但其相差不显著,而较对照组有心肌酶漏出量明显减少,两者相差非常显著（P＜0．01）。说明HOE642对缺氧／再复氧后未成熟兔心肌细胞内游离钙超载具有明显的抑制作用。结论HOE642对未成熟心肌的保护机制可能是抑制心肌细胞内游离钙超载引起的心肌缺血／再灌注损伤。     

Electrophysiological response of rat ventricular myocytes to acidosis

The effects of acidosis on the action potential, resting potential, L-type Ca(2+) (I(Ca)), inward rectifier potassium (I(K1)), delayed rectifier potassium (I(K)), steady-state (I(SS)), and inwardly rectifying chloride (I(Cl,ir)) currents of rat subepicardial (Epi) and subendocardial (Endo) ventricular myocytes were investigated using the patch-clamp technique. Action potential duration was shorter in Epi than in Endo cells. Acidosis (extracellular pH decreased from 7.4 to 6.5) depolarized the resting membrane potential and prolonged the time for 50% repolarization of the action potential in Epi and Endo cells, although the prolongation was larger in Endo cells. At control pH, I(Ca), I(K1), and I(SS) were not significantly different in Epi and Endo cells, but I(K) was larger in Epi cells. Acidosis did not alter I(Ca), I(K1), or I(K) but decreased I(SS); this decrease was larger in Endo cells. It is suggested that the acidosis-induced decrease in I(SS) underlies the prolongation of the action potential. I(Cl,ir) at control pH was Cd(2+) sensitive but 4,4'-disothiocyanato-stilbene-2,2'-disulfonic acid resistant. Acidosis increased I(Cl,ir); it is suggested that the acidosis-induced increase in I(Cl,ir) underlies the depolarization of the resting membrane potential.     

Functionally distinct sodium channels in ventricular epicardial and endocardial cells contribute to a greater sensitivity of the epicardium to electrical depression

A greater depression of the action potential (AP) of the ventricular epicardium (Epi) versus endocardium (Endo) is readily observed in experimental models of acute ischemia and Brugada syndrome. Endo and Epi differences in transient outward K(+) current and/or ATP-sensitive K(+) channel current are believed to contribute to the differential response. The present study tested the hypothesis that the greater sensitivity of Epi is due in part to its functionally distinct early fast Na(+) current (I(Na)). APs were recorded from isolated Epi and Endo tissue slices and coronary-perfused wedge preparations before and after exposures to elevated extracellular K(+) concentration ([K(+)](o); 6-12 mM). I(Na) was recorded from Epi and Endo myocytes using whole cell patch-clamp techniques. In tissue slices, increasing [K(+)](o) to 12 mM reduced V(max) to 51.1 +/- 5.3% and 26.8 +/- 9.6% of control in Endo (n = 9) and Epi (n = 14), respectively (P < 0.05). In wedge preparations (n = 12), the increase in [K(+)](o) caused selective depression of Epi APs and transmural conduction slowing and block. I(Na) density was not significantly different between Epi (n = 14) and Endo (n = 15) cells, but Epi cells displayed a more negative half-inactivation voltage [-83.6 +/- 0.1 and -75.5 +/- 0.3 mV for Epi (n = 16) and Endo (n = 16), respectively, P < 0.05]. Our data suggest that reduced I(Na) availability in ventricular Epi may contribute to its greater sensitivity to electrical depression and thus may contribute to the R-ST segment changes observed under a variety of clinical conditions including acute myocardial ischemia, severe hyperkalemia, and Brugada syndrome.     

Altered spatial calcium regulation enhances electrical heterogeneity in the failing canine left ventricle: implications for electrical instability

Myocytes across the left ventricular (LV) wall of the mammalian heart are known to exhibit heterogeneity of electrophysiological properties; however, the transmural variation of cellular electrophysiology and Ca(2+) homeostasis in the failing LV is incompletely understood. We studied action potentials (APs), the L-type calcium (Ca(2+)) current (I(Ca,L)), and intracellular Ca(2+) transients ([Ca(2+)](i)) of subendocardial (Endo), midmyocardial (Mid), and subepicardial (Epi) tissue layers in the canine normal and tachycardia pacing-induced failing left ventricles. Heart failure (HF) was associated with significant prolongation of the AP duration in Mid myocytes. There were no differences in I(Ca,L) density in normal Endo, Mid, and Epi myocytes, whereas in the failing heart, I(Ca,L) density was downregulated by 45% and 26% (at +10 mV) in Endo and Mid myocytes, respectively. The rates of sarcoplasmic reticulum (SR) Ca(2+) release and decay of the [Ca(2+)](i) were slowed, and the amplitude of the [Ca(2+)](i) was depressed in Endo and Epi myocytes isolated from failing, compared with normal, hearts. Experiments in sodium (Na(+))-free solutions showed that Epi and Mid myocytes of the failing ventricle exhibit a greater reliance on the Na(+)-Ca(2+) exchanger to remove cytosolic Ca(2+) than myocytes isolated from normal hearts. Simulation studies in Endo, Mid, and Epi canine myocytes demonstrate the importance of L-type current density and SR Ca(2+) uptake in modulating the potentially arrhythmogenic repolarization in HF. In conclusion, these results demonstrate that spatially heterogeneous decreases in I(Ca,L) and defective cytosolic Ca(2+) removal contribute to the altered [Ca(2+)](i) and AP profiles across the canine failing LV. These distinct electrophysiological features in myocytes from a failing heart contribute to a characteristic electrogram arising from increased dispersion of refractoriness across the LV, which may result in significant arrhythmogenic sequellae.     

Regional differences in effects of exercise training on contractile and biochemical properties of rat cardiac myocytes.

Myocardial function is enhanced by endurance exercise training, but the cellular mechanisms underlying this improved function remain unclear. A number of studies have shown that the characteristics of cardiac myocytes vary across the width of the ventricular wall. We have previously shown that endurance exercise training alters the Ca2+ sensitivity of tension as well as contractile protein isoform expression in rat cardiac myocytes. We tested the hypothesis that these effects of training are not uniform across the ventricular wall but are more pronounced in the subendocardial (Endo) region of the myocardium. Female Sprague-Dawley rats were divided into sedentary control (C) and exercise trained (T) groups. T rats underwent 11 wk of progressive treadmill exercise. Myocytes were isolated from the Endo region of the myocardium and from the subepicardial (Epi) region of both T and C hearts. We found an increase in the Ca2+ sensitivity of tension in T cells compared with C cells, but this difference was larger in the Endo cells than in the Epi cells. In addition, we found a training-induced increase in atrial myosin light chain 1 (aMLC1) expression that was larger in the Endo compared with Epi samples. We conclude that effects of exercise training on myocyte contractile and biochemical properties are greater in myocytes from the Endo region of the myocardium than those from the Epi region. In addition, these results provide evidence that the increase in aMLC1 expression may be responsible for some of the training-induced increase in myocyte Ca2+ sensitivity of tension.     

Targeting intracellular calcium cycling in catecholaminergic polymorphic ventricular tachycardia: a theoretical investigation

Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a malignant arrhythmogenic disorder linked to mutations in the cardiac ryanodine receptor (RyR2) and calsequestrin, predisposing the young to syncope and cardiac arrest. To define the role of β-adrenergic stimulation (BAS) and to identify potential therapeutic targeted sites relating to intracellular calcium cycling, we used a Luo-Rudy dynamic ventricular myocyte model incorporated with interacting Markov models of the L-type Ca(2+) channel (I(Ca,L)) and RyR2 to simulate the heterozygous state of mouse RyR2 R4496C mutation (RyR2(R4496C+/-)) comparable with CPVT patients with RyR2 R4497C mutation. Characteristically, in simulated cells, pacing at 4 Hz or faster or pacing at 2 Hz under BAS with effects equivalent to those of isoproterenol at ≥ 0.1 μM could readily induce delayed afterdepolarizations (DADs) and DAD-mediated triggered activity (TA) in RyR2(R4496C+/-) but not in the wild-type via enhancing both I(Ca,L) and sarcoplasmic reticulum (SR) Ca(2+) ATPase (I(UP)). Moreover, with the use of steady state values of isolated endocardial (Endo), mid-myocardial (M), and epicardial (Epi) cells as initial data for conducting single cell and one-dimensional strand studies, the M cell was more vulnerable for developing DADs and DAD-mediated TA than Endo and Epi cells, and the gap junction coupling represented by diffusion coefficient (D) of ≤ 0.000766*98 cm(2)/ms was required for generating DAD-mediated TA in RyR2(R4496C+/-). Whereas individual reduction of Ca(2+) release channel of SR and Na-Ca exchanger up to 50% was ineffective, 30% or more reduction of either I(Ca,L) or I(UP) could totally suppress the inducibility of arrhythmia under BAS. Of note, 15% reduction of both I(Ca,L) and I(UP) exerted a synergistic antiarrhythmic efficacy. Findings of this model study confirm that BAS facilitates induction of ventricular tachyarrhythmias via its action on intracellular Ca(2+) cycling and a pharmacological regimen capable of reducing I(Ca,L) could be an effective adjunctive to β-adrenergic blockers for suppressing ventricular tachyarrhythmias during CPVT.     

The contribution of ventricular apicobasal and transmural repolarization patterns to the development of the T wave body surface potentials in frogs (Rana temporaria) and pike (Esox lucius)

The study aimed at the simultaneous determination of the transmural and apicobasal differences in the repolarization timing and the comparison of the contributions of these two repolarization gradients to the development of the body surface T wave potentials in animals with the single heart ventricle (fishes and amphibians). Unipolar potentials were measured on the body surface, epicardium and in the intramural (subepicardial, Epi; midmyocardial; and subendocardial, Endo) ventricular layers of 9 pike and 8 frogs. Activation times, repolarization times and activation-recovery intervals were determined. A transmural gradient in repolarization durations in frogs (Endo>Epi, P<0.024) corresponds to the gradient in repolarization times. No significant transmural difference in repolarization duration is observed in pike that produces a repolarization sequence from Endo to Epi (Endo相似文献   

Coronary sinus occlusion enhances coronary collateral flow and reduces subendocardial ischemia

On the hypothesis that coronary sinus occlusion (CSO) may reduce myocardial ischemia, we examined the effects of CSO on coronary collateral blood flow and on the distribution of regional myocardial blood flow (RMBF) in dogs. Thirty-eight anesthetized dogs underwent occlusion of the left anterior descending coronary artery with or without CSO and intact vasomotor tone. We measured RMBF and intramyocardial pressure (IMP) in the subendocardium (Endo) and subepicardium (Epi) separately. With intact vasomotor tone, CSO during ischemia significantly increased RMBF in the ischemic region (IR), particularly in Endo from 0.17 +/- 0.03 to 0.33 +/- 0.05 ml x min(-1) x g(-1) (P < 0.05), and increased the Endo/Epi from 0.59 +/- 0.10 to 1.15 +/- 0.15 (P < 0.01). These effects of CSO were partially abolished by adenosine. However, the Endo/Epi was still increased from 0.90 +/- 0.13 to 2.09 +/- 0.30 (P < 0.01). The changes in RMBF in IR were significantly correlated with the peak CS pressure during CSO. The Endo/Epi of IMP in IR was significantly decreased during CSO. In conclusion, CSO potentially enhances coronary collateral flow, and preserves the ischemic myocardium, especially in Endo.     

兔心室肌细胞电生理异质性研究--缺血对动作电位和钾流的影响

实验用全细胞膜片箝技术,观察正常及缺血条件下,兔心内膜下心室肌细胞与心外膜下心室肌细胞的动作电位和稳态外向钾流及其变化。结果显示：（１）正常条件下,心外膜下心室肌细胞与心内膜下心室肌细胞动作电位形态有差异,心外膜下心室肌细胞动作电位时程（ＡＰＤ）较短,复极１期后有明显的初迹,动作电位形态是“锋和圆顶”,而心内膜下心室肌细胞ＡＰＤ较长,并且没有上述动作电位形态特征。这两类细胞静息电位无差异。（２）在     

In vivo visualization of subendocardial arteriolar response in renovascular hypertensive hearts

Time-sequential responses to endothelium-dependent and -independent vasodilators and angiotensin-converting enzyme (ACE) inhibitors were studied in the subendocardial arterioles (Endo) of canine renovascular hypertension (HT) compared with subepicardial arterioles (Epi; both <120 microm) by charge-coupled device intravital microscope. Vascular responses to acetylcholine, papaverine, and cilazaprilat were compared between normotensive (NT) and HT dogs [4 wk and 12 wk of HT (4wHT and 12wHT)]. The acetylcholine-induced vasodilation of Endo in both 4wHT and 12wHT was smaller than that of NT (both P < 0.01 vs. 4wHT and 12wHT), and that of Epi was smaller than that of NT only in 12wHT (P < 0.05). The papaverine-induced vasodilation of Endo, but not Epi, was impaired only in 12wHT (both P < 0.01 vs. NT and 4wHT). Vasodilation by cilazaprilat remained unchanged at 4wHT and 12wHT in both Epi and Endo. In conclusion, at the early stage, the endothelium-dependent response of Endo was impaired, whereas at the later stage, the endothelium-dependent and -independent responses of Endo and the endothelium-dependent response of Epi were impaired. However, the vasodilatory responses to the ACE inhibitor were maintained in both Endo and Epi of HT.