参麦注射液联合丹红注射液对体外循环心肌缺血再灌注损伤患者的保护作用

目的探讨参麦注射液联合丹红注射液对体外循环心肌缺血再灌注损伤患者的保护作用。方法体外循环心肌缺血再灌注损伤患者78例,随机分成对照组和观察组各39例。对照组:应用丹红注射液静脉注射治疗。观察组:应用丹红注射液联合参麦注射液治疗。结果治疗后,观察组心率、心律失常持续时间、心律失常发生率均低于对照组(均P0.01);肌酸激酶同工酶(CK-MB)、肌钙蛋白(c Tn)I、血管紧张素(Ang)Ⅱ水平低于对照组(P0.01);超氧化物歧化酶(SOD)、一氧化氮(NO)水平高于对照组,丙二醛(MDA)水平低于对照组(P0.01)。结论参麦注射液联合丹红注射液能够有效改善体外循环心肌缺血再灌注损伤患者的心律失常、降低心率,并有助于改善患者的氧化应激状态,保护心肌功能和促进受损心肌的恢复。     

丹参、参麦注射液对急性心肌梗死再灌注后脂蛋白相关磷脂酶A的影响

目的通过丹参、参麦注射液干预,观察心肌缺血再灌注损伤时脂蛋白相关磷脂酶A2(LP—PLA2)的变化,从而探讨其对心肌缺血再灌注损伤的保护机制。方法选择我院2013年05月-2015年05月急性ST抬高型心肌梗死(STEMI)患者60例,分三组:1.心肌缺血再灌注组20例,2.丹参注射液干预组20例,3.参脉注射液干预组20例。另设对照组20例。所有急性心肌梗死患者入院后均急诊行经皮冠状动脉腔内成形术(PCI),开通闭塞血管。在行PCI前、后即刻、24小时、3天、7天(共5次)抽静脉血2ml于促凝管送检,通过酶联免疫法测定LP—PLA2。丹参注射液干预组于入院后即刻(PCI前)静脉滴注20ml/天,持续7天;参脉注射液干预组静脉滴注40ml/天,持续7天。结果各组Lp-PLA2的变化及分析三组之间总体存在差异。缺血再灌注组和丹参干预组、参麦干预组比较,干预组Lp-PLA2明显降低,P值分别(P=0.031)、(P=0.034),丹参干预组和参麦干预组比较无统计学差异(P0.05)。结论通过这项研究发现,丹参、参麦注射液能够干预LP—PLA2的变化,从而认为它们可能通过降低炎症介质,达到保护心肌细胞的作用,为中医中药在心肌缺血再灌注损伤的保护方面提供理论依据。     

黄芪预处理对心脏瓣膜置换术心肌保护作用的临床研究

目的探讨黄芪在心脏瓣膜置换术中对心肌缺血再灌注损伤的保护作用.方法将30例心脏瓣膜置换术患者随机分为试验组和对照组,两组灌注方法及体外循环方法相同.试验组在转机前于预充液中加入黄芪注射液20 ml.分别于主动脉阻断前、开放多时点采血检测心肌酶CK-MB、cTnI的水平;记录两组患者的体外循环时间、主动脉阻断时间及术中、术后各时点血管活性药物多巴胺的用量及心肌收缩能力(dp/dtmax)恢复情况;观察开放后心脏自动复跳率、室性心律失常发生率等心肌电生理指标;电镜观察手术前、后心肌超微结构变化.结果对照组术后室性心律失常发生率、除颤次数明显高于试验组;试验组缺血再灌注后心肌收缩能力(dp/dtmax)恢复情况优于对照组.开放后6 h、12 h血清心肌酶CK-MB水平对照组和试验组分别为(91.6±20.4)U/L和(52.7±17.3)U/L,(148.7±24.2)U/L和(94.3±16.3)U/L;开放后6 h、12 h血清cTnI水平对照组和试验组分别为(4.973±1.431)ng/ml和(2.622±1.024)ng/ml,(5.054±1.419)ng/ml和(1.908±0.984)ng/ml,对照组明显高于试验组(P＜0.05或P＜0.01).试验组心肌超微结构保存较好,损伤较对照组轻.结论黄芪对心脏瓣膜置换术患者心肌缺血再灌注损伤具有明显保护作用.     

大鼠心脏缺血再灌注后发生复杂室性心律失常对左心室功能的影响

目的探讨心脏缺血再灌注后发生复杂室性心律失常对左心室功能的影响。方法雄性(Sprague Dawley,SD)大鼠按随机数字表法分成3组:心肌梗死再灌注A组、延迟再灌注B组和假手术对照组,每组至少12只。观察并记录再灌注后及术后3 d内大鼠心律失常情况。术后3 d行超声检查评估大鼠左心室功能;Masson′s染色评估及TUNEL染色检测细胞凋亡。结果再灌注A组和延迟再灌注B组每搏射血量、射血分数、左心室内径缩短率和心排血量较对照组明显下降,差异有统计学意义(P0.05)。复杂室性心律失常主要表现为室性期前收缩二联律或短阵室性心动过速。再灌注A组和延迟再灌注B组复杂室性心律失常发生率比较,差异无统计学意义[33%(4/12)vs. 50%(6/12),P=0.41]。再灌注后并发室性心律失常可致左心室收缩功能进一步下降:收缩末直径和容积增加(P=0.004、P=0.005);每搏射血量、左心室射血分数、内径缩短率和心排血量均显著减低(P=0.038、P0.001、P=0.001、P=0.01),差异均有统计学意义。Masson′s染色可见并发心律失常亚组大鼠心肌纤维断裂范围大且伴明显纤维化,TUNEL染色示细胞凋亡在再灌注并发室性心律失常亚组大鼠中均增多。结论心肌梗死再灌注后并发复杂室性心律失常可致左心室收缩功能进一步下降;同时伴有更加明显的心肌细胞萎缩、细胞凋亡和组织纤维化。     

镁离子对急性心肌梗塞溶栓后再灌注心律失常的疗效观察（附40例临床分析）

目的观察镁离子在急性心肌梗塞溶栓后再灌注心律失常治疗中的作用。方法选取84例急性心肌梗塞住院确诊病人随机分为两组。治疗组40例用门冬氨酸钾镁20ml加入5%葡萄糖注射液500ml中静滴,同时另开放静脉,选用天普乐欣(注射用尿激酶)150万U加入生理盐水100ml中于30min内静脉滴入。对照组44例仅用天普乐欣治疗(用法用量同治疗组)。两组同时用心电监护或动态心电图监测24～48h。结果治疗组发生再灌注心律失常8例占20%,对照组26例占50%。结论急性心肌梗塞早期补镁能降低再灌注心律失常的发生率。     

益母草和当归注射液对兔心肌缺血-再灌注损伤的保护作用比较

当归、益母草为妇科常用中药 ,当归偏养血活血 ,益母草偏去瘀生新 ,益母草使子宫收缩 ,当归抑制子宫收缩。但二者在治疗心肌缺血 再灌注损伤作用有无差异 ,尚未见报道。本文对此进行对比研究。资料与方法　兔 4 8只 ,随机等分为 4组 ,各组均结扎冠脉缺血 4 0ｍｉｎ ,再灌注 4 0ｍｉｎ ,Ⅰ组于结扎冠脉前 10ｍｉｎ ,静滴益母草注射液 10ｍｇ ｋｇ,稀释至 30ｍｌ(成都制药一厂生产 ,1ｍｌ含益母草生物碱 2 0ｍｇ) ,Ⅱ组按上法注射当归注射液 5 0ｍｇ ｋｇ稀释至 30ｍｌ。Ⅲ组按上法注射维拉帕米注射液 0 2 5ｍｇ ｋｇ ,稀释至 30ｍｌ。Ⅳ组滴…     

绞股蓝总皂甙对抗大鼠再灌注心律失常的作用

用结扎和解除结扎大鼠冠状动脉法复制心肌缺血再灌注模型,观察绞股蓝总皂甙(GP)对再灌注心律失常的影响。结果表明对照组和绞股蓝给药组(5mg/kg、10mg/kg、20mg/kg)心律失常发生率分别为91.91％(10/11)、81.82％(9/11)、45.45％(5/11)和27.23％(3/11),提示GP具有对抗大鼠再灌注心律失常作用,并且存在剂量依赖性关系。     

苦碟子注射液对急性心肌梗死患者心肌保护作用的临床观察

目的　探讨苦碟子注射液对急性心肌梗死 (AMI)患者心肌的保护作用及机制。方法　 10 2例AMI患者随机分为治疗组 (予苦碟子注射液 )和对照组 ,每组各 5 1例。两组患者均接受常规西药治疗及行经皮冠状动脉腔内成形术 (PTCA)。治疗组患者在行PTCA前 7天开始给予苦碟子注射液 4 0ml溶于 5 %葡萄糖注射液 5 0 0ml中静脉滴注 ,1次 d ,连用 4周。结果　治疗组患者治疗后心电图各导联抬高的ST段振幅之和除以ST段抬高导联数的值下降≥ 5 0 %率与完全回落率显著提高 ,梗死部位收缩期室壁增厚率、左心室射血分数显著提高 ,左心室收缩末期容量显著下降 ,核素分布异常节段计数、计分及核素心肌显像缺损范围份数和严重程度积分下降 ,与对照组比较差异有显著性意义 (P <0 .0 1)。结论　苦碟子注射液具有改善冠状动脉血流量 ,增加心肌缺血区灌注的作用 ,对AMI心肌具有保护作用。     

潘南金防治急性心肌梗死再灌注性心律失常

目的观察急性心肌梗死(AMI)溶栓治疗早期应用潘南金防治再灌注性心律失常疗效。方法将64例AMI患者随机分为治疗组和对照组,治疗组于溶栓前开始使用潘南金注射液静脉滴注,观察两组再灌注性心律失常发生情况。结果治疗组频发室早(20.6%)、短阵室速(8.8%)发生率分别明显低于对照组的53.3%、30%(P<0.05);而加速性室性自搏心律和室颤发生率,两组相比无明显差异(P>0.05)。结论AMI早期应用潘南金可以降低溶栓的再灌注性心律失常,从而降低AMI的死亡率,改善预后。     

复方甘草酸苷治疗抗结核药物性肝炎的临床疗效分析

目的观察复方甘草酸苷治疗抗结核药物性肝炎的临床疗效。方法将65例由应用抗结核药物所引起的药物性肝损伤患者随机分为治疗组和对照组,治疗组给予复方甘草酸苷(复方甘草酸苷注射液60 ml加5%葡萄糖注射液250 ml,静脉滴注,每日1次)治疗4周,对照组给予还原型谷胱甘肽(还原型谷胱甘肽1.2 g加入5%葡萄糖注射液250 ml中静脉滴注,每日1次)治疗4周,对两组进行疗效比较。结果治疗组在肝功能恢复,症状、体征的改善方面差异均有显著性(P0.05)。结论复方甘草酸苷治疗药物性肝炎疗效可靠,值得临床推广。     

冠心病慢性心力衰竭患者室性心律失常临床治疗

目的：讨论在临床中对冠心病慢性心力衰竭患者存在的室性心律失常进行治疗的临床效果。方法选取我院2012年1月-2014年6月收治治疗的冠心病心力衰竭患者100例，随机的把其分成观察组与对照组，其中观察组患者通过胺碘酮进行治疗，而对照组患者选择常规治疗手段进行治疗，对两组患者的临床治疗效果进行对比分析。结果两组患者经过治疗后，对照组患者的治疗总有效率为76.0％，显效率为48.0％；而观察组患者的治疗总有效率为94.0％，显效率为80.0％；两组患者进行对比，观察组患者的临床疗效明显的高于对照组。100例冠心病衰竭患者中，出现室性心律失常的患者为46例，随着左心室内径的逐渐增大，其出现室性心律失常的概率则越高。结论对于冠心病心力衰竭来说，出现室性心律失常的概率较高，应用胺碘酮对其进行治疗，具备着非常显著的效果，在临床中值得推广与应用。     

温肾活血汤治疗冠心病缓慢型心律失常

目的 观察温肾活血汤治疗冠心痛缓慢型心律失常的临床疗效。方法 将42例缓慢型心律失常病人随机分成两组，对照组采用西医常规治疗，治疗组在对照组基础上加服温肾活血汤，疗程4周，观察两组临床症状和疗效、心电图变化，疗程4周。结果 治疗组总有效率为90．48％，明显优于对照组的61．90％（P〈0．05），治疗组在提高心率、改善心电图及临床症状方面优于对照组（P〈0．05）。结论 温肾活血汤治疗缓慢型心律失常疗效优于单纯西药治疗。     

急性心肌梗死再灌注心律失常不增加心肌损伤

目的探讨急性心肌梗死（AMI）患者PCI再灌注心律失常的临床意义。方法回顾性分析近年在我院接受直接PCI且成功开通梗死相关血管（IRA）的AMI患者228例。将其中开通IRA后数分钟内发生心肌缺血再灌注损伤（MIRI）的119例患者（MIRI组）分为3个亚组,即严重心动过缓和低血压（缓慢性心律失常组）、需电复律的严重室性心律失常（快速性心律失常组）和IRA前向血流≤TIMI2级且除外急性闭塞（无复流组）。结果（1）临床和造影资料：与无MIRI组相比,MIRI组缺血时间短,梗死前心绞痛所占比例低,多支血管病变、下壁梗死、右冠状动脉IRA、PCI前IRA血流TIM10级和肾功能不全所占比例高,住院病死率较高（13．4％比4．6％,P=0．021）。（2）血清心肌酶水平：缓慢性心律失常组肌酸激酶（OK）峰值中位数显著低于无MIRI组（20LOIU／L比2521IU／L,P=0．039）,肌酸激酶同工酶（CK．MB）峰值中位数有低于无MIRI组的趋势（98IU／L比142IU／L,P=0．091）;快速性心律失常组CK峰值中位数（2317IU／L）和CK-MB峰值中位数（134IU／L）与无MIRI组相比差异无统计学意义（P=0．627,0．500）;无复流组CK峰值中位数（4573IU／L）和CK-MB峰值中位数（338IU／L）均显著高于无MIRI组（P均=0．000）。（3）超声心功能：无复流组左心室射血分数显著低于无MIRI组（38．7％±8．3％比51．2％±8．1％,P=0．000）,左心室舒张末期容积显著大于快速性心律失常组[（135±32）ml比（105±19）ml,P=0．029],左心室收缩末期容积显著大于无MIRI组[（82±33）ml比（54±24）ml,P=0．008]和缓慢性心律失常组[（56±19）ml,P=0．025]。结论再灌注心律失常可能提示梗死区存活心肌多,而且不增加心肌损伤;无复流增加心肌损伤,导致永久的心功能障碍。     

电话传输心电图在PTCA术后患者康复医疗中的应用

目的:探讨电话传输心电图(TTEM)在冠心病患者心脏介入手术后康复医疗中的应用价值。方法:对160例行冠状动脉腔内血管成形术(PTCA)后的冠心病患者应用TTEM进行监测,并与常规心电图(RECG)检查进行对照分析,观察其对心律失常和心肌缺血的检出情况。结果:TTEM的心律失常和心肌缺血检出率分别为63.9％和66.3％,较RECG显著提高(P<0.01,<0.05)。结论:TTEM能及时检出阵发性、无规律的心律失常,及时发现无症状的心肌缺血,在冠心病的二、三级防治工作中有重要作用。     

Outcome of direct current cardioversion for atrial arrhythmias in adults with congenital heart disease

Objectives

We sought to evaluate safety, efficacy, and outcome of direct current cardioversion (DCCV) for atrial arrhythmias in adults with congenital heart disease (CHD).

Background

Atrial arrhythmias are increasingly noted in adults with CHD. The outcome of DCCV for atrial arrhythmias in this population is unknown.

Methods

Our study was a retrospective review of patients 18 years or older with CHD who underwent DCCV between June 2000 and July 2003. This constituted the CHD group. Patient characteristics reviewed included the specific cardiac diagnosis and arrhythmia history. A subset of patients had transesophageal echocardiography (TEE) before DCCV; this subset was reviewed to evaluate spontaneous echocardiographic contrast. The outcome data evaluated included success of DCCV, complications, recurrence of arrhythmia, antiarrhythmic medication use, electrophysiology or pacemaker procedure in follow-up, and all-cause mortality. The recurrence rate of the arrhythmia was compared to a control group consisting of an age, gender, and rhythm matched group of patients who have no CHD and who underwent DCCV for atrial arrhythmias.

Results

Sixty-three patients in the CHD group underwent 80 DCCVs, 59 of which were TEE-guided. Atrial flutter was more common in the CHD group (37 of 80 DCCV, 46%) than in the control group (13 of 56, 23%) (p < 0.001). DCCV was successful in 75 (94%). Mean follow-up was 387 days. No thromboembolic events were noted. All-cause mortality on follow-up was 11%. There was no death related to DCCV. Twenty-five patients in the CHD group (40%) remained in sinus rhythm throughout follow-up. This was similar to that observed in the control group (30/56, 54%, p = 0.13). Recurrent arrhythmia in the CHD group was predicted by the presence of atrial fibrillation (p = 0.009) and less so spontaneous echo contrast in the left atrium (p = 0.05).

Conclusions

DCCV with appropriate anticoagulation is safe and effective for patients with CHD, even in the presence of an intracardiac shunt and spontaneous contrast on TEE. However, the recurrence rate is substantial. Spontaneous echo contrast in the left atrium along with atrial fibrillation predicts arrhythmia recurrence following DCCV in patients with CHD.     

Silymarin and Vitamin E do not Attenuate and Vitamin E Might Even Enhance the Antiarrhythmic Activity of Amiodarone in a Rat Reperfusion Arrhythmia Model

Oxidative stress and lysosomal phospholipoidosis, which also might be partly attributed to free radicals induced by amiodarone (AM), may be involved in AM toxicity, which can be prevented by antioxidants. Our aim was to study if vitamin E (E) or silymarin (S), a lipid and a water-soluble antioxidant, modified the antiarrhythmic efficacy of AM in a rat reperfusion arrhythmia test. The following groups of male Sprague-Dawley rats (15 rats/group) were treated by gavage once a day for 4 weeks: 1. methylcellulose (MC, 0.4%), 2. sunflower seed oil (SSO), 3. AM, suspended in MC (30 mg/kg), 4. E, dissolved in SSO (100 mg/kg), 5. AM + E, 6. S, suspended in MC (80 mg/kg), 7. AM + S. The mean duration of ventricular tachycardia + fibrillation (MDVT + VF) and sinus rhythm (MDSR) the incidence of ventricular fibrillation (VF) and ventricular tachycardia (VT) and mortality were measured during a 10-min reperfusion after a 5-min coronary artery occlusion in anaesthetized rats. An arrhythmia score, representing the combined incidence and duration of different types of ventricular arrhythmia, was calculated. Compared with the MC group, MDSR was longer and MDVT + VF was shorter in all drug treated groups and in the SSO group. In the AM + E treated group MDSR was prolonged more and MDVT + VF was shortened more than in the AM, E or SSO groups. Compared with the MC group, the incidence of VF and mortality was similarly decreased in the SSO group and in most drug treated groups. No significant difference in the incidence of VT was found among all groups. The arrhythmia score was reduced by all drug treatments. Combined treatment with AM + E decreased arrhythmia score more than treatment with AM or SSO alone, but arrhythmia score was similar in the AM + E and E groups. In conclusion, both AM and antioxidant treatments alone or together resulted in a marked reduction of reperfusion arrhythmias in this model. SSO also exerted a moderate antiarrhythmic effect. Antioxidants administered together with AM did not attenuate and E might have even enhanced the antiarrhythmic effect of AM, therefore the combination of antioxidants with AM may be advantageous to reduce AM toxicity.     

缺血预适应减少缺血再灌注冠状窦血浆内皮素的含量

目的:观察缺血预适应(PC)对缺血再灌注(IR)后冠状窦血浆内皮素(ET)含量的影响。方法:以单纯的心肌缺血(阻闭家免冠脉左前降支近端)30min+再灌注30min为对照,观察经PC(缺血5min+再灌注10min)后IR心肌的梗死范围、超微结构以及室颤(VF)或室速(VT)的发生率,并采用均相放射免疫竞争法,测量比较两组1R后冠状窦血浆ET含量。结果:PC后心肌梗死范围缩小约60％、VF／VT的发生率降低(P<0.05);电镜下,心肌细胞的损伤减轻;血浆ET含量明显减少(P<0.01)。结论:PC减少IR时冠脉ET的分泌,可能是PC保护心肌组织结构及抗IR心律失常的部分病理生理机制。     

Attenuation of reperfusion phenomenon by reperfusion using leukocyte-depleted blood during direct percutaneous transluminal coronary angioplasty for acute myocardial infarction

Leukocytes are important in the occurrence of reperfusion injury in coronary intervention for acute myocardial infarction (AMI). This study compared reperfusion injury caused by reperfusion using leukocyte-depleted blood (LD) and that by conventional angioplasty (control) through the reperfusion phenomenon including reperfusion arrhythmia and additional ST elevation during direct percutaneous transluminal coronary angioplasty (PTCA) in 41 patients with 21 left anterior descending artery (LAD) lesions and 20 right coronary artery (RCA) lesions. LD was prepared from 20 ml of venous blood, 20 ml of mixed blood and 60 ml of arterial blood from the patients (LD group; LAD-LD: n = 10, RCA-LD: n = 10) which was passed through a leukocyte removal filter. The blood was injected from the tip of the balloon catheter at 10 ml/min during inflation for 10 min before balloon deflation. The control group (LAD-control: n = 11, RCA-control: n = 10) underwent conventional angioplasty. The appearance of reperfusion arrhythmia [atrioventricular block (AVB) > II, accelerated idioventricular rhythm (AIVR), ventricular tachycardia (VT), ventricular fibrillation (Vf)] and measurements of STmax deviation before and after reperfusion, the differences of the STmax deviation (delta ST) and additional ST elevation (LAD: > or = 0.5 mV increase of sigma ST in lead V1-V6, RCA: > or = 0.3 mV increase of sigma ST in lead II, III and aVF) were studied. The appearance of reperfusion arrhythmias was as follows; LAD-LD: AVB 0, AIVR 1, VT 1, Vf 0, LAD-control: AVB 0, AIVR 4, VT 2, Vf 1, NS, and RCA-LD: AVB 0, AIVR 0, VT 0, Vf 0, RCA-control: AVB 2, AIVR 0, VT 1, Vf 0, NS. There was no reperfusion arrhythmia in the RCA-LD group. There was no significant difference in the appearance of reperfusion arrhythmias between the LAD-LD and LAD-control or RCA-LD and RCA-control groups. Before reperfusion the STmax deviation (mV) was LAD-LD 0.86 +/- 0.46 vs LAD-control 0.74 +/- 0.49 and RCA-LD 0.29 +/- 0.18 vs RCA-control 0.15 +/- 0.09 and after reperfusion LAD-LD 0.63 +/- 0.35 vs LAD-control 0.81 +/- 0.49 and RCA-LD 0.13 +/- 0.15 vs RCA-control 0.20 +/- 0.12, respectively. There were no significant differences between LAD-LD and LAD-control or RCA-LD and RCA-control groups. delta ST (mV) was LAD-LD 0.23 +/- 0.56 vs LAD-control 0.07 +/- 0.60, p = 0.09 and RCA-LD 0.16 +/- 0.12 vs RCA-control 0.06 +/- 0.14, p = 0.002, respectively. The number of patients with additional ST elevation soon after reperfusion was LAD-LD 3 vs LAD-control 10, p < 0.05 and RCA-LD 0 vs RCA-control 8, p < 0.001, respectively.     

The effect of verapamil on reperfusion arrhythmia in canine heart

This study was designed to clarify the mechanism of reperfusion arrhythmia and with the effect of verapamil on arrhythmia. In vivo study: Fifty anesthetized dogs were divided into two groups the control group (n = 37) and the verapamil group (n = 13). The left anterior descending coronary artery (LAD) was occluded for 15 min and then reperfused for 5 min. Physiological saline or verapamil (0.4 mg/kg) was infused 5 min prior to the LAD reperfusion. Eleven (30%) of the control dogs developed "reperfusion arrhythmia" (arrhythmia group) but 26 did not (non-arrhythmia group), while in the verapamil group, none of the 13 dogs developed arrhythmia. Immediately after 5 min reperfusion, myocardial plasma membrane and mitochondria were prepared from the normal and the reperfused area. In the arrhythmia group, an increase in free fatty acids (FFA) and a decrease in phospholipids were observed in membrane samples, and the content of calcium in the mitochondria increased in the reperfused myocardium; these changes were not observed in the non-arrhythmia group or the verapamil group. In vitro study: In vitro study consisted of two experiments. In experiment 1, incubation of myocardial plasma membrane with phospholipase (PLase) A2 increased only the unsaturated FFA, while PLase C increased all the detected FFA. In experiment 2, the effects on myocardial membrane potentials induced by PLase A2 and PLase C were studied by using microelectrodes. Each PLase caused a decrease in the resting potential and in the magitude and duration of the action potential.(ABSTRACT TRUNCATED AT 250 WORDS)