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。     

药物对实验血吸虫病 家兔机体反应的影响

(一)本文报告了药物对于血吸虫病病兔及正常家兔的红血球沉降率,血浆纤维蛋白,丙种球蛋白,凝血酶元时值及体重的影响。(二)酒石酸锑钾的治疗,无论在家兔患病的早期或后期,均可抑制其血沉的加速,而以早期治疗的抑制作用更为显著。同时这个抑制血沉的作用与治疗后的成虫发育率是符合的。因此利用这种方法,可以考虑作为研究一些治疗血吸虫病药物的疗效指标。(三)酒石酸锑钾及士的宁本身对正常家兔的血沉并不引起改变,士的宁对于病兔的血沉也无明显作用,但士的宁可以影响酒石酸锑钾对病兔血沉的抑制作用。 (四)半疗程剂量酒石酸锑钾并用士的宁之疗效较单独应用半疗程剂量酒石酸锑钾者为高(10—20%),而单独应用士的宁并无任何疗效,轻度激动量士的宁也不增加酒石酸锑钾的毒性。(五)酒石酸锑钾的治疗剂量对于正常家兔之血浆纤维蛋白元无明显影响,但能使病兔增高之血浆纤维蛋白元回复正常。(六)酒石酸锑钾的治疗可以使病兔的丙种球蛋白在一定时期内保持在接近正常值范围内,这一抑制作用与感染对照组相比,甚为明显,而氨苯氧烷却无此作用,这一点可能与疗效是有关系的。(七)酒石酸锑钾治疗后的病兔之体重较感染对照组病兔显著增高,而经氨苯氧烷治疗后之病兔,其体重仍日见减轻。(八)氨苯氧烷有较高的毒性,但疗效甚低,它对病兔的血沉及纤维蛋白元所出现的抑制作用,究竟属于对血吸虫或其虫卵的作用,抑系对于病兔机体的毒性作用,目前还不能肯定。     

用新型四极单导管技术同时测定在体心脏同一位点的APD和ERP

动作电位间期(APD)与有效不应期(ERP)及其比值(ERP/APD)是评价抗心律失常药物的重要指标。以往测定在体心脏的APD和ERP是采用分离的两根导管。一根是记录单相动作电位(MAP)的接触电极导管;另一根是起搏导管。用这种方法测定的APD和ERP之间的相关性很差,这可能是由于两根导管处在心室     

酒石酸锑钾对麻醉兔电致心室颤动的影响

在戊巴比妥钠麻醉兔观察酒石酸锑钾(锑钾)对电致颤阈的影响,锑钾本身所致的心室颤动,以及心脏神经对锑钾作用的影响。结果发现:一定剂量的锑鉮(依次地静脉注射3,6,12毫克/公斤)能显著地降低电致颤阈(9/10兔),并使心率稍有加速(8/10兔),血压缓慢而逐步下降;大剂量(24—36毫克/公斤)使血压迅速而显著下降,6/10兔出现锑致性心室颤动。在切断迷走神经,切除交感神经或利血平化以后,锑钾的降低电致颤阈的作用不仅被防止并且全部翻轉,阿托品(0.2或2毫克/公斤)均不能显著地影响这种致颤阈的降低。锑钾所致的心率加速作用为切除交感神经,利血平化或大剂量阿托品所防止而且翻轉,相反,在切断迷走神经与小剂量阿托品后,心率加速仍然出现。切断迷走神经与小剂量阿托品完全不能防止锑致性心室颤动,分别仍有4/5与5/6兔出现颤动,而切除交感神经,利血平化或大剂量阿托品则能完全防止之。此外,于不麻醉兔小剂量阿托品不影响,而大剂量阿托品能防止去甲腎上腺素的心律紊乱。根据实验结果,可以作出推论如下:在本实验条件下锑钾的降低电致颤阈的作用是与心脏交感神经的完整性或心内儿茶酚胺储存量有关;至于迷走神经的意义尚待阐明,可能为组成此反射弧的传入通路,而以交感神经为其传出通路。锑钾加速心率的作用及大剂量所致的锑致性心室颤动则与迷走神经无关,而是取决于交感神经的完整性或心肌内的儿茶酚胺储存量。大剂量阿托品对锑致性心室颤动与去甲腎上腺素的心律紊乱均有保护作用,这可能是通过对抗迷走神经以外的机制。     

锑剂对于心脏毒性作用的机制

锑剂是目前治疗日本血吸虫病的主要药物,但对机体有显著的毒性作用。现在主要就这种制剂对于心脏的毒性作用来进行研究。早在1927年 Chopra 曾在动物实验上注意到锑剂对于心脏的毒性作用,但在药理学书籍上关于锑剂对于心脏的毒性作用,很少注意和分析。至于以往临床方面,只强调锑剂对于肝脏功能的影响,亦不很重视它对于心脏的毒性作用。近年来,由于大规模地应用酒石酸锑钾治疗日本血吸虫病,曾发生突然死亡的病     

鳖心对迷走刺激的时相依赖性反应

在27只毁脑和脊髓的中华鳖上,研究了时相耦联式刺激迷走神经对心率的影响。结果心脏的负变时性反应取决于刺激猝发所在的心动周期时相。首先A-A间期逐渐延长,然后突然缩短。在注射心得安的鳖中,常温下右迷走刺激引起的时相反应曲线的幅度(AT)为1484.10±213.10ms,从最大至最小反应的时相差异为804,00±210.90 ms。AT及(St-A)_(max)(产生最大A-A间期的刺激开始至下一A波开始的间期)直接随AA(最大及最小反应的均值)的改变而改变,皆呈正线性相关,但(St-A)_(min)(产生最小A-A间期的刺激开始至下一A波开始的间期)与AA无显著相关性。冬眠期4只鳖的AT,AA及(St-A)_(min)都显著增大,其中3只鳖在特定时相刺激引起心率加快。左迷走的时相反应明显较小或无作用。 上述反应可被阿托品消除,提示是由于静脉窦起搏细胞在其活动周期的不同时相对迷走传出末梢所释放的ACh的反应性不同所致。     

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     

除草剂草甘膦异丙胺盐水剂对中华大蟾蜍心电活动的影响

采用生物信号采集处理系统对草甘膦异丙胺盐胁迫条件下中华大蟾蜍(BufogargarizansCantor)的心率和心电活动的相关指标进行了测定和分析。不同浓度的草甘膦异丙胺盐溶液被喷施到中华大蟾蜍的体表,由皮肤进入体内而作用于心脏。试验结果表明:随着草甘膦异丙胺盐处理浓度的增大,中华大蟾蜍的心率减慢,心电图中P波、R波和T波的电压峰值降低,而P-R间期、QRS期和Q-T间期的时值延长。草甘膦异丙胺盐胁迫条件下,蟾蜍心率与心电图的各项指标有显著相关性,可用多元线性回归模型分别对蟾蜍心率与心电图中P、R、T波和P-R、QRS、Q-T间期的相关关系进行拟合。多元回归分析结果表明,蟾蜍心电图中Q-T间期值对心率的影响最大,可以推断草甘膦异丙胺盐主要是通过延长蟾蜍心电活动周期中Q-T间期时值即心室收缩期而延长心动周期,导致蟾蜍心率减慢。由此可见草甘膦异丙胺盐水剂的喷施对中华大蟾蜍心脏的电活动周期和机械活动周期均造成了一定影响。     

动态心电图评价2型糖尿病患者心脏自主神经功能的价值

目的:研究动态心电图在评价2型糖尿病患者心脏自主神经功能中的价值。方法:选择2012年2月~2015年2月在我院进行诊治的2型糖尿病患者260例,按照心血管自主神经功能分为损伤组152例和正常组108例,采用动态心电图检查两组的心率变异、心脏变时功能不全和心率震荡。结果:两组间平均心率相比无明显差异(P0.05),损伤组的最慢心率明显高于正常组(P0.05),最快心率和差值明显低于正常组(P0.05);两组间震荡初始无明显差异(P0.05),损伤组的震荡斜率明显低于正常组(P0.05);损伤组的窦性心搏间期均值的标准差、相邻R-R间期差值的均方根值和5 min心搏间期均值的标准差均明显低于正常组(P0.05)。结论:应用动态心电图检测心脏变时性功能不全指标和心率震荡、心率变异指标能准确评价2型糖尿病患者的心脏自主神经功能,具有较高的诊断价值。     

24小时动态心电图检查在起搏器植入心律失常诊断中应用价值分析

目的:分析24 h动态心电图检查在起搏器植入心律失常诊断中的应用价值。方法:选择2013年2月～2016年1月于医院接受起搏器植入术治疗的60例患者作为研究对象,均采用常规12导联及24 h动态心电图进行检查,比较两种不同检查方法对心律失常的诊断价值。结果:①24 h动态心电图对心室过感知、心房感知不良、心室感知不良检出率均高于12导联心电图(P0.05)。②24 h动态心电图心律失常总检出率明显高于12导联心电图(P0.05)。③24 h动态心电图HRV时域指标24 h内所有正常R-R间期标准差(SDNN)、24 h内相邻正常R-R间期之差均方根值(RMSDD)、全程每5 min时间段R-R间期均值标准差(SDANN)均高于12导联心电图(P0.05)。结论:24 h动态心电图对起搏器植入术后起搏功能异常、感知功能异常及心律失常检出率高,且对心率变异性诊断相对敏感,对起搏器植入心律失常诊断的临床应用价值较12导联心电图更高。     

牵张所致心室不应性变化的频率依赖现象及其机制

本文旨在探讨牵张所致麻醉兔心室不应性变化的频率依赖现象及其机制。采用部分夹闭兔主动脉根部以增加左室后负荷的在体心脏模型 ,观察不同起搏周长时左室后负荷增加后心室有效不应期 (effectiverefractoryperi od ,ERP)的变化及链霉素对此的影响。结果显示 ,当起搏周长为 10 0 0和 5 0 0ms时 ,左室收缩期内压增加后的心室ERP较主动脉夹闭前略有缩短 ( 10 0 0ms,3± 2ms,1 5 % ;5 0 0ms,7± 3ms,4 0 % .P >0 0 5 ) ,而起搏周长 3 0 0和 2 0 0ms时则明显缩短 ( 3 0 0ms,2 1± 5ms ,17 0 % ;2 0 0ms,19± 3ms,18 8% P <0 0 1) ;( 2 )链霉素可有效消除基本驱动周长 3 0 0和 2 0 0ms时左心室后负荷增加对ERP的影响 (P >0 0 5 ,组内比较 )。结果提示 ,牵张所致心室ERP变化具有快频率依赖性 ,且链霉素通过抑制牵张激活性离子通道的活化而消除这种电生理效应     

Effects of propafenone on sinus node function in the rabbit heart

Propafenone is a type 1C antiarrhythmic drug with efficacy for both ventricular and supraventricular arrhythmias. We investigated the effects of propafenone on properties of sinus node function in an in vitro preparation of rabbit sinus node and surrounding atrium. Spontaneous sinus cycle length (SCL), atriosinus conduction time (ASCT), and sinus node effective refractory period (SNERP) at multiple pacing cycle lengths were measured in the control state and during superfusion with propafenone (2.3 microM). SNERP prolonged from 175 +/- 25 ms in the control state to 220 +/- 45 ms (p less than 0.001) with propafenone. ASCT also prolonged significantly (p less than 0.01) from 50 +/- 20 to 65 +/- 20 ms whereas SCL did not change. In four experiments, multiple concentrations of propafenone were utilized and there appeared to a dose-dependent prolongation of SNERP. Thus, propafenone has a significant effect on SNERP and ASCT in an isolated rabbit sinus node preparation.     

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.     

The effect of lidocaine compared with verapamil on the enhanced ventricular rhythm in the infarcted canine heart

Myocardial ischemia was produced in dogs by the occlusion of the left anterior descending (LAD) coronary artery for 24 or 48 h. After complete atrioventricular block was produced, enhanced ventricular rhythm was observed in all animals. The enhanced ventricular rhythm showed multiple QRS configurations and had spontaneous cycle lengths (SCL) of 397 +/- 18 ms (n = 20) after 24 h of LAD occlusion and 446 +/- 23 ms (n = 20) after 48 h of LAD occlusion. Overdrive pacing did not result in the termination of the enhanced ventricular rhythm in any experiment. Propranolol, as a cumulative dose of 1.5-2.0 mg/kg i.v., also did not abolish the enhanced ventricular rhythm. In 24-h infarcted hearts, lidocaine abolished the enhanced ventricular rhythm in 1 of 11 experiments. In the remaining 10 experiments, the ventricular SCL was increased from 401 +/- 22 to 491 +/- 26 ms after a cumulative dose of 8.8 +/- 0.7 mg/kg of lidocaine. In the presence of verapamil, given as a cumulative dose of 0.60 +/- 0.11 mg/kg, the ventricular SCL was increased from 401 +/- 33 to 482 +/- 64 ms (n = 9). In 48-h infarcted hearts, lidocaine abolished the enhanced ventricular rhythm in 5 of 11 experiments. Both lidocaine and verapamil increased the SCL of hearts in which the enhanced ventricular rhythm persisted. Analysis of variance showed that only the increase in SCL by lidocaine in 48-h infarcted hearts was statistically significant. The atrial and idioventricular rhythms in noninfarcted hearts responded differently to lidocaine and verapamil. The results suggest that some electrophysiological effects of antiarrhythmic drugs in the normal heart may not be applicable to those in the diseased situation.     

Hemodynamic effects of pacing-induced tachycardia in valvular aortic stenosis.

The hemodynamic effects of tachycardia were studied in 13 patients with valvular aortic stenosis. Observations were made during sinus rhythm (average heart rate 80 beats/min) and two periods (P1 and P2) when atrial pacing increased the heart rate to 109 and 131 beats/min respectively. The cardiac index did not change, but the left ventricular stroke work index fell from 61.8 to 39.5 g X m/m2 (p less than 0.001) as the heart rate increased. The left ventricular end-diastolic pressure averaged 18 mm Hg during sinus rhythm and fell to about 11.5 mm Hg at P1 and P2 (p less than 0.001). The brachial arterial systolic pressure did not change during pacing, but the left ventricular systolic pressure fell from 208 mm Hg to 201 mm Hg during P1 (p less than 0.05) and 193 mm Hg during P2 (p less than 0.001). The mean systolic aortic valve gradient averaged 64 mm Hg during sinus rhythm and fell to 51 mm Hg during P2 (p less than 0.001), and the peak aortic valve gradient fell from 82 to 69 mm Hg during P2 (p less than 0.001). The left ventricular ejection time fraction increased from 26.9% during sinus rhythm to 31.9% during P1 (p less than 0.05) and 34.7% during P2 (p less than 0.005). Because of the prolonged left ventricular ejection time fraction and smaller stroke volume, a smaller pressure gradient developed across the stenosed valve at higher heart rates. The pacing test was of little value in assessing left ventricular function and thus is not useful during invasive investigations of valvular aortic stenosis.     

Roles of the AV junction in determining the ventricular response to atrial fibrillation.

The statistical properties of RR interval sequences during cholinergic atrial fibrillation were studied in anesthetized dogs both in control conditions and after the selective injection of dromotropic agents into the atrioventricular (AV) node artery. It was observed that RR interval histogram configurations depended mainly on the mean heart rate, regardless of whether it was a control or a post-injection sequence. The sequences were found to vary from almost regular at fast rates to highly irregular at slow rates, covering all intermediate possibilities. Since the injections of dromotropic agents into the AV node artery were carried out during sinus rhythm between the episodes of fibrillation, their influences on the AV junction, as reflected both on the length of the PR interval during sinus rhythm and on the RR interval dispersion during fibrillation, could be compared. The dispersion of RR intervals was found to increase as the PR interval duration became longer. In addition, it was observed that the generally random character of the RR interval sequences during fibrillation was not affected by the injection of dromotropic agents into the AV node artery. These results were interpreted as an indication that, for a well-established atrial fibrillation, the degree of ventricular irregularity (dispersion of RR intervals) is related to the conductivity within the AV junction and that the random character of RR interval sequences is related to the atrial fibrillatory activity itself.     

Ventricular pump function under ectopic excitation of the frog heart

The ventricular pump function under ectopic excitation of the heart was studied in decapitated and pithed adult frogs Rana temporaria (n = 21) at 18-19 degrees C. The intraventricular pressure was recorded with a catheter via ventricular wall. During pacing of the ventricular base and apex, the systolic pressure decreased (6.1 +/- 4.5 mm Hg and 8.9 +/- 5.0 mm Hg, respectively) as compared to the supraventricular rhythm (8.9 +/- 5.0 mm Hg, p < 0.05). The end-diastolic pressure decreased insignificantly both under basal and apical pacing. The systolic rate of pressure rise during dP/dtmax decreased under ventricular pacing, especially during pacing of the ventricular apex, as compared to the supraventricular rhythm (14.4 +/- 6/9 mm Hg/s and 22.1 +/- 11.2 mm Hg/s, respectively, p < 0.003). The isovolumetric relaxation (dP/dtmin) slowed during apical pacing as compared to the supraventricular rhythm (-25.1 +/- 13.6 and -35.6 +/- 18.3 mm Hg/s, respectively, p < 0.03). Ectopic excitation of the ventricular base and apex resulted in increase of the QRS duration (93 +/- 33 ms and 81 +/- 30 ms, respectively) as compared to the supraventricular rhythm (63 +/- 13 ms, p < 0.05). Thus, pacing of different ventricular areas ventricular myocardium with the ventricular pump function being reduced more obviously during the apical pacing compared to the pacing of ventricular base.     

家兔离体心脏组织的不应期及房室结的滤波特性

一般认为房室结具有滤波特性,即它能阻止过快或过于提前的心房冲动传到心室。本实验旨在研究家兔离体心脏组织的不应期及房室结的滤波牧场生（ｎ＝１８）。实验中发现：（１）在短基础周期（２００－３００ｍｓ）房室结的相对不应期最长,而在长基础周期（６００,７００ｍｓ）希浦系（ＨｉｓＰｕｒｋｉｎｊｅ ｓｙｔｅｍ）的相对不应期最长;（２）在多种基础周期下,大多数心脏（１６／１８）房室结有效不应期小于心房功能不应期     

高钙对兔窦房结的负性变时作用

本文采用常规微电极技术在离体兔心窦房结标本上研究了细胞外钙离子浓度([Ca~(2 )]_0)对窦房结的变时性作用。结果显示,[Ca~(2 )]_0的递增(1.1—5.5mM),对窦性周期(CL)大于400ms 的标本引起双相变时作用,但对CL小于400ms的标本却引起负性变时作用。阿托品(0.5mg/l)和心得安(0.2mg/l)对[Ca~(2 )]_0 的变时作用无明显影响。随着[Ca~(2 )]_0的递增,窦房结优势起搏细胞的动作电位幅度、最大舒张期电位和0期最大除极速度均降低,舒张期自动除极化斜率增加,起始电位上移,动作电位时程(APD)延长。高[Ca~(2 )]_0时窦房结起搏细胞的有效不应期(ERP)延长、ERP/APD增大,ERP点的阈值提高(P<0.01)。 上述结果表明,高[Ca~(2 )]_0引起窦房结的负性变时效应,这种作用不是通过交感和副交感神经的传递,而可能是 Ca~(2 )直接作用于窦房结起搏细胞引起其电活动改变的结果。     

Thoracic vein ablation terminates chronic atrial fibrillation in dogs

The thoracic vein hypothesis of chronic atrial fibrillation (AF) posits that rapid, repetitive activations from muscle sleeves within thoracic veins underlie the mechanism of sustained AF. If this is so, thoracic vein ablation should terminate sustained AF and prevent its reinduction. Six female mongrel dogs underwent chronic pulmonary vein (PV) pacing at 20 Hz to induce sustained (>48 h) AF. Bipolar electrodes were used to record from the atria and thoracic veins, including the vein of Marshall, four PVs, and the superior vena cava. Radio frequency (RF) application was applied around the PVs and superior vena cava and along the vein of Marshall until electrical activity was eliminated. Computerized mapping (1,792 electrodes, 1 mm resolution) was also performed. Sustained AF was induced in 30.6 +/- 6.5 days, and ablation was done 17.3 +/- 8.5 days afterward. Before ablation, the PVs had shorter activation cycle lengths than the atria, and rapid, repetitive activations were observed in the PVs. All dogs converted to sinus rhythm during (n = 4 dogs) or within 90 min of completion of RF ablation. Rapid atrial pacing afterward induced only nonsustained (<60 s) AF in all dogs. Average AF cycle lengths after reinduction were significantly (P = 0.01) longer (183 +/- 31.5 ms) than baseline (106 +/- 16.2 ms). There were no activation cycle length gradients after RF application. We conclude that thoracic vein ablation converts canine sustained AF into sinus rhythm and prevents the reinduction of sustained AF. These findings suggest that thoracic veins are important in the maintenance of AF in dogs.