Electrophysiological effects of haloperidol on isolated rabbit Purkinje fibers and guinea pigs papillary muscles under normal and simulated ischemia

Aim： Overdoses of haloperidol are associated with major ventricular arrhythmias, cardiac conduction block, and sudden death. The aim of this experiment was to study the effect of haloperidol on the action potentials in cardiac Purkinje fibers and papillary muscles under normal and simulated ischemia conditions in rabbits and guinea pigs. Methods： Using the standard intracellular microelectrode technique, we examined the effects of haloperidol on the action potential parameters [action potential amplitude （APA）, phase 0 maximum upstroke velocity （Vmax）, action potential amplitude at 90% of repolarization （APD90）, and effective refractory period （ERP）] in rabbit cardiac Purkinje fibers and guinea pig cardiac papillary cells, in which both tissues were under simulated ischemic conditions. Results： Under ischemic conditions, different concentrations of haloperidol depressed APA and prolonged APD90 in a concentration-dependent manner in rabbit Purkinje fibers. Haloperidol （3 μmol/L） significantly depressed APA and prolonged APD90, and from 1 μmol/L, haloperidol showed significant depression on Vmax; ERP was not significantly affected. In guinea pig cardiac papillary muscles, the thresholds of significant reduction in APA, Vmax, EPR, and APD90 were 10, 0.3, 1, and 1 μmol/L, respectively, for haloperidol. Conclusion： Compared with cardiac conductive tissues, papillary muscles were more sensitive to ischemic conditions. Under ischemia, haloperidol prolonged ERP and APD90 in a concentration-dependent manner and precipitated the decrease in Vmax induced by ischemia. The shortening of ERP and APD90 in papillary muscle action potentials may be inhibited by haloperidol.     

赛庚啶对豚鼠乳头状肌的收缩性与动作电位的影响

Cyp对豚鼠孔头状肌有浓度依赖性负性肌力作用,提高浴液钙浓度此作用减弱,对高K~+除极后ISO恢复的收缩抑制作用更强。较高浓度的Cyp使频率依赖性正阶梯现象取消和翻转。对乳头状肌AP,Cyp浓度依赖性地使APD_(20),APD_(50),APD_(90)和ERP缩短。灌流液中Ca~(2+)降低或升高分别使该作用增强或减弱,K~+的改变对其作用影响较小。提示Cyp对豚鼠乳头状肌收缩性和AP的作用可能主要是抑制心肌跨膜Ca~(2+)内流所致。     

Effects of 3,6-dimethamidodibenzopyriodonium citrate (I-65) on action potentials and contractions in guinea pig papillary muscles

Synchronous recordings of action potentials and contractile force in isolated guinea pig papillary muscles administered 3,6-dimethamidodibenzopyriodonium citrate (I-65) 30 mumol/L showed excitation-contraction uncoupling, ie, the contractile force was markedly depressed although the Vmax and amplitudes of the action potentials were unaffected. At the same concentration, I-65 shortened the duration of the action potentials at 50% and 90% repolarization. However, I-65 at lower concentrations (1-10 mumol/L) decreased Vmax and the amplitude of the slow action potentials which were elicited by isoprenaline in papillary muscles were rendered partially depolarized by KCl 25 mmol/L Tyrode solution. These effects were partially reversed by elevation of the concentration of Ca2+ from 2.7 to 5.4 mmol/L. I-65 also suppressed the abnormal automaticity elicited by BaCl2 and DAD and triggered activity induced by ouabain. The results suggest that I-65 may be a calcium channel blocker.     

Electrophysiologic effect of dipfluzine on guinea pig papillary muscles in vitro

用细胞内微电极技术记录正常和部分除极豚鼠乳头肌动作电位,研究双苯氟嗪（３－３０μｍｏｌ·Ｌ－１）对豚鼠乳头肌细胞电生理的影响．结果表明,双苯氟嗪轻度缩短正常乳头肌动作电位的平台期（ＰＰＤ）,５０％和９０％复极化时程（ＡＰＤ５０和ＡＰＤ９０）,但对静息电位（ＲＰ）,动作电位幅度（ＡＰＡ）,超射（ＯＳ）和０相最大上升速率（Ｖｍａｘ）均无显著影响．在高Ｋ＋部分去极化的豚鼠乳头肌标本,双苯氟嗪可轻度降低慢反应动作电位的ＯＳ,ＡＰＡ和Ｖｍａｘ,并缩短ＰＰＤ,ＡＰＤ５０和ＡＰＤ９０,对ＲＰ同样无显著影响．在相同浓度下,双苯氟嗪对离体豚鼠乳头肌动作电位的影响与氟桂利嗪无显著差别．提示双苯氟嗪在较高浓度时,可轻度缩短豚鼠乳头肌的复极过程及降低部分除极乳头肌的ＯＳ,ＡＰＡ和Ｖｍａｘ．     

DDPH对豚鼠心室乳头状肌细胞电压与频率依赖性的电生理作用

目的　观察１ （２,６ 二甲基苯氧基） ２ （３,４ 二甲氧基苯乙氨基） 丙烷盐酸盐〔１ （２,６ ｄｉｍｅｔｈｙｌｐｈｅｎｏｘｙ） ２ （３ ,４ ｄｉｍｅｔｈｏｘｙｐｈｅｎｙｌｅｔｈｙｌａｍｉｎｏ） ｐｒｏｐａｎｅ ｈｙｄｒｏｃｈｌｏｒｉｄｅ, ＤＤＰＨ〕对豚鼠右心室乳头状肌细胞电压与频率依赖性的电生理作用。方法　采用常规细胞内玻璃微电极技术,分别以０－０２Ｈｚ、２ Ｈｚ 的刺激频率,观察ＤＤＰＨ（１ ～５０ μｍｏｌ·Ｌ－１） 对豚鼠右心室乳头状肌细胞动作电位（ＡＰ） 各参数的影响,并采用０－１ ～３－３ Ｈｚ 的刺激频率和提高Ｋ＋ 浓度（２－７ ～１５ ｍｍｏｌ·Ｌ－ １）将静息膜电位除极化到不同的水平,观察了ＤＤＰＨ（１０μｍｏｌ·Ｌ－１）对豚鼠右心室乳头状肌细胞动作电位零相最大除极化速率（ Ｖｍａｘ）频率与电压依赖性的抑制作用。结果　ＤＤＰＨ以浓度依赖降低豚鼠右心室乳头状肌细胞动作电位振幅（ＡＰＡ） 、缩短动作电位复极５０ ％ 时程（ＡＰＤ５０） 、延长动作电位复极９０％ 时程（ＡＰＤ９０） 并抑制Ｖｍａｘ ,但不明显改变静息膜电位（ＲＰ）,其作用在刺激频率为２ Ｈｚ 时较０－０２ Ｈｚ 时更为明显。对Ｖｍａｘ 呈现出刺激频率     

1—（2，6—二甲基苯氧基）—2—（3，4—二甲氧基苯乙氨基）丙烷盐酸盐抑制豚鼠心室肌细胞内向整流和延迟整流钾电流

目的:研究1-(2,6-二甲基苯氧基)-2-(3,4-二甲氧基苯乙氨基)丙烷盐酸盐(DDPH)对心室肌细胞动作电位(AP)、内向整流钾通道电流(I_(K1))及延迟整流钾通道电流(I_K)的影响。方法:全细胞膜片箝技术。结果:DDPH 10,100μmol·L~(-1)使豚鼠心室肌细胞AP时程APD_(50)明显缩短;但DDPH(>1μmol·L~(-1))延长APD_(90)。DDPH浓度依赖性地抑制I_K尾电流(I_(K·tail)),EC_(50)为13.3(11.6.6-16.7)μmol·L~(-1)。DDPH(>1.0μmol·L~(-1))明显抑制I_(Kl);同时,DDPH使I_(Kl)翻转电位向正电位方向移动。结论:DDPH对豚鼠心室肌细胞I_(Kl)和I_K具有明显的抑制作用。     

Electrophysiologic effects of sophocarpine on papillary muscle in guinea pig

Sophocarpine prolonged the action potential duration of guinea pig papillary muscle in a dose-dependent manner. After the preparations were exposed to sophocarpine 50 mumol/L for 30 min, APD50 and APD90 were prolonged from 189 +/- 21 and 216 +/- 24 ms to 205 +/- 27 and 241 +/- 25 ms (P less than 0.01). Simultaneously, ERP was prolonged from 202 +/- 14 to 211 +/- 16 ms, although the ERP/APD90 ratio was not changed. Sophocarpine had no significant effects on other AP parameters. Propranolol did not block sophocarpine effects.