Antiarrhythmic and electrophysiologic actions of clofilium in experimental canine models.
Antiarrhythmic and electrophysiologic actions of clofilium in experimental canine models.
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氯非铵在实验犬模型中的抗心律失常和电生理作用。
DOI：
10.1016/0014-2999(85)90184-0
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发表时间：
1985
影响因子：
5
通讯作者：
Lucchesi,BR
中科院分区：
文献类型：
--
作者：
Kopia,GA;Eller,BT;Patterson,E;Shea,MJ;Lucchesi,BR
在三个实验模型中研究了Clofilium。在非缺血和慢性梗塞的犬心脏中，氯非铵（0.5-2 mg/kg）产生剂量依赖性的心室颤动阈值（VFT）增加，但仅延长非缺血心脏正常心肌的有效不应期（ERP）。当对慢性梗塞心脏进行程控电刺激时，1 mg/kg氯非铵抑制了6只动物中5只的室性心动过速或室颤的再诱导，并减缓了第6只动物的诱导心动过速的速率。氯非铵对正常心肌的心室不应期无明显影响，在舒张期阈值电流为2倍时（对照组176 ± 5 ms，氯非铵后187 ± 9 ms，P > 0.05），在10 mA时（对照组134 ± 6 ms，氯非铵后137 ± 13 ms，P > 0.05）。此外，慢性给予氯非铵（2 mg/kg，i. v.，随后每12小时给药1 mg/kg）对降低冠状动脉猝死犬模型的死亡率无效。在10只生理盐水处理的清醒动物中，在存在先前缺血性损伤的情况下对左回旋支冠状动脉进行电诱导内膜损伤，所有10只动物在电流应用后173 ± 45 min内突然死于心室颤动。在相似条件下，7只动物在249 ± 88 min内突然死亡（P > 0.05），3只动物存活（P > 0.10）。然而，氯非铵确实延长了这些动物的有效不应期（生理盐水处理组为150 ± 3 ms，氯非铵处理组为195 ± 7 ms）。从我们的数据中可以得出结论，氯非铵在正常心肌中的电生理作用与抗心律失常作用之间几乎没有关系。此外，简单延长正常非缺血心肌中的不应期可能不足以预防心室颤动，心室颤动是对叠加在慢性损伤心肌上的短暂性缺血事件的响应而发展的。
Clofilium was studied in three experimental models. In non-ischemic and chronically infarcted canine hearts, clofilium (0.5–2 mg/kg) produced a dose-dependent increase in electrical ventricular fibrillation threshold (VFT), but prolonged the effective refractory period (ERP) of normal myocardium in only the non-ischemic heart. When chronically infarcted hearts were subjected to programmed electrical stimulation, 1 mg/kg of clofilium inhibited the re-induction of either ventricular tachycardia or ventricular fibrillation in 5 of 6 animals and slowed the rate of the induced tachycardia in the sixth. Clofilium, however, failed to alter ventricular refractory periods of normal myocardium at either twice diastolic threshold current (176 ± 5 ms control vs. 187 ± 9 ms post-clofilium, P > 0.05) or at 10 mA (134 ± 6 ms control vs. 137 ± 13 ms post-clofilium, P > 0.05). In addition, chronic administration of clofilium (2 mg/kg, i.v., followed by 1 mg/kg every 12 h) was ineffective in decreasing mortality in a canine model of sudden coronary death. Of 10 saline-treated conscious animals subjected to an electrically-induced intimal lesion of the left circumflex coronary artery in the presence of a previous ischemic insult, all 10 died suddenly of ventricular fibrillation within 173 ± 45 min after current application. Under similar conditions, 7 clofilium-treated animals died suddenly within 249 ± 88 min (P > 0.05) after current application while 3 animals survived (P > 0.10). Clofilium did, however, elevate the effective refractory period in these animals (150 ± 3 ms saline-treated vs. 195 ± 7 ms clofilium-reated). It is concluded from our data that there is little relationship between clofilium's electrophysiologic actions in normal myocardium and antiarrhythmic effects. Furthermore, simple prolongation of refractorines in normal non-ischemic myocardium may be insufficient for the prevention of ventricular fibrillation which develops in response to a transient ischemic event superimposed on a chronically injured myocardium.
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