Nakanishi H, Ono T, Shirasaka M, Yoshida H
Department of Pharmacology, Fukushima Medical College, Japan.
Fukushima J Med Sci. 1992 Dec;38(2):105-10.
Arrhythmia was produced by the rapid intravenous injection of ouabain 200 micrograms/kg in anesthetized guinea-pigs. The incidence of ventricular fibrillation (V.F.) induced by the ouabain challenge was significantly decreased by the pretreatment with prostaglandin (PG) E1 5 micrograms/kg or propranolol 0.5 mg/kg, but not with prostacyclin (PGI2) 0.5 or 5 micrograms/kg. Also, a significant number of animals treated with PGE1 or propranolol, but not PGI2, showed recurrent reversion to sinus or ventricular rhythm from V.F. and survived more than 20 min after the ouabain challenge. On the other hand, almost all animals treated with PGI2 produced V.F., which converted to cardiac arrest within 20 min after the ouabain challenge. The finding shows that PGI2 has no protective action on V.F. induced by ouabain in anesthetized guinea-pigs. Involvement of norepinephrine released from sympathetic nerve terminals in ouabain-induced V.F. was assumed.
在麻醉的豚鼠中,通过快速静脉注射200微克/千克哇巴因诱发心律失常。用5微克/千克前列腺素(PG)E1或0.5毫克/千克普萘洛尔预处理可显著降低哇巴因激发诱导的心室颤动(V.F.)发生率,但0.5或5微克/千克前列环素(PGI2)预处理则无此作用。此外,用PGE1或普萘洛尔治疗的相当数量动物(而非PGI2治疗的动物)显示从心室颤动复归窦性或室性节律,并在哇巴因激发后存活超过20分钟。另一方面,几乎所有用PGI2治疗的动物均发生心室颤动,并在哇巴因激发后20分钟内转为心脏停搏。该发现表明PGI2对麻醉豚鼠中哇巴因诱导的心室颤动无保护作用。推测交感神经末梢释放的去甲肾上腺素参与了哇巴因诱导的心室颤动。