Rao T S, Seth S D, Manchanda S C, Nayar U
Prostaglandins. 1987 Mar;33(3):339-50. doi: 10.1016/0090-6980(87)90017-7.
The role of the central nervous system (CNS) in the antiarrhythmic effects of prostaglandins (PGs) E2, F2 alpha, and I2 was studied by administering each agent into the left lateral cerebral ventricle (i.c.v. administration) of chloralose-anaesthetized cats. The cardiac arrhythmias were produced by intravenous (i.v.) infusion of ouabain (1 microgram/kg/min). The PGs E2, F2 alpha and I2 on i.c.v. administration in the dose range of 1 ng to 10 micrograms failed to inhibit ouabain-induced cardiac arrhythmias. However, when infused i.v., PGE2 (1 microgram/kg/min), PGF2 alpha (5 micrograms/kg/min), and PGI2 (2 micrograms/kg/min) effectively suppressed these arrhythmias. The standard antiarrhythmic drug propranolol (0.5-8.0 mg) on i.c.v. administration also significantly reduced the ouabain-induced cardiac arrhythmias. It is suggested that the CNS is not the site of action of PGs E2, F2 alpha, and I2 in antagonising the ouabain-induced cardiotoxicity in cats.
通过将前列腺素E2、F2α和I2分别注入水合氯醛麻醉猫的左侧脑室(脑室内给药),研究了中枢神经系统(CNS)在前列腺素(PGs)E2、F2α和I2抗心律失常作用中的作用。心律失常通过静脉输注哇巴因(1微克/千克/分钟)诱发。脑室内给予剂量范围为1纳克至10微克的PGs E2、F2α和I2未能抑制哇巴因诱发的心律失常。然而,静脉输注时,前列腺素E2(1微克/千克/分钟)、前列腺素F2α(5微克/千克/分钟)和前列环素I2(2微克/千克/分钟)可有效抑制这些心律失常。标准抗心律失常药物普萘洛尔(0.5 - 8.0毫克)脑室内给药也可显著减少哇巴因诱发的心律失常。提示在拮抗哇巴因诱发的猫心脏毒性方面,中枢神经系统不是PGs E2、F2α和I2的作用部位。