吡喹酮引起心律失常的中枢机制

清醒家兔静注吡喹酮45mg/kg后,心律失常发生率为76.5%。侧脑室注入吡喹酮3mg/kg后78.9%的兔出现与静注时性质相同的心律失常。从椎动脉注入苯妥英钠3mg/kg能即刻对抗静注吡喹酮所致的心律失常。毁坏双侧肾上腺體质,利血平化及中枢应用心得安后,吡喹酮侧脑室注射所致心律失常发生率显著降低。中枢应用心得安及心得宁后,吡喹酮静注所致心律失常发生率也显著降低,但椎动脉注射可乐宁却无效。吡喹酮引起心律失常可能与中枢β受体兴奋而导致肾上腺髓质分泌肾上腺素及交感神经释放去甲肾上腺素有关。

CENTRAL MECHANISM OF PYQUITON INDUCED ARRHYTHMIA

Heart rhythm disturbances in normal rabbits induced by intravenous (ⅳ 45 mg/kg) or intracerebroventricular(i c v 3 mg/kg) administration of pyquiton were quite similar in frequency(76.5% or 78.9%, respectively) and in ECG (ventricular premature beats or ventricular tachycardia). Injection of phenytoin sodium(3 mg/kg) into the vertebral artery immediately abolished the arrhythmia induced by iv pyquiton. Destruction of the adrenal medulla, reserpinization or icy propranolol significantly decreased the frequency of the arrhythmia induced by icv Pyquiton. Ⅰ cv propranolol or practolol significantly decreased the frequency of the arrhythmia induced by iv pyquiton, but administration of clonidineinto the vertebral artery did not. Our results seem to suggest that pyquiton-induced heart rhythm disturbances in normal rabbits possibly originated from the stimulation of certain central β-adrenergic areas which caused overactivity of the peripheral sympathetic system.