Ganglionic and cardiac actions of batrachotoxin.
Ganglionic and cardiac actions of batrachotoxin.
复制标题
箭毒毒素的神经节和心脏作用。
DOI：
10.1016/0014-2999(70)90023-3
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发表时间：
1970
影响因子：
5
通讯作者：
J. E. Warnick
中科院分区：
文献类型：
--
作者：
S. Kayaalp;E. Albuquerque;J. E. Warnick
从哥伦比亚箭毒蛙（phylloates aurotaenia）中纯化的活性成分Batrachotoxin (BTX)，当给药0.3 ~ 1.3 μg时，可阻断其在兔颈上神经节制剂中的传播。初始神经节电位比晚期电位更易受BTX抑制的影响；正后电位被消除，甚至逆转。在较高剂量（1.0 μg或更高）下，该毒物引起神经节传导的长时间阻断；在服用BTX后的两小时内，只观察到晚期尖峰的部分恢复。BTX对神经节的作用部分是由于其对神经节前交感神经冲动传导的影响，其中毒素不同程度地阻断了神经节前反节律诱发动作电位的初始通道。BTX后神经节传导和神经传导的功能障碍均与刺激剂量和频率有关。在大多数实验中，在BTX产生的神经节传导阻滞过程中，神经节细胞对去极化剂尼古丁、乙酰胆碱和氯化钾有反应。该药还可引起多种心律失常，包括a - v传导阻滞、多灶性室性异搏、室性心动过速和纤颤。
Batrachotoxin (BTX), the purified active principle from the Colombian Arrow Poison Frog (Phyllobates aurotaenia), blocked transmission in thein siturabbit superior cervical ganglion preparation when administered intraarterially in doses of 0.3 to 1.3 μg. The initial ganglionic potential was more susceptible to BTX depression than the late potential; the positive afterpotential was abolished and even reversed. At higher doses (1.0 μg or more), the poison caused a prolonged blockade of the ganglionic transmission; a partial recovery of only the late spike was observed within two hours following the administration of BTX. These actions of BTX on the ganglion were partly due to its effect on the impulse conduction in the preganglionic sympathetic nerve in which the poison differentially blocked the initial spake of the preganglionic antidromically evoked action potential. Both the failure of ganglionic transmission and of nerve conduction occuring after BTX were functions of the dose and frequency of stimulation. In most experiments during the blockade of the ganglionic transmission produced by BTX, the ganglion cells were responsive to the depolarizing agents, nicotine, acetylcholine and potassium chloride. The poison also produced a large variety of cardiac arrhythmias including A-V block, multifocal ventricular ectopic beats, ventricular tachycardia and fibrillation.