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感觉神经与炎症:关于泰氏蝎毒素释放一种神经源性通透性因子的证据

Sensory nerves and inflammation: evidence for the release of a neurogenic permeability factor by tityustoxin.

作者信息

Leme J G, Pimenta A F, Raulino-Filho M, Diniz C R

出版信息

J Pathol. 1978 Mar;124(3):165-76. doi: 10.1002/path.1711240307.

DOI:10.1002/path.1711240307
PMID:722379
Abstract

Venom of the scorpion Tityus serrulatus and its active principle tityustoxin (TsTX), kept in contact with the peripheral cut end of the sciatic or saphenous nerve of the rat, induced inflammatory reactions in the areas supplied by the nerves. The reactions include increased vascular permeability and oedema formation below the tibio-tarsal articulation, and were similar to those evoked by electrical antidromic stimulation of these nerves. When electrical stimulation of the peripheral nerve ending preceded its contact with the toxin or, conversely, when the application of electrical pulses closely followed contact with TsTX, no marked increase in the vascular permeability and oedematous respones, subsequent to the second stimulation, was observed. Anti-histamine and anti-serotonin drugs, as well as substances capable of blocking synthesis of prostaglandins or activation of the kinin system, and also atropine, were ineffective in reducing the responses to TsTX or electrical stimuli. Since the responses were evoked at a distance, in the areas supplied by the nerves, they must be chemically mediated. It is concluded that TsTX and electrical antidromic stimuli affect sensory nerves inducing the release of a permeability-increasing factor, which is responsible for the observed reactions. This factor can be depleted from storage sites by prolonged stimulation of the nerves, is not inhibited by antagonists of known mediators of inflammatory reactions and most probably originates in sensory fibres.

摘要

将锯脂鲤属毒蝎毒液及其活性成分锯脂鲤毒素(TsTX)与大鼠坐骨神经或隐神经的外周切断端接触,会在神经所支配的区域引发炎症反应。这些反应包括胫跗关节下方血管通透性增加和水肿形成,且与这些神经的电逆向刺激所引发的反应相似。当在毒素接触外周神经末梢之前进行电刺激,或者相反,当在接触TsTX后紧接着施加电脉冲时,在第二次刺激后未观察到血管通透性和水肿反应有明显增加。抗组胺药、抗5-羟色胺药,以及能够阻断前列腺素合成或激肽系统激活的物质,还有阿托品,在减轻对TsTX或电刺激的反应方面均无效。由于这些反应是在神经所支配的远距离区域诱发的,所以它们必定是由化学物质介导的。得出的结论是,TsTX和电逆向刺激会影响感觉神经,诱导释放一种增加通透性的因子,该因子导致了所观察到的反应。通过长时间刺激神经,这种因子可从储存部位耗竭,不受已知炎症反应介质拮抗剂的抑制,并且很可能起源于感觉纤维。

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