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前列腺素E2对豚鼠气管神经节传递的影响。

Effects of prostaglandin E2 on ganglionic transmission in the guinea pig trachea.

作者信息

DeLisle S, Biggs D, Wang A, Martin J G

机构信息

Meakins-Christie Laboratories, McGill University, Montreal, Quebec, Canada.

出版信息

Respir Physiol. 1992 Jan;87(1):131-9. doi: 10.1016/0034-5687(92)90105-6.

Abstract

We studied the effects of prostaglandin E2 (PGE2) on the contractile responses of in vitro guinea pig tracheal preparations with intact vagal innervation. The preparation was stimulated either through the vagal nerves (NS) or with an electrical field (EFS) and trachealis response was assessed from the pressure change inside the tracheal tube. Ganglionic blockade by hexamethonium inhibited responses to NS but did not affect EFS while both responses to NS and EFS were abolished by atropine or tetrodotoxin. This indicates that responses to both stimulation modalities were mediated by cholinergic nerves but that NS involved a ganglionic relay whereas EFS did not. Within the frequency range of 0.1-20 Hz, there was a gradual increase in the pressure generated by the trachealis muscle with increasing frequency of stimulation. The frequency-response relationship was similar for NS and EFS. Thus, the ganglion does not appear to play an important filtering or amplifying role under those conditions. PGE2 (1-50 mM) produced a concentration-dependent inhibition of NS and EFS without affecting responses to exogenous acetylcholine (ACh). This suggests that the main action of PGE2 is to reduce ACh release from post-ganglionic nerve terminals. PGE2 inhibited EFS to a larger extent than NS; we postulate a possible excitatory effect of PGE2 on neurotransmission in the airway ganglia.

摘要

我们研究了前列腺素E2(PGE2)对具有完整迷走神经支配的体外豚鼠气管制备物收缩反应的影响。通过迷走神经(NS)或电场(EFS)刺激该制备物,并根据气管插管内的压力变化评估气管肌反应。六甲铵引起的神经节阻滞抑制了对NS的反应,但不影响EFS,而阿托品或河豚毒素则消除了对NS和EFS的反应。这表明对两种刺激方式的反应均由胆碱能神经介导,但NS涉及神经节中继,而EFS则不涉及。在0.1 - 20 Hz的频率范围内,随着刺激频率的增加,气管肌产生的压力逐渐增加。NS和EFS的频率 - 反应关系相似。因此,在这些条件下,神经节似乎并未发挥重要的滤波或放大作用。PGE2(1 - 50 mM)对NS和EFS产生浓度依赖性抑制,而不影响对外源性乙酰胆碱(ACh)的反应。这表明PGE2的主要作用是减少节后神经末梢的ACh释放。PGE2对EFS的抑制程度大于NS;我们推测PGE2对气道神经节神经传递可能具有兴奋作用。

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