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香烟烟雾诱导的豚鼠肺支气管收缩和速激肽释放。

Cigarette smoke-induced bronchoconstriction and release of tachykinins in guinea pig lungs.

作者信息

Lee L Y, Lou Y P, Hong J L, Lundberg J M

机构信息

Department of Pharmacology, Karolinska Institute, Stockholm, Sweden.

出版信息

Respir Physiol. 1995 Jan;99(1):173-81. doi: 10.1016/0034-5687(94)00088-h.

Abstract

Two series of experiments were carried out to determine whether the release of tachykinins is involved in the bronchoconstriction induced by inhalation of cigarette smoke in guinea pigs. In the first series, cigarette smoke consistently induced bronchoconstriction (delta RL = +203% and delta Cdyn = -46%) in anesthetized guinea pigs, and the response was only partially blocked by bilateral cervical vagotomy. However, the smoke-induced bronchial constriction was completely abolished in animals receiving a systemic capsaicin pretreatment to destroy the tachykinin-containing C-fiber afferents. In the second series, the bronchoconstrictive effect of cigarette smoke was increased by approx. three times in isolated perfused guinea pig lungs when phosphoramidon (3 x 10(-6) M) was added to the perfusate to prevent the degradation of tachykinins after their release. Moreover, the enhanced bronchomotor response to smoke was accompanied by an overflow of neurokinin A-like immunoreactivity (LI) and calcitonin gene-related peptide -LI in the pulmonary effluent. These studies showed that cigarette smoke triggers the release of tachykinins in the lungs, which plays an important role in the smoke-induced bronchoconstrictive effect in guinea pigs.

摘要

进行了两个系列的实验,以确定速激肽的释放是否参与豚鼠吸入香烟烟雾诱导的支气管收缩。在第一个系列中,香烟烟雾在麻醉的豚鼠中持续诱导支气管收缩(ΔRL = +203%,ΔCdyn = -46%),并且该反应仅被双侧颈迷走神经切断术部分阻断。然而,在接受全身性辣椒素预处理以破坏含速激肽的C纤维传入神经的动物中,烟雾诱导的支气管收缩被完全消除。在第二个系列中,当向灌注液中加入磷酰胺(3×10(-6) M)以防止速激肽释放后降解时,香烟烟雾在离体灌注的豚鼠肺中的支气管收缩作用增加了约三倍。此外,对烟雾增强的支气管运动反应伴随着肺流出物中神经激肽A样免疫反应性(LI)和降钙素基因相关肽-LI的溢出。这些研究表明,香烟烟雾触发肺中速激肽的释放,这在豚鼠烟雾诱导的支气管收缩作用中起重要作用。

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