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神经肽 Y(2)受体的激活对麻醉大鼠的心肺变量产生兴奋作用。

Activation of neuropeptide Y(2) receptors exerts an excitatory action on cardio-respiratory variables in anaesthetized rats.

机构信息

Laboratory of Respiratory Reflexes, Mossakowski Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland.

出版信息

Neuropeptides. 2011 Aug;45(4):281-6. doi: 10.1016/j.npep.2011.05.003. Epub 2011 Jun 11.

DOI:10.1016/j.npep.2011.05.003
PMID:21658765
Abstract

The respiratory effects of stimulation of NPYY(2) receptors were studied in spontaneously breathing rats that were either (i) neurally intact and subsequently bilaterally vagotomized in the neck, or (ii) neurally intact and subjected to supranodosal vagotomy or (iii) neurally intact treated with pharmacological blockade of NPY(1-2) receptors. Before neural interventions an intravenous (iv) bolus of the NPYY(2) receptor agonist NPY 13-36 (10 μg/kg) increased breathing rate, tidal volume and mean arterial blood pressure (MAP). Section of the midcervical vagi abrogated NPY 13-36-evoked increase in respiratory rate but had no effect on augmented tidal volume, minute ventilation and blood pressure. Supranodosal vagotomy prevented the increase in tidal volume and slightly reduced the pressor response. Blockade of NPYY(2) receptor with intravenous doses of BIIE 0246 eliminated cardio-respiratory effects of NPY 13-36 injection. BMS 193885 - an antagonist of NPYY(1) receptor-was not effective in abrogating cardio-respiratory response. The present study showed that (i) NPY 13-36 induced stimulation of breathing results from activation of NPYY(2) receptors associated with pulmonary vagal afferentation; (ii) the increase in the frequency of breathing is mediated by midcervical vagi and augmentation of tidal volume relies on the intact supranodosal trunks (iii) the pressor response results from the excitation of NPYY(2) receptors outside of the vagal pathway.

摘要

刺激 NPYY(2) 受体对呼吸的影响在自主呼吸的大鼠中进行研究,这些大鼠要么(i)神经完整,随后在颈部双侧迷走神经切断,要么(ii)神经完整,接受超神经干迷走神经切断术,要么(iii)神经完整,用 NPY(1-2) 受体的药理学阻断治疗。在神经干预之前,静脉内(iv)注射 NPYY(2) 受体激动剂 NPY 13-36(10 μg/kg)会增加呼吸频率、潮气量和平均动脉血压(MAP)。中颈迷走神经切断术消除了 NPY 13-36 引起的呼吸频率增加,但对潮气量增加、分钟通气量和血压没有影响。超神经干迷走神经切断术阻止了潮气量的增加,并略微降低了升压反应。静脉内给予 BIIE 0246 阻断 NPYY(2) 受体消除了 NPY 13-36 注射引起的心肺作用。NPYY(1) 受体拮抗剂 BMS 193885 不能有效阻断心肺反应。本研究表明:(i)NPY 13-36 诱导的呼吸刺激是由于与肺迷走传入有关的 NPYY(2) 受体的激活引起的;(ii)呼吸频率的增加是由中颈迷走神经介导的,潮气量的增加依赖于完整的超神经干(iii)升压反应是由迷走神经通路外的 NPYY(2) 受体兴奋引起的。

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