Department of Pharmacology, Institute of Biomedical Science, University of São Paulo, Sao Paulo, Brazil.
Department of Physiology and Biophysics, Institute of Biomedical Science, University of São Paulo, Sao Paulo, Brazil.
Am J Physiol Lung Cell Mol Physiol. 2019 Sep 1;317(3):L402-L413. doi: 10.1152/ajplung.00467.2018. Epub 2019 Jun 26.
Active expiration (AE) is part of the breathing phase; it is conditional and occurs when we increase our metabolic demand, such as during hypercapnia, hypoxia, or exercise. The parafacial respiratory group (pFRG) is involved in AE. Data from the literature suggest that excitatory and the absence of inhibitory inputs to the pFRG are necessary to determine AE. However, the source of the inputs to the pFRG that trigger AE remains unclear. We show in adult urethane-anesthetized Wistar rats that the pharmacological inhibition of the medial aspect of the nucleus of the solitary tract (mNTS) or the rostral aspect of the pedunculopontine tegmental nucleus (rPPTg) is able to generate AE. In addition, direct inhibitory projection from the mNTS or indirect cholinergic projection from the rPPTg is able to contact pFRG to trigger AE. The inhibition of the mNTS or the rPPTg under conditions of high metabolic demand, such as hypercapnia (9-10% CO), did not affect the AE. The present results suggest for the first time that inhibitory sources from the mNTS and a cholinergic pathway from the rPPTg, involving M2/M4 muscarinic receptors, could be important sources to modulate and sustain AE.
主动呼气（AE）是呼吸阶段的一部分；它是有条件的，发生在我们增加代谢需求时，例如在高碳酸血症、缺氧或运动期间。副面神经呼吸组（pFRG）参与 AE。文献中的数据表明，pFRG 兴奋性输入和抑制性输入的缺失对于确定 AE 是必要的。然而，触发 AE 的 pFRG 输入的来源仍不清楚。我们在成年乌拉坦麻醉的 Wistar 大鼠中表明，中缝核复合体（mNTS）的内侧部分或脑桥被盖网状核（rPPTg）的前部的药理学抑制能够产生 AE。此外，来自 mNTS 的直接抑制性投射或来自 rPPTg 的间接胆碱能投射能够接触 pFRG 以触发 AE。在高代谢需求的情况下，如高碳酸血症（9-10% CO），抑制 mNTS 或 rPPTg 并不影响 AE。本研究结果首次表明，来自 mNTS 的抑制性来源和来自 rPPTg 的胆碱能途径，涉及 M2/M4 毒蕈碱受体，可能是调节和维持 AE 的重要来源。
