Delpierre S, Pugnat C, Duté N, Jammes Y
Laboratoire de Physiologie Respiratoire, Faculté de Médecine Timone, Marseille, France.
Neurosci Lett. 1995 Feb 15;186(1):69-73. doi: 10.1016/0304-3940(95)11266-y.
It was previously shown that inspiratory resistive loading (IRL) increases the cerebrospinal fluid (CSF) level of beta endorphin in awake goats, and also that the slower ventilation induced by injection of this substance into the CSF of anesthetized dogs is suppressed after vagotomy. In the present study, performed on anesthetized rabbits, we evaluated the part played by vagal afferents in the ventilatory response to IRL after opioid receptor blockade by naloxone. During unloaded breathing, naloxone injection did not modify baseline ventilation. Conversely, naloxone partially reversed IRL-induced hypoventilation through an increase in respiratory rate. This effect was abolished after either vagotomy or cold blockade of large vagal fibers, but it persisted after procaine blockade of thin vagal fibers. These results suggest that pulmonary stretch receptors, which are connected to some large vagal afferent fibers, would play a major role in the ventilatory response to IRL under opioid receptor inhibition.
先前的研究表明，吸气性阻力负荷（IRL）可提高清醒山羊脑脊液（CSF）中β内啡肽的水平，还表明，将该物质注入麻醉犬的脑脊液所诱导的较慢通气，在迷走神经切断术后受到抑制。在本研究中，我们对麻醉兔进行实验，评估了纳洛酮阻断阿片受体后迷走神经传入纤维在对IRL的通气反应中所起的作用。在无负荷呼吸期间，注射纳洛酮并未改变基线通气。相反，纳洛酮通过增加呼吸频率部分逆转了IRL诱导的通气不足。迷走神经切断术或大迷走神经纤维冷阻断后，这种效应消失，但在普鲁卡因阻断细迷走神经纤维后仍持续存在。这些结果表明，与一些大的迷走神经传入纤维相连的肺牵张感受器，在阿片受体抑制下对IRL的通气反应中起主要作用。
