The role of the different components of the respiratory network in the mediation of opioid-induced respiratory depression is still unclear. We investigated the contribution of the preBötzinger Complex (preBötC) and the neighbouring Bötzinger Complex (BötC) and inspiratory portion of the ventral respiratory group (iVRG) in anesthetized, vagotomized, paralyzed and artificially ventilated adult rabbits making use of bilateral microinjections (30−50 nl) of the μ-opioid receptor agonist [D-Ala², N-Me-Phe⁴, Gly⁵-ol]-enkephalin (DAMGO). Dose-dependent effects were observed. In the preBötC and the BötC 0.1 mM DAMGO microinjections caused mainly reductions in peak phrenic amplitude associated with tonic phrenic activity and irregular (ataxic) patterns of breathing that were more pronounced in the preBötC. Apneic effects developed at 0.5 mM. In the iVRG DAMGO provoked decreases in amplitude and frequency of phrenic bursts at 0.1 mM and apnea at 0.5 mM. Local 5 mM naloxone reversed the apneic effects. The results imply that different components of the respiratory network may contribute to opioid-induced respiratory disorders.

呼吸网络的不同成分在介导阿片类药物引起的呼吸抑制中的作用尚不清楚。我们研究了 preBötzinger 复合体 (preBötC) 和邻近的 Bötzinger 复合体 (BötC) 以及腹侧呼吸组 (iVRG) 的吸气部分对麻醉、迷走神经切断术、瘫痪和人工通气的成年兔的贡献，利用双侧显微注射 (30-50 nl) μ-阿片受体激动剂 [D-Ala ² , N-Me-Phe ⁴ , Gly ⁵-ol]-脑啡肽 (DAMGO)。观察到剂量依赖性效应。在 preBötC 和 BötC 中，0.1 mM DAMGO 显微注射主要导致与强直膈活动和不规则（共济失调）呼吸模式相关的峰值膈振幅降低，这在 preBötC 中更为明显。在 0.5 mM 时出现窒息效应。在 iVRG 中，DAMGO 在 0.1 mM 和 0.5 mM 时引起膈肌爆发的振幅和频率降低。局部 5 mM 纳洛酮逆转了呼吸暂停效应。结果表明呼吸网络的不同组成部分可能导致阿片类药物引起的呼吸系统疾病。