Acute intermittent hypoxia (AIH) modifies the functioning of the respiratory network, causing respiratory motor facilitation in anesthetized animals and a compensatory increase in pulmonary ventilation in freely behaving animals. However, it is still unclear whether the ventilatory facilitation induced by AIH in unanesthetized animals is associated with changes in the respiratory pattern. We found that Holtzman male rats (80–150 g) exposed to AIH (10 × 6% O₂ for 30–40 s every 5 min, n = 9) exhibited a prolonged (30 min) increase in baseline minute ventilation (P < 0.05) compared to control animals (n = 13), combined with the occurrence of late expiratory peak flow events, suggesting the presence of active expiration. The increase in ventilation after AIH was also accompanied by reductions in arterial CO₂ and body temperature (n = 5–6, P < 0.05). The systemic treatment with ketanserin (a 5-HT₂ receptor antagonist) before AIH prevented the changes in ventilation and active expiration (n = 11) but potentiated the hypothermic response (n = 5, P < 0.05) when compared to appropriate control rats (n = 13). Our findings indicate that the ventilatory long-term facilitation elicited by AIH exposure in unanesthetized rats is linked to the generation of active expiration by mechanisms that may depend on the activation of serotonin receptors. In contrast, the decrease in body temperature induced by AIH may not require 5-HT₂ receptor activation.

急性间歇性缺氧 (AIH) 会改变呼吸网络的功能，导致麻醉动物的呼吸运动促进和自由行为动物的肺通气量补偿性增加。然而，目前尚不清楚 AIH 在未麻醉动物中引起的通气促进是否与呼吸模式的变化有关。我们发现，Holtzman 雄性大鼠 (80-150 g) 暴露于 AIH (10 × 6% O ₂每 5 分钟 30-40 秒，n = 9) 表现出基线分钟通气量延长 (30 分钟) 增加 (P < 0.05）与对照动物（n = 13）相比，结合晚期呼气峰值流量事件的发生，表明存在主动呼气。AIH 后通气的增加也伴随着动脉 CO2 的减少₂和体温（n = 5-6，P < 0.05）。_{与适当的对照大鼠相比，AIH 前用酮色林（一种 5-HT 2}受体拮抗剂）进行全身治疗可防止通气和主动呼气的变化（n = 11），但增强了低温反应（n = 5，P < 0.05）。 n = 13)。我们的研究结果表明，在未麻醉的大鼠中，AIH 暴露引起的长期通气促进与可能依赖于血清素受体激活的机制产生的主动呼气有关。相反，AIH 引起的体温降低可能不需要 5-HT ₂受体激活。