Influence of estrus cycle and timing of lipopolysaccharide (LPS)‐induced inflammation on inspiratory motor activity and the acute hypoxic ventilatory response (HVR) in urethane‐anesthetized spontaneously breathing adult female Sprague‐Dawley rat

In humans, the hypoxic ventilatory response (HVR) is augmented when preceded by a short hyperoxic exposure (Y. Honda, H. Tani, A. Masuda, T. Kobayashi, T. Nishino, H. Kimura, S. Masuyama, and T. Kuriyama. J. Appl. Physiol. 81: 1627–1632, 1996). To examine whether neuronal nitric oxide synthase (nNOS) is involved in such hyperoxia-induced HVR potentiation, 17 male Sprague-Dawley adult rats underwent hypoxic challenges (10% O2-5% CO2-balance N2) preceded either by 10 min of room air (−O2) or of 100% O2(+O2). At least 48 h later, similar challenges were performed after the animals received the selective nNOS inhibitor 7-nitroindazole (25 mg/kg ip). In −O2 runs, minute ventilation (V˙e) increased from 121.3 ± 20.5 (SD) ml/min in room air to 191.7 ± 23.8 ml/min in hypoxia ( P< 0.01). After +O2,V˙e increased from 114.1 ± 19.8 ml/min in room air to 218.4 ± 47.0 ml/min in hypoxia (+O2 vs. −O2: P < 0.005, ANOVA). After 7-nitroindazole administration, HVR was not affected in the −O2 treatment group withV˙e increasing from 113.7 ± 17.8 ml/min in room air to 185.8 ± 35.0 ml/min in hypoxia ( P < 0.01). However, HVR potentiation in +O2-exposed animals was abolished (111.8 ± 18.0 ml/min in room air to 184.1 ± 35.6 ml/min in hypoxia; +O2 vs. −O2: P not significant). We conclude that in the conscious rat nNOS activation mediates essential components of the HVR potentiation elicited by a previous short hyperoxic exposure.

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Intratracheal Lipopolysaccharide (LPS) Administration Attenuates Acute Hypoxic Ventilatory Response (HVR) in Spontaneously Breathing Adult C57BL/6 Male Mice

The FASEB Journal ◽

10.1096/fasebj.29.1_supplement.1012.22 ◽

2015 ◽

Vol 29 (S1) ◽

Author(s):

Jonathan Conyers ◽

Keeley Rice ◽

Mohammed Ahmad ◽

Muzammil Hyder ◽

Irene Solomon

Keyword(s):

Ventilatory Response ◽

Male Mice ◽

Hypoxic Ventilatory Response ◽

Spontaneously Breathing

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Interleukin-1beta suppresses the ventilatory hypoxic response in rats via prostaglandin-dependent pathways

Canadian Journal of Physiology and Pharmacology ◽

10.1139/cjpp-2016-0419 ◽

2017 ◽

Vol 95 (6) ◽

pp. 681-685 ◽

Cited By ~ 4

Author(s):

Nina P. Aleksandrova ◽

Galina A. Danilova ◽

Viacheslav G. Aleksandrov

Keyword(s):

Ventilatory Response ◽

Prostaglandin Synthesis ◽

Respiratory Neurons ◽

Hypoxic Ventilatory Response ◽

Hypoxic Response ◽

Interleukin 1Beta ◽

Spontaneously Breathing ◽

The Brain ◽

Ventilatory Response To Hypoxia

We investigated the effect of the major inflammatory cytokine interleukin-1beta (IL-1β) on the ventilatory response to hypoxia. The goal was to test the hypothesis that IL-1β impairs the hypoxic ventilatory response in vivo by indirectly inhibiting respiratory neurons in the brainstem via prostaglandins. Thus, IL-1β was delivered by cerebroventricular injection, and the ventilatory hypoxic response was assessed in anesthetized, spontaneously breathing rats pretreated with or without diclofenac, a nonspecific inhibitor of prostaglandin synthesis. We found that the slope of the ventilatory response to hypoxia decreased almost 2-fold from 10.4 ± 3.02 to 4.06 ± 0.86 mL·min−1·(mm Hg)−1 (–61%) 90 min after administration of IL-1β (p < 0.05). The slope of tidal volume and mean inspiratory flow also decreased from 0.074 ± 0.02 to 0.039 ± 0.01 mL·(mm Hg)−1 (–45%, p < 0.05), and from 0.36 ± 0.07 to 0.2 ± 0.04 mL·s−1·(mm Hg)−1 (–46%, p < 0.05), respectively. Pretreatment with diclofenac blocked these effects. Thus, the data indicate that IL-1β degrades the ventilatory hypoxic response by stimulating production of prostaglandin. The increase of cerebral levels of IL-1β, which is induced by the activation of immune cells in the brain, may impair respiratory chemoreflexes.

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