Atmospheric respiration and the complex cycles in mammalian breathing mechanisms

McCutcheon, F. H.

doi:10.1002/jcp.1030410207

Cited by 39 publications

(29 citation statements)

References 14 publications

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“…We are not aware of any study to date that has specifically examined the effect of metabolic rate per se on the incidence of augmented breaths. However, it is known that larger mammals are known to express less frequent augmented breaths compared with small mammals (46,47). Indeed, one of the benefits of using rats to study mechanisms involved in the generation of augmented breaths is that they express them relatively frequently, several times per hour in normal conditions.…”

Section: Discussionmentioning

confidence: 98%

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Hypocapnia increases the prevalence of hypoxia-induced augmented breaths

Bell

Ferguson

Kehoe

et al. 2009

American Journal of Physiology-Regulatory, Integrative and Comp

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Augmented breaths promote respiratory instability and have been implicated in triggering periods of sleep-disordered breathing. Since respiratory instability is well known to be exacerbated by hypocapnia, we asked whether one of the destabilizing effects of hypocapnia might be related to an increased prevalence of augmented breaths. With this question in mind, we first sought to determine whether hypoxia-induced augmented breaths are more prevalent when hypocapnia is also present. To do this, we studied the breath-by-breath ventilatory responses of a group of freely behaving adult rats in a variety of different respiratory background conditions. We found that the prevalence of augmented breaths was dramatically increased during hypocapnic-hypoxia compared with room air conditions. When hypocapnia was prevented during exposure to hypoxia by adding 5% CO2 to the inspired air, the rate of occurrence of augmented breaths was no greater than that observed in room air. The addition of CO2 alone to room air had no effect on the prevalence of augmented breaths. We conclude that in spontaneously breathing rats, hypoxia promotes the generation of augmented breaths, but only in poikilocapnic conditions, where hypocapnia develops. Our results, therefore, reveal a means by which CO2 exerts a stabilizing influence on breathing, which may be of particular relevance during sleep in conditions commonly associated with respiratory instability.

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Section: Discussionmentioning

confidence: 98%

“…Augmented breaths have been documented and studied across a diverse spectrum of species (46,47), and their ubiquitous presence alludes to the physiological importance of their function in the animal. Augmented breaths function to prevent atelectisis, which otherwise results in collapsed and hypoventilated regions of the lung (58).…”

mentioning

confidence: 99%

Hypocapnia increases the prevalence of hypoxia-induced augmented breaths

Bell

Ferguson

Kehoe

et al. 2009

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Sighs also occur spontaneously, from several per hour in humans to dozens per hour in rodents 1,2 . Their recurrence during normal breathing enhances gas exchange and may preserve lung integrity by reinflating collapsed alveoli 2-4 .…”

Section: Introductionmentioning

confidence: 99%

The peptidergic control circuit for sighing

Janczewski

Yackle

et al. 2016

Nature

184

175

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Sighs are long, deep breaths expressing sadness, relief, or exhaustion. Sighs also occur spontaneously every few minutes to reinflate alveoli, and sighing increases under hypoxia, stress, and certain psychiatric conditions. Here we use molecular, genetic, and pharmacologic approaches to identify a peptidergic sigh control circuit in murine brain. Small neural subpopulations in a key breathing control center (RTN/pFRG) express bombesin-like neuropeptide genes neuromedin B (Nmb) or gastrin releasing peptide (Grp). These project to the preBötzinger Complex (preBötC), the respiratory rhythm generator, which expresses NMB and GRP receptors in overlapping subsets of ~200 neurons. Introducing either neuropeptide into preBötC, or onto preBötC slices, induced sighing, whereas elimination or inhibition of either receptor reduced basal sighing and inhibition of both abolished it. Ablating receptor-expressing neurons eliminated basal and hypoxia-induced sighing, but left breathing otherwise intact initially. We propose these overlapping peptidergic pathways comprise the core of a sigh control circuit that integrates physiological and perhaps emotional input to transform normal breaths into sighs.

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“…OCCASIONAL RESPIRATORY DISTURBANCES, in the form of augmented breaths, are a typical feature of the resting breathing rhythm of all mammalian species studied, including humans (4,34,35). Augmented breaths, also referred to as "sighs," are distinct from normal background eupneic breaths for a number of reasons.…”

mentioning

confidence: 99%

Acetazolamide suppresses the prevalence of augmented breaths during exposure to hypoxia

Bell¹,

Haouzi²

2009

American Journal of Physiology-Regulatory, Integrative and Comp

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Augmented breaths, or "sighs," commonly destabilize respiratory rhythm, precipitating apneas and variability in the depth and rate of breathing, which may then exacerbate sleep-disordered breathing in vulnerable individuals. We previously demonstrated that hypocapnia is a unique condition associated with a high prevalence of augmented breaths during exposure to hypoxia; the prevalence of augmented breaths during hypoxia can be returned to normal simply by the addition of CO(2) to the inspired air. We hypothesized that counteracting the effect of respiratory alkalosis during hypocapnic hypoxia by blocking carbonic anhydrase would yield a similar effect. We, therefore, investigated the effect of acetazolamide on the prevalence of augmented breaths in the resting breathing cycle in five awake, adult male rats. We found a 475% increase in the prevalence of augmented breaths in animals exposed to hypocapnic hypoxia compared with room air. Acetazolamide treatment (100 mg/kg i.p. bid) for 3 days resulted in a rapid and potent suppression of the generation of augmented breaths during hypoxia. Within 90 min of the first dose of acetazolamide, the prevalence of augmented breaths in hypoxia fell to levels that were no greater than those observed in room air. On cessation of treatment, exposure to hypocapnic hypoxia once again caused a large increase in the prevalence of augmented breaths. These results reveal a novel means by which acetazolamide acts to stabilize breathing and may help explain the beneficial effects of the drug on breathing stability at altitude and in patients with central forms of sleep-disordered breathing.

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Atmospheric respiration and the complex cycles in mammalian breathing mechanisms

Cited by 39 publications

References 14 publications

Hypocapnia increases the prevalence of hypoxia-induced augmented breaths

Hypocapnia increases the prevalence of hypoxia-induced augmented breaths

The peptidergic control circuit for sighing

Acetazolamide suppresses the prevalence of augmented breaths during exposure to hypoxia

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