Respiratory volume-time relationships during resistive loading in the cat

Zechman, F. W.; Frazier, Donald T.; Lally, D A

doi:10.1152/jappl.1976.40.2.177

Cited by 47 publications

(28 citation statements)

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“…This load compensation response has been reported in anesthetized animals using external resistive loads to breathing and is characterized by the recruitment of respiratory muscle activity, an increase in breath duration, and a decrease in tidal volume (6,8,(13)(14)(15)(16)57). Depending on the timing within the breath phase of the added resistive load (end-inspiratory vs. endexpiratory), inspiratory or expiratory duration is increased.…”

Section: Itto Load Compensationmentioning

confidence: 74%

“…A similar volume-timing relationship was found when a mechanical stimulus in the form of an external resistive load was applied. Loading of the inspiratory (57) or expiratory (33) phase caused a decrease in volume and an increase in the duration of the respective loaded breath phase. The response to the added loads was called the respiratory load compensation reflex.…”

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confidence: 99%

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Tracheal occlusion modulates the gene expression profile of the medial thalamus in anesthetized rats

Bernhardt¹,

García-Reyero

Vovk³

et al. 2011

Journal of Applied Physiology

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scious awareness of breathing requires the activation of higher brain centers and is believed to be a neural gated process. The thalamus could be responsible for the gating of respiratory sensory information to the cortex. It was reasoned that if the thalamus is the neural gate, then tracheal obstructions will modulate the gene expression profile of the thalamus. Anesthetized rats were instrumented with an inflatable cuff sutured around the trachea. The cuff was inflated to obstruct 2-4 breaths, then deflated for a minimum of 15 breaths. Obstructions were repeated for 10 min followed by immediate dissection of the medial thalamus. Following the occlusion protocol, 588 genes were found to be altered (P Ͻ 0.05; log2 fold change Ն 0.4), with 327 genes downregulated and 261 genes upregulated. A significant upregulation of the serotonin HTR2A receptor and significant downregulation of the dopamine DRD1 receptor genes were found. A pathway analysis was performed that targeted serotonin and dopamine receptor pathways. The mitogen-activated protein kinase 1 (MAPK1) gene was significantly downregulated. MAPK1 is an inhibitory regulator of HTR2A and facilitatory regulator for DRD1. Downregulation of MAPK1 may be related to the significant upregulation of HTR2A and downregulation of DRD1, suggesting an interaction in the medial thalamus serotonin-dopamine pathway elicited by airway obstruction. These results demonstrate an immediate change in gene expression in thalamic arousal, fear, anxiety motivation-related serotonin and dopamine receptors in response to airway obstruction. The results support the hypothesis that the thalamus is a component in the respiratory mechanosensory neural pathway. respiratory loading; microarray; stress; serotonin; dopamine THE RESPIRATORY SYSTEM is continually active, and any prolonged interruption is a threat to an animal's survival. Thus it is of critical importance to maintain ventilation in the face of a variety of stimuli by adjusting the breathing pattern. Clark and von Euler (13) described the relationship between lung volume and breath timing in anesthetized cats. They demonstrated that inspiratory time (TI) depends on inspiratory volume and that the subsequent expiratory time (TE) depends on the preceding TI. A similar volume-timing relationship was found when a mechanical stimulus in the form of an external resistive load was applied. Loading of the inspiratory (57) or expiratory (33) phase caused a decrease in volume and an increase in the duration of the respective loaded breath phase. The response to the added loads was called the respiratory load compensation reflex. Load compensation is a sensory motor response.A sufficiently high load on the respiratory system results in the sensation of dyspnea, or breathlessness, which is one of the primary symptoms in pulmonary and cardiovascular diseases (40, 44). It is one of the main symptoms that limits patients with obstructive pulmonary diseases, and it can also be considered one of the most important factors in determining the severi...

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Section: Itto Load Compensationmentioning

confidence: 74%

mentioning

confidence: 99%

Tracheal occlusion modulates the gene expression profile of the medial thalamus in anesthetized rats

Bernhardt¹,

García-Reyero

Vovk³

et al. 2011

Journal of Applied Physiology

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“…The volume-timing (Vt-T) parameters of the unloaded phase of the breath were unchanged. The Vt-T values obtained from complete respiratory occlusion approached those seen after vagotomy (50). Load compensation is also characterized by increased respiratory motor output, measured from respiratory muscle electromyography (EMG) primarily in the diaphragm (37), although abdominal muscle responses are also observed (35).…”

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confidence: 87%

“…diaphragm; c-Fos; respiratory control; PAG; intrinsic occlusion RESPIRATORY LOAD COMPENSATION in anesthetized animals has been characterized as reflexive and vagal dependent (50), specifically mediated by pulmonary stretch receptors (15,16,24). Load compensation has been observed in response to mechanical challenges to breathing such as resistive or elastic loads applied to the respiratory circuit (49).…”

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confidence: 99%

“…Load compensation has been observed in response to mechanical challenges to breathing such as resistive or elastic loads applied to the respiratory circuit (49). The stereotypical response to a resistive load applied to one phase of the breath included a decrease in volume inspired (Vi) or expired (Ve) for the duration of the load and an increase in the loaded breath phase duration (50). The volume-timing (Vt-T) parameters of the unloaded phase of the breath were unchanged.…”

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Tracheal occlusions evoke respiratory load compensation and neural activation in anesthetized rats

Pate

Davenport

2012

Journal of Applied Physiology

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Pate KM, Davenport PW. Tracheal occlusions evoke respiratory load compensation and neural activation in anesthetized rats. J Appl Physiol 112: 435-442, 2012. First published November 10, 2011 doi:10.1152/japplphysiol.01321.2010.-Airway obstruction in animals leads to compensation and avoidance behavior and elicits respiratory mechanosensation. The pattern of respiratory load compensation and neural activation in response to intrinsic, transient, tracheal occlusions (ITTO) via an inflatable tracheal cuff are unknown. We hypothesized that ITTO would cause increased diaphragm activity, decreased breathing frequency, and activation of neurons within the medullary and pontine respiratory centers without changing airway compliance. Obstructions were performed for 2-3 breaths followed by a minimum of 15 unobstructed breaths with an inflatable cuff sutured around the trachea in rats. The obstruction procedure was repeated for 10 min. The brains of obstructed and control animals were removed, fixed, sectioned, and stained for c-Fos. Respiratory pattern was measured from esophageal pressure (Pes) and diaphragm electromyography (EMGdia). The obstructed breaths resulted in a prolonged inspiratory and expiratory time, an increase in EMGdia amplitude, and a more negative Pes compared with control breaths. Neurons labeled with c-Fos were found in brain stem and suprapontine nuclei, with a significant increase in c-Fos expression for the occluded experimental group compared with the control groups in the nucleus ambiguus, nucleus of the solitary tract, lateral parabrachial nucleus, and periaqueductal gray matter. The results of this study demonstrate tracheal occlusion-elicited activation of neurons in brain stem respiratory nuclei and neural areas involved in stress responses and defensive behaviors, suggesting that these neurons mediate the load compensation breathing pattern response and may be part of the neural pathway for respiratory mechanosensation.diaphragm; c-Fos; respiratory control; PAG; intrinsic occlusion RESPIRATORY LOAD COMPENSATION in anesthetized animals has been characterized as reflexive and vagal dependent (50), specifically mediated by pulmonary stretch receptors (15,16,24). Load compensation has been observed in response to mechanical challenges to breathing such as resistive or elastic loads applied to the respiratory circuit (49). The stereotypical response to a resistive load applied to one phase of the breath included a decrease in volume inspired (Vi) or expired (Ve) for the duration of the load and an increase in the loaded breath phase duration (50). The volume-timing (Vt-T) parameters of the unloaded phase of the breath were unchanged. The Vt-T values obtained from complete respiratory occlusion approached those seen after vagotomy (50). Load compensation is also characterized by increased respiratory motor output, measured from respiratory muscle electromyography (EMG) primarily in the diaphragm (37), although abdominal muscle responses are also observed (35).Load compensation has brain stem and...

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