The Abdominal Muscles
Alan D. Miller, Armand L. Bianchi, Beverly P. Bishop in Neural Control of the Respiratory Muscles, 2019
Peripheral chemoreceptors, located in the carotid and aortic bodies, are served by afferent fibers in the IXth and Xth nerves, respectively, and are excited by a fall in PaO2 or in arterial pH, or a rise in PaCO2. Their increased firing evokes deeper breathing which, in turn, evokes abdominal expiratory activity via the enhanced vagal feedback. Early results on anesthetized cats suggested that chemo-feedback, in the absence of concurrent facilitatory input from lung receptors, was insufficient to excite abdominal expiratory activity.14,15 Subsequent studies disputed these results,47,49 but recently Yasuma et al.82 elegantly demonstrated that in conscious dogs a reversible cold block of the vagi abolished the abdominal expiratory activity evoked by hypoxia or hypercapnia. Therefore, even though central expiratory neurons may receive projections from the peripheral chemoreceptors,49 concomitant facilitatory inputs at either the bulbar or spinal levels appear to be required for abdominal expiratory activity in the cat.
Control of Ventilation
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal in Principles of Physiology for the Anaesthetist, 2020
The carotid and aortic bodies are composed of type 1 or glomus cells and type 2 or sustentacular cells. The glomus cells contain large amounts of dopamine and nerve endings, whereas the type 2 cells resemble glia with a supporting function. Stimulation of the peripheral chemoreceptors blocks the potassium currents and causes membrane depolarization. The voltage-gated Ca++ channels open, and the influx of Ca++ provokes exocytosis of neurotransmitters, which stimulate the nerve endings to produce an action potential. The peripheral chemoreceptors are stimulated by low oxygen tension, not low oxygen content, of the blood. Conditions with low blood oxygen content, but relatively normal oxygen tension (anaemia, carboxyhaemoglobin), do not stimulate ventilation via the peripheral chemoreceptors. A high can cause a smaller but quicker response resulting in mild hyperventilation.
Control of breathing
Andrew M. Luks, Philip N. Ainslie, Justin S. Lawley, Robert C. Roach, Tatum S. Simonson in Ward, Milledge and West's High Altitude Medicine and Physiology, 2021
Dopamine is the most abundant transmitter found in the carotid body. Hypoxia increases the rate of release of dopamine from glomus cells. Norepinephrine (noradrenalin) and 5-hydroxytryptamine (i.e., serotonin) are next in abundance. There are also small quantities of acetylcholine, ATP, and enkephalin-like peptides in some glomus cells (Leonard et al. 2018). Substance P, endothelin-1, adenosine, angiotensin erythropoietin, and purinergic receptors are also present and may be involved in modulating the hypoxic response (Leonard et al. 2018; Wilson et al. 2005). It should be noted that, although in the context of high altitude, the most important function of the peripheral chemoreceptors (carotid and, to a lesser extent, aortic bodies) is to respond to hypoxia, they also respond to changes in pH and PaCO2 in dependent fashion through stimulus interaction; there is also growing consensus that the peripheral chemoreceptors also act as general metabolic sensors and, for example, are stimulated by changes in glucose and/or insulin (Conde et al. 2018). The greatest systemic response to PaCO2 is via the central chemoreceptors in the brainstem. As an example of the relative contribution of the chemoreceptors, a study by Fatemian et al. (2003) revealed that subjects who had had both carotid bodies removed had about 36% lower hypercapnic ventilatory response (HCVR) than normal subjects.
Association between heart rate variability and haemodynamic response to exercise in chronic heart failure
Published in Scandinavian Cardiovascular Journal, 2019
Aaron Koshy, Nduka C. Okwose, David Nunan, Anet Toms, David A. Brodie, Patrick Doherty, Petar Seferovic, Arsen Ristic, Lazar Velicki, Nenad Filipovic, Dejana Popovic, Jane Skinner, Kristian Bailey, Guy A. MacGowan, Djordje G. Jakovljevic
Chronic heart failure manifests an overactivation of the sympathetic system and parasympathetic withdrawal. This derangement in heart rate variability is further associated with excessive levels of circulating catecholamines [25]. It is expected that sympathetic drive may improve cardiac contractility and response to exercise resulting in higher values of cardiac output, stroke volume, heart rate, blood pressure and cardiac power output. Our results confirm the trend of positive relationship between HRV and exercise heamodynamics. This association may partially be explained by the role of peripheral chemoreceptors [26]. In heart failure, chemoreceptor sensitivity is increased in response to sympathetic overactivity and is associated with improved exercise capacity and measures of heart rate variability as previously documented [26,27].
Physiological and oxidative stress responses to intermittent hypoxia training in Sprague Dawley rats
Published in Experimental Lung Research, 2020
Megha A. Nimje, Himadri Patir, Rajesh Kumar Tirpude, Prasanna K. Reddy, Bhuvnesh Kumar
These changes can be attributed to the fact that at normoxic condition (21% FiO2); heart rate is modulated beat to beat mainly by arterial baroreceptors.38 However, during exposure to hypoxia, peripheral chemoreceptors act as regulators of autonomic activity and reset baroreflex control of heart rate and sympathetic activity, allowing higher levels of heart rate, blood pressure and sympathetic drive.39 The reduction in SpO2 level followed by hyperventilation and tachycardia during IHT in the present investigation may be due to the reason that hypoxia reduces the partial pressure of arterial oxygen leading to decreased arterial oxygen saturation (SpO2), which further stimulate peripheral chemoreceptors to hyperventilate in order to restore arterial oxygen levels as observed by.40 Breathing pattern and the activity of the chemoreceptors influence the modulation of heart rate during exposure to hypoxia.41 This results in cardiovascular system adjustments to deliver more blood to tissues to compensate for reduced oxygen delivery.42 In our study, rats exposed to hypoxia showed hyperventilation which further modulated the heart rate to beat faster in other to increase the cardiac output resulting in efficient tissue oxygenation.
Congenital central hypoventilation syndrome: diagnosis and management
Published in Expert Review of Respiratory Medicine, 2018
Melissa A. Maloney, Sheila S. Kun, Thomas G. Keens, Iris A. Perez
While individuals with CCHS lack ventilatory responses to gradual hypercapnia and hypoxia in rebreathing challenges [7], other aspects of ventilatory control appear intact. In order to test peripheral chemoreceptor function in CCHS patients, Gozal et al. [31] tested awake ventilatory responses to abrupt hypoxia, hyperoxia, and hypercapnia. In this study, CCHS patients demonstrated a ventilatory response similar to that of control subjects, suggesting that peripheral chemoreceptor function is at least partially intact [31]. This pattern is consistent with observations in healthy controls, who also demonstrate a more robust ventilatory response to abrupt hypoxia and hypercapnia than to gradual hypoxia and hypercapnia [32]. CCHS patients are also able to increase minute ventilation and tidal volume in response to exercise, although not to the same degree as normal subjects [33]. Passive lower extremity movement in both awake and sleep states leads to increased alveolar ventilation [34,35]. This finding demonstrates that CCHS patients have intact mechanoreceptor function and the pathway by which mechanoreceptors stimulate breathing remains intact.
Related Knowledge Centers
- Aortic Body
- Carotid Body
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- Peripheral Nervous System
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- Proprioception
- Sensory Neuron
- Taste Bud
- Blood Vessel
- Stimulus Modality