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Respiratory neuroplasticity following carotid body denervation: Central and peripheral adaptations.

Hodges MR, Forster HV - Neural Regen Res (2012)

Bottom Line: Historically, the role of the carotid bodies in ventilatory control has been understated, but the current view suggests that the carotid bodies (1) provide a tonic, facilitory input to the respiratory network, (2) serve as the major site of peripheral O2 chemoreception and minor contributor to CO2/H(+) chemoreception, and (3) are required for ventilatory adaptation to high altitude.Respiratory plasticity following carotid body denervation is also dependent on species, with contributions from peripheral and central sites/mechanisms driving the respiratory plasticity.We speculate that after carotid body denervation there are altered excitatory and/or inhibitory neuromodulator mechanisms that contribute to the initial respiratory depression and the subsequent respiratory plasticity, and further suggest that the continued exploration of central effects of carotid body denervation might provide useful information regarding the capacity of the respiratory network for plasticity following neurologic injury in humans.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology, Medical College of Wisconsin, Milwaukee, WI 53226, USA ; Neuroscience Research Center, Medical College of Wisconsin, Milwaukee, WI 53226, USA.

ABSTRACT
Historically, the role of the carotid bodies in ventilatory control has been understated, but the current view suggests that the carotid bodies (1) provide a tonic, facilitory input to the respiratory network, (2) serve as the major site of peripheral O2 chemoreception and minor contributor to CO2/H(+) chemoreception, and (3) are required for ventilatory adaptation to high altitude. Each of these roles has been demonstrated in studies of ventilation in mammals after carotid body denervation. Following carotid body denervation, many of the compromised ventilatory "functions" show a time-dependent recovery plasticity that varies in the degree of recovery and time required for recovery. Respiratory plasticity following carotid body denervation is also dependent on species, with contributions from peripheral and central sites/mechanisms driving the respiratory plasticity. The purpose of this review is to provide a summary of the data pointing to peripheral and central mechanisms of plasticity following carotid body denervation. We speculate that after carotid body denervation there are altered excitatory and/or inhibitory neuromodulator mechanisms that contribute to the initial respiratory depression and the subsequent respiratory plasticity, and further suggest that the continued exploration of central effects of carotid body denervation might provide useful information regarding the capacity of the respiratory network for plasticity following neurologic injury in humans.

No MeSH data available.


Related in: MedlinePlus

Chronic effects of carotid body denervation (CBD) on eupneic PaCO2 (Torr) and the NaCN response ratio (index of peripheral chemosensitivity to hypoxia) in ponies before and up to 52 months after CBD.Note the recovery in resting PaCO2 is greater that the minimal, but significant recovery peripheral chemoreflex. Adapted from[25].
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Figure 3: Chronic effects of carotid body denervation (CBD) on eupneic PaCO2 (Torr) and the NaCN response ratio (index of peripheral chemosensitivity to hypoxia) in ponies before and up to 52 months after CBD.Note the recovery in resting PaCO2 is greater that the minimal, but significant recovery peripheral chemoreflex. Adapted from[25].

Mentions: Clearly, CBD acutely causes hypoventilation at rest (PaCO2 + 8-15 mm Hg), and blood and brain acidosis, and decreases CO2 sensitivity[67]. This period of significant hypoventilation, increased PaCO2, and decreased CSF pH should provide an increased stimulus to central CO2/pH chemoreceptors. Specifically, increasing PaCO2 by 8 mm Hg (by increasing inspired CO2) increases ventilation from 5 to 20 L/min in goats prior to CBD[6] (Figure 3). However, PaCO2 increases 10 mmHg at rest due to decreased ventilation by day 4 after CBD, and further increases in PaCO2 by increasing inspired CO2 have far less of a stimulatory effect on ventilation. Why is breathing not stimulated under these conditions? One possibility is that the sensitivity of central chemoreceptors is reduced following CBD, as shown by a reduced ventilatory response to focal acidification of the medullary raphé nuclei in goats after bilateral CBD[30] (Figure 4).


Respiratory neuroplasticity following carotid body denervation: Central and peripheral adaptations.

Hodges MR, Forster HV - Neural Regen Res (2012)

Chronic effects of carotid body denervation (CBD) on eupneic PaCO2 (Torr) and the NaCN response ratio (index of peripheral chemosensitivity to hypoxia) in ponies before and up to 52 months after CBD.Note the recovery in resting PaCO2 is greater that the minimal, but significant recovery peripheral chemoreflex. Adapted from[25].
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4340020&req=5

Figure 3: Chronic effects of carotid body denervation (CBD) on eupneic PaCO2 (Torr) and the NaCN response ratio (index of peripheral chemosensitivity to hypoxia) in ponies before and up to 52 months after CBD.Note the recovery in resting PaCO2 is greater that the minimal, but significant recovery peripheral chemoreflex. Adapted from[25].
Mentions: Clearly, CBD acutely causes hypoventilation at rest (PaCO2 + 8-15 mm Hg), and blood and brain acidosis, and decreases CO2 sensitivity[67]. This period of significant hypoventilation, increased PaCO2, and decreased CSF pH should provide an increased stimulus to central CO2/pH chemoreceptors. Specifically, increasing PaCO2 by 8 mm Hg (by increasing inspired CO2) increases ventilation from 5 to 20 L/min in goats prior to CBD[6] (Figure 3). However, PaCO2 increases 10 mmHg at rest due to decreased ventilation by day 4 after CBD, and further increases in PaCO2 by increasing inspired CO2 have far less of a stimulatory effect on ventilation. Why is breathing not stimulated under these conditions? One possibility is that the sensitivity of central chemoreceptors is reduced following CBD, as shown by a reduced ventilatory response to focal acidification of the medullary raphé nuclei in goats after bilateral CBD[30] (Figure 4).

Bottom Line: Historically, the role of the carotid bodies in ventilatory control has been understated, but the current view suggests that the carotid bodies (1) provide a tonic, facilitory input to the respiratory network, (2) serve as the major site of peripheral O2 chemoreception and minor contributor to CO2/H(+) chemoreception, and (3) are required for ventilatory adaptation to high altitude.Respiratory plasticity following carotid body denervation is also dependent on species, with contributions from peripheral and central sites/mechanisms driving the respiratory plasticity.We speculate that after carotid body denervation there are altered excitatory and/or inhibitory neuromodulator mechanisms that contribute to the initial respiratory depression and the subsequent respiratory plasticity, and further suggest that the continued exploration of central effects of carotid body denervation might provide useful information regarding the capacity of the respiratory network for plasticity following neurologic injury in humans.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology, Medical College of Wisconsin, Milwaukee, WI 53226, USA ; Neuroscience Research Center, Medical College of Wisconsin, Milwaukee, WI 53226, USA.

ABSTRACT
Historically, the role of the carotid bodies in ventilatory control has been understated, but the current view suggests that the carotid bodies (1) provide a tonic, facilitory input to the respiratory network, (2) serve as the major site of peripheral O2 chemoreception and minor contributor to CO2/H(+) chemoreception, and (3) are required for ventilatory adaptation to high altitude. Each of these roles has been demonstrated in studies of ventilation in mammals after carotid body denervation. Following carotid body denervation, many of the compromised ventilatory "functions" show a time-dependent recovery plasticity that varies in the degree of recovery and time required for recovery. Respiratory plasticity following carotid body denervation is also dependent on species, with contributions from peripheral and central sites/mechanisms driving the respiratory plasticity. The purpose of this review is to provide a summary of the data pointing to peripheral and central mechanisms of plasticity following carotid body denervation. We speculate that after carotid body denervation there are altered excitatory and/or inhibitory neuromodulator mechanisms that contribute to the initial respiratory depression and the subsequent respiratory plasticity, and further suggest that the continued exploration of central effects of carotid body denervation might provide useful information regarding the capacity of the respiratory network for plasticity following neurologic injury in humans.

No MeSH data available.


Related in: MedlinePlus