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16 Cards in this Set

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What role does the dorsal respiratory group play in the neuronal genesis of rhythmic breathing?
The dorsal respiratory group neurons [DRG] are the respiratory center responsible for PASSIVE RESTING INSPIRATION. It is located in Nucleus Tractus Solitarius(NTS) bilaterally in the medulla. It receives & integrates sensory information from chemoreceptors & mechanoreceptors. Chemoreceptor input results in a tonic drive for ventilation. It is thought that some respiratory pacemaker activity may lie here or outside the DRG in the pre-Botzinger complex near the nucleus ambiguous(NA). Output from the DRG projects to the diaphragm and inspiratory muscles, it also projects to VRG to inhibit activities of “expiratory neurons”

Note: in quiet breathing it is the periodic pause in action potentials of inspiratory neurons (DRG)that allows for passive expiration, as inspiratory muscles relax.
What role does the ventral respiratory group(VRG) play in the neuronal genesis of rhythmic breathing?
Ventral Respiratory Group (VRG) neurons are the respiratory center involved in active expiration and inspiration. They are found in the nucleus ambiguous(NA) & nucleus retroambiguous (NRA) bilaterally in the medulla. Some books say VRG neurons are assoc. primarily with active expirations. These “expiratory neurons" are the origin of active respiratory effects but NOT passive expirations of quiet breathing. Active VRG neurons inhibit activity of “inspiratory neurons.” VRG appear to be driven by input from DRG and do not appear to have spontaneous activity (except possibly for “pre-Botzinger complex” near NA)
Describe how the pneumotaxic center may contribute to the pattern of rhythmic breathing?
The pneumotactic center is located in the parabrachealis medialis (NPBM) in the upper pons. It appears to contribute to “switching off” inspiration, via neural pathways to medullary DRG neurons and to “apneustic center neurons” in the lower pons. Increased activity in PC increases the number of breaths per minute by decreasing the duration of inspiration and expiration. The PC receives input from the DRG and afferent vagal input from pulmonary stretch receptors.
Describe the results of interrupting neural input to the apneustic center from the pneumotaxic center and vagus nerves on the pattern of breathing?
Apneustic center is located in the lower pons and it’s exact role is still debated. It receives input from pneumotaxic center & vagus nerve. If you cut these inputs leaving output pathways to DRG intact you produce prolonged deep inspirations (apneusis). This suggest apneustic center neurons have an excitatory influance on the inspiratory neurons of the DRG.
Describe the results of interrupting the neural input to the medullary respiratory groups from the pons on the pattern of breathing?
The pons not required for spontaneous rhythmic breathing but without the pons, breathing tends to have a variable, less regular pattern. Pons represents a “fine tuning” of the control of ventilation
Describe the roles of expiratory neurons of the medulla and expiratory muscles in a) quiet breathing and b) forceful breathing efforts.
Expiratory neurons play no role in quiet breathing, in which expiration is passive. Forceful expirations result from firing of VRG expiratory neurons.
Describe the roles of the cerebral cortex, limbic system and hypothalamus in the control of breathing.
The cerebral cortex is involved in voluntary ventilation efforts. The
limbic center & hypothalamus is involved in ventilary patterns in emotional states, anger & fear.
Describe the effects of CO2 on a) the level of ventilation and b) the response of the respiratory system to hypoxemia
Hypercapnia causes a reflex increase in alveolar ventilation rate.

Ventilation can also be depressed somewhat by hypocapnia. For example, hyperventilation of an anesthetized patient can result in apnea when the ventilator is initially removed.

The responses of ventilation to increases in arterial PCO2 are enhanced by simultaneous hypoxemia. Lowering alveolar PO2 below 110 mm Hg increases the slope of the response curves of Ventilation vs. Alveolar PCO2. (see graph):
Describe the role of the central chemoreceptors in the response of the respiratory system to changes in arterial PCO2:
The stimulation of ventilation by hypercapnia is largely the result of stimulation of the central (medullary) chemoreceptors (located in the ventrolateral medulla, distinct from the DRG & VRG). These are the primary CO2 sensors for the chemical control of ventilation. Stimulation of the central chemoreceptors by hypercapnia increases action potential frequencies of medullary inspiratory neurons. The responses of ventilation to increases in arterial PCO2 are enhanced by simultaneous hypoxemia. However, Hypoxemia itself does not stimulate the central chemoreceptors.

Decreases in arterial PCO2 result in changes opposite to those above.


Note: Chronic hypercapnia results in diminished central chemoreceptor responsiveness to hypercapnia, due to secretion of additional HCO3- ions into the CSF and brain interstitial fluid. This buffers some of the H+ ions.
Describe the effects of hypoxemia on a) the level of ventilation and b) the response of the respiratory system to hypercapnia:
Hypoxemia causes a reflex increase in alveolar ventilation rate:

The responses of ventilation to decreases in arterial PO2 are enhanced by simultaneous hypercapnia (see graph). Increasing alveolar PCO2 above 35.8 mm Hg shifts the response curve of Ventilation vs. Alveolar PO2 upward and to the right.
See graph
Describe the role of the peripheral chemoreceptors in the responses of the respiratory system to changes in arterial PO2, PCO2 and pH.
The peripheral chemoreceptors are located in the carotid bodies and aortic bodies. They are responsible for the responses to changes in arterial PO2. The peripheral chemoreceptors respond to the PO2, not the O2 content (or concentration) of blood. In humans, the aortic bodies are apparently less sensitive to hypoxemia than are the carotid bodies. In some individuals, aortic bodies may respond very little to arterial hypoxemia.

The responses of ventilation to decreases in arterial PO2 are enhanced and stimulated to a lesser extent by hypercapnia. Other stimuli are nicotine and cyanide.

The Carotid bodies are stimulated by increased [H+]. In humans, the aortic bodies appear to respond much less strongly to changes in arterial pH than the carotid bodies. In some individuals, the aortic bodies appear unresponsive to changes in arterial pH.
Describe the Hering-Breuer inflation reflex
Lung inflation is sensed by stretch receptors located in airway smooth muscle fo the bronchi and bronchioles. Vagal afferent neurons from stretch receptors signal to DRG in medulla & also to pons to inhibit inspiration and augment expiration. This reflex may be of limited importance in humans when tidal volume is less than 1 liter. It may be more important with larger tidal volumes, e.g., during exercise.
Describe the Hering-Breuer Deflation Reflex
Lung deflation is sensed by stretch receptors in bronchi and bronchioles (probably distinct from those involved in the Hering-Breur Inflation reflex). Vagal afferent neurons signal reflex stimulation of inspiration and inhibition of expiration to medulla
Describe the roles of pulmonary irritant receptors
Mechanical and chemical irritants are sensed by “irritant receptors” located in the airway epithelium. There is a reflex increase in respiratory frequency and a decrease in tidal volume. This is often accompanied by coughing or sneezing & bronchoconstriction. This is an important defense mechanism of the lung.
Describe the roles of juxtacapillary (J) receptors in the control of breathing
The J receptors, located in the pulmonary interstitium adjacent to pulmonary capillaries, sense pulmonary interstitial edema and pulmonary capillary distenion. There is a reflex response of laryngeal closure, apnea, followed by rapid, shallow breathing. This reflex may be involved in producing dyspnea associated with increased pulmonary capillary pressure and pulmonary edema.
Describe the role of the muscle spindles of the intercostal muscles in the control of breathing.
Muscle spindle reflexes of the intercostals muscles respond to stretch of the spindle by reflex contraction of the intercostals muscle. Possible functions include augmentation of inspiratory efforts. Maintenance of tidal volume when inspiratory movements are restricted and possible contribution to sensations of dyspnea.