Resp Lecture 14

Front 1

What are the neural controls of the ventilation?

Back 1

generation of rhythmic pattern of alternating inspiration and expiration
• regulation of rate and depth of ventilation to match changing requirements (breathing more quickly or more deeply, or opposite)
• modification of respiratory activity for other purposes (voluntary: breathe holding and speech; involuntary: coughing and sneezing)

Front 2

Respiratory centre

Back 2

• located within brainstem (brainstem = rostral continuation of spinal cord; whatremains when cerebral cortex and cerebellum removed):
• made up of 5 aggregations of neuronal cell bodies

Front 3

What are the 5 neuonral cell bodies that play a role in respiratory regulation?

Back 3

• dorsal respiratory group (DRG), ventral respiratory group (VRG) and pre-Bötzinger complex within medulla oblongata (caudal continuation of the spinal cord)
• apneustic centre and pneumotaxic centre within the pons

Front 4

Dorsal Respiratory Group?

Back 4

• efferent fibres from DRG stimulate inspiratory spinal motor neurons innervatingdiaphragm (the axons go down the spinal cord and synapse with the motor neurons and the phrenic nerve, these are the neurons that innervate the diaphragm)
• rhythmic firing of DRG in response to pacemaker activity (i.e. repetitiveself-induced action potentials) of pre-Bötzinger complex
• firing of DRG neurons causes inspiration; with cessation of firingexpiration occurs.
• rate of rhythmic firing regulated by excitatory or inhibitory synaptic inputfrom other brain areas or elsewhere in body (Þ altered rate and depth ofventilation) DRG is able to integrate information coming from various parts of the body and creating a pattern of respiration.

Front 5

pre-Bötzinger complex

Back 5

Sends repeated action potentials to the DRG which cause it to fire resulting in contraction of the diaphragm. There's little bursts of firing followed by a pause when the diaphragm relaxes.

Front 6

Ventral Respiratory Group?

Back 6

The same axons from the DRG extend to the VRG. The VRG axons project to spinal motor neurons of both expiratory andaccessory inspiratory muscles (It's axons travel further down the spinal cord)
• VRG activated by DRG when demands for ventilation increased

Front 7

DRG receives input from:

Back 7

Pneumotaxic and apneustic centres
Stretch receptors in smooth muscle of airways
Mechanoreceptors in airways
Chemoreceptors in the peripheral and central locations.

Front 8

Pneumotaxic and apneustic centres

Back 8

• fine-tuning of output from medullary centres => normal smooth inspirationand expiration
• pneumotaxic centre acts to terminate inspiration (if the stimulation from the DRG is going on for too long)
• apneustic centre prevents switching off of inspiratory neurons

Not nearly as important as the VRG or the DRG, more just fine tuning of the ventilation

Front 9

Stretch receptors in smooth muscle of airways

Back 9

Initiate Hering-Breuer reflex, i.e. inhibition of firing of inspiratoryneurons to prevent over-inflation of lungs

Front 10

Mechanoreceptors in airways

Back 10

• initiate coughing/sneezing reflex to remove unwanted material

Front 11

peripheral chemoreceptors

Back 11

Located in the carotid bodies and the aortic bodies

Front 12

Carotid body chemoreceptors

Back 12

located at origin of internal carotid a. Transmit their sensory information to the DRG via CNIX (glossopharyngeal nerve)

Front 13

Aortic Bodies

Back 13

Located at the aortic arch transmit their sensory information to DRG via CN X (vagus)

Front 14

Central chemoreceptors

Back 14

Located in the ventral part of the medulla oblongata

Front 15

Regulation of rate and depth of ventilation

Back 15

carried out by medullary centre (i.e. DRG and VRG) in response to informationabout body’s need for gas exchange
Constantly monitoring O2, CO2, also H+ levels in circulation. DRG and VRG respond accordingly.

Front 16

Regulation by lowered arterial PO2

Back 16

(hypoxic drive)
• Arterial PO2 monitored by peripheral chemoreceptors, only sensitive to dramatic change in arterial PO2, i.e. < 60 mm Hg (pointwhere %Hb saturation 90%)=>stimulate medullary inspiratory neurons => increased ventilation (rate and depth)
• necessary life-saving mechanism, since low PO2 depresses all neuralfunction except chemoreceptors (only the respiratory center become activated during low PO2 levels)
• only respond to arterial PO2, not O2 content of blood, i.e. not O2 bound toHb. In cases of anaemia, O2 content may be extremely low, but nostimulus for hypoxic drive because arterial PO2 maintained at 100 mm Hg

normally arterial PO2 coincidentally maintained at normal level by responseof central chemoreceptors to [H+] in brain ECF (if there's too much CO2, probably not enough O2, but the breathing will increase anyhow to blow off CO2)

Front 17

Regulation by varying arterial PCO2 levels

Back 17

• increased ventilation in response to elevated PCO2 = hypercapnic drive
• arterial PCO2 most important input regulating ventilation under normal conditions
• stimulation of peripheral chemoreceptors - weak response
• stimulation of central chemoreceptors, most important regulation of ventilation in response to changing PCO2

Front 18

What happens when the PCO2 levels increase?

Back 18

Respond to [H+ ] generated from CO2 in brain extracellular fluid (ECF) rather than to PCO2 (CO2 diffuses much more readily across blood-brain barrier than does [H+ ]. So the H+ are a mark of PCO2 levels, not pH.

Elevated H+ in brain ECF => stimulation of medullary respiratory center => stimulation of ventilation (leading to CO2 removal from the lungs)

very high levels of CO2 in blood (> 75 mm Hg) directly depress neural function => depression of ventilation => death (animal trapped in airtight space rebreathing own CO2)

Front 19

What happens when the PCO2 levels are too low?

Back 19

Low PCO2 levels=> Lowered H+ levels in the brain ECF => Decreased stimulation of the medullary respiratory center by central chemoreceptors=> decreased ventilation (rate and depth) NOT hypoventilation

Front 20

Regulation by arterial [H+]

Back 20

• cannot influence central chemoreceptors ([H+] does not cross blood-brain barrier)
• does influence peripheral chemoreceptors (increased H+ => increased respiration to blow off CO2; decreased H+ => decreased respiration to increase CO2)

Front 21

Decreased PO2 <60mmHG

Back 21

Peripheral chemoreceptors are stimulated, there is no effect on central chemoreceptors but a general depression of neural function.

Front 22

Increased PCO2 (H+ in the ECF of the brain)

Back 22

Weak stimulation of the peripheral chemoreceptors, strong stimulation on the central chemoreceptors (except where PCO2 > 70-80 mm Hg => depression of entire nervous system)

Front 23

Increased H+

Back 23

Stimulation of the peripheral chemoreceptors, no effect on the central chemoreceptors

Front 24

Decreased PCO2 (decreased H+ in the ECF of the brain)

Back 24

No effect on the peripheral chemoreceptors, depression of the central cemoreceptors

Front 25

Higher control of ventilation

Back 25

From the cerebral cortex, the part of the brain responsible for conscious control

Front 26

conscious control of ventilation by higher (cortical) centres occurs in associationwith what activities

Back 26

• stopping breathing during swallowing (so food doesn't enter the respiratory tract)
• vocalization (modify breathing patterns)
• defaecation
• parturition (contraction of abdominal muscles will impact breathing)
• breath holding (diving, etc)
• changes in gait in some species, e.g. in horse, ventilation synchronised withgait at canter and gallop (but not walk or trot); inhalation occurs asforelimbs extended, and exhalation occurs when forelimbs in contact withground