Regulation of respiration

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Presentation transcript:

Regulation of respiration Breathing is controlled by the central neuronal network to meet the metabolic demands of the body Neural regulation Chemical regulation

Respiratory center Definition: A collection of functionally similar neurons that help to regulate the respiratory movement

Respiratory center Spinal cord: Medulla Pons respiratory motor neurons Medulla Pons Higher respiratory center: cerebral cortex, hypothalamus & limbic system Basic respiratory center: produce and control the respiratory rhythm

Neural regulation of respiration Voluntary breathing center Cerebral cortex Automatic (involuntary) breathing center Medulla Pons

Neural generation of rhythmical breathing 1. The discharge of medullary inspiratory neurons provides rhythmic input to the motor neurons innervating the inspiratory muscles. 2. Then the action potential cease, the inspiratory muscles relax, and expiration occurs as the elastic lungs recoil.

Inspiratory neurons Expiratory neurons

Respiratory center Dorsal respiratory group (medulla) – mainly causes inspiration Ventral respiratory group (medulla) – causes either expiration or inspiration Pneumotaxic center (upper pons) – inhibits apneustic center & inhibits inspiration,helps control the rate and pattern of breathing Apneustic center (lower pons) – to promote inspiration

Hering-Breuer inflation reflex (Pulmonary stretch reflex) The reflex is originated in the lungs and mediated by the fibers of the vagus nerve: Pulmonary inflation reflex: inflation of the lungs, eliciting expiration. Pulmonary deflation reflex: deflation, stimulating inspiration.

Pulmonary inflation reflex Inflation of the lungs  +pulmonary stretch receptor +vagus nerve  -medually inspiratory neurons  +eliciting expiration

Pulmonary inflation reflex Role: Feedback from the lungs helps terminate inspiration and enhance inspiration/expiration transition, thus increasing respiratory rate.

Chemical control of respiration Chemoreceptors Central chemoreceptors: medulla Stimulated by [H+] in the CSF Peripheral chemoreceptors Carotid body Stimulated by arterial PO2 or [H+] Aortic body

Central chemoreceptors

Peripheral chemoreceptors Chemosensory neurons that respond to changes in blood pH and gas content are located in the aorta and in the carotid sinuses; these sensory afferent neurons alter CNS regulation of the rate of ventilation.

Peripheral chemoreceptors and their afferent nerves

Effect of carbon dioxide on pulmonary ventilation Small changes in the carbon dioxide content of the blood quickly trigger changes in ventilation rate. CO2    respiratory activity

BBB CO2 H+

Central and peripheral chemosensory neurons that respond to increased carbon dioxide levels in the blood are also stimulated by the acidity from carbonic acid, so they “inform” the ventilation control center in the medulla to increase the rate of ventilation. CO2+H2O  H2CO3  H++HCO3-

Effect of carbon dioxide on pulmonary ventilation Very high levels of CO2 actually inhibits ventilation and may be lethal. This is because high concentration of CO2 act directly on the medulla to inhibit the respiratory neurons by an anesthesia-like effect.

Effect of hydrogen ion on pulmonary ventilation [H+]    respiratory activity Regardless of the source, increases in the acidity of the blood cause hyperventilation.

Regardless of the source, increases in the acidity of the blood cause hyperventilation, even if carbon dioxide levels are driven to abnormally low levels.

Effect of low arterial PO2 on pulmonary ventilation PO2    respiratory activity A severe reduction in the arterial concentration of oxygen in the blood can stimulate hyperventilation.

Chemosensory neurons that respond to decreased oxygen levels in the blood “inform” the ventilation control center in the medulla to increase the rate of ventilation.

In summary: The levels of oxygen, carbon dioxide, and hydrogen ions in blood and CSF provide information that alters the rate of ventilation.

Regulation of respiration

Questions 1. Why is increased depth of breathing far more effective in evaluating alveolar ventilation than is an equivalent increase in breathing rate?

Questions 2. Describes the effects of PCO2, [H+] and PO2 on alveolar ventilation and their mechanisms. CO2 ­-­  respiratory activity; Peripheral mechanism and central mechanism, the latter is the main one. [H+]  ­-­  respiratory activity; Peripheral mechanism and central mechanism, the former is the main one. PO2  ­-­  respiratory activity; Peripheral mechanism is excitatory.

Questions 3. What is the major result of the ventilation-perfusion inequalities throughout the lungs? 1) An increase of the ventilation-perfusion ratio will result in an increase of alveolar dead space. 2) A decrease of the ventilation-perfusion ratio will result in the functional A-V shunt. 3) The major result of the ventilation-perfusion inequality is to decrease the PO2 of systemic arterial blood. Because the diffusion coeffient for CO2 is about 20 times that for O2.

Questions 4. Describe the factors that influence gas exchange in the lungs.

Questions 5. If an experimental rabbit’s vagi were obstructed to prevent them from sending action potential, what will happen to respiration? 1) Pulmonary stretch reflex: Inflation of the lungs  +pulmonary stretch receptor +vagus nerve  -medually inspiratory neurons  +eliciting expiration. 2) The feedback from the lungs helps terminate inspiration and enhance inspiration/expiration transition, thus increasing respiratory rate. 3) In the animal experiment, if the vagi were destrcted, prolonged inspiration and deep slow breathing could be observed.