3- mammals :

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3- mammals

• Skin o2 is trivial
• Children and gold ---- died
• toxicity not hypoxia
• O2 is barely measured through skin but co2 is
  about 1
• Bats - larger skin surface
• Thin, hairless, and highly vascularized wings
• Play about (0.4----to 11.5) of total co2
  excretion ( temperature arise percent)
• Why co2 yes but o2 no !!!!!!!!!!!!!

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Mammals lungs

• The lung is founded in amphibians as divided sac
  but
• Frog lung 1 cubic cm of lung tissue 20
  squarecm of gas-exchange surface
• Mouse lung 1 cubic cm of lung tissue 800
  square cm of gas-exchange tissue
• Surface area of human lung 100 square m size
  of tennis court!
• Large surface area essential for high rate of
  oxygen uptake required for high metabolic rate of
  endothermic organisms

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• Membrane that separates the air in the lungs from
  the blood is thin 2micrometers thick (thickness
  of page 50 micrometers
• Large surface ( tennis court) 100m2 thin
  membrane very high rate of gaze exchange

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Lung volume

• In mammals about 5 of body weight

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inhalation and expiration

• Volume of air taken in single breath is termed
  tidal volume
• A person at rest has a tidal volume 500 cubic
  cm
• Dead space already present in lungs (150 cubic
  cm)
• Therefore, only about 350 Cubic cm of fresh air
  reach the lungs
• Dead space space already occupied with air in
  passageways, resulting in less volume for
  incoming air

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inhalation and expiration

• Lungs never completely devoid of air
• For a human, 1000 cubic cm of air left in lungs
  after exhalation thus impossible for person to
  fill lungs with fresh air
• In respiration at rest, a person may have about
  1650 cubic cm of air in the lungs when inhalation
  begins
• If 350 cubic cm reach the lungs, and mixed with
  the 1650 already there, then renewal of air is
  only about 1 in 5 (20) Result Alveolar gas
  remains constant 15 oxygen 5 carbon dioxide

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Tidal Ventilation

• Inhalation
• diaphragm, intercostals contract
• negative pressure

• Exhalation
• muscles relax
• elastic recoil pushes air out

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• Mechanical work of breathing
• Movement of air in and out of the lungs requires
  work how much?
• During rest (human) 1.2 of total resting
  oxygen consumption
• During exercise (human) increases 3

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Respiratory Membrane
Figure 22.9b
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Respiratory Membrane
Figure 22.9c ,d
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Physical Properties of the Lungs

• Ventilation occurs as a result of pressure
  differences induced by changes in lung volume.
• Physical properties that affect lung function
• Compliance.
• Elasticity.
• Surface tension.

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Compliance

• Distensibility (stretchability)
• Ease with which the lungs can expand.
• Change in lung volume per change in
  transpulmonary pressure.
• 100 x more distensible than a balloon.
• Compliance is reduced by factors that produce
  resistance to distension.

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Elasticity

• Tendency to return to initial size after
  distension.
• High content of elastin proteins.
• Very elastic and resist distension.
• Recoil ability.
• Elastic tension increases during inspiration and
  is reduced by recoil during expiration.

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Surface Tension

• Force exerted by fluid in alveoli to resist
  distension.
• Lungs secrete and absorb fluid, leaving a very
  thin film of fluid.
• This film of fluid causes surface tension.
• Fluid absorption is driven (osmosis) by Na
  active transport.
• Fluid secretion is driven by the active transport
  of Cl- out of the alveolar epithelial cells.
• H20 molecules at the surface are attracted to
  other H20 molecules by attractive forces.
• Force is directed inward, raising pressure in
  alveoli.

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(Silverthorn, Fig. 17-12)
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Surfactant

• Phospholipid produced by alveolar type II cells.
• Lowers surface tension.
• Reduces attractive forces of hydrogen bonding by
  becoming interspersed between H20 molecules.
• Surface tension in alveoli is reduced.
• As alveoli radius decreases, surfactants ability
  to lower surface tension increases.

Insert fig. 16.12
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Respiratory Distress Syndrome (RDS)

• Leading cause of death and illness in infants,
  especially premature infants
• 2 surfactant production pathways
• One develops 22-24 weeks
• The other develops at 35 weeks (very soon to
  birth)
• If type II alveolar cells do not produce enough
  surfactant
• Lungs collapse easily
• Hard to inflate strains diaphragm

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Respiratory control centers
1- Medullary respiratory center
2- Pons respiratory center
(Sherwood, Fig. 13-33)
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III. Gas exchange in air

• 4. Regulation of breathing
• Two major respiratory centers in the brain stem
• Medullary respiratory center
• Controls inspiration and expiration
• Consists of dorsal respiratory group (DRG) and
  ventral respiratory group (VRG)
• DRG contain mostly inspiratory neurons
  (I-neurons)
• VRG contain expiratory neurons (E-neurons) and I
  neurons (greater than normal ventilation)
• Rhythmic breathing produced by pacemaker neurons
  (rostral ventromedial medulla?)

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III. Gas exchange in air

• 2) Pons respiratory center
• Influences output from medullary respiratory
  center
• Pneumotaxic neurons switch off I-neurons
  (limits duration of inspiration)
• Apneustic neurons prevent I neurons from being
  switched off
• Pneumotaxic dominant over apneustic, allowing for
  smooth breathing

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III. Gas exchange in air

• Control of ventilation by PO2, PCO2 and H
• Achieved via chemoreceptors (2 types)
• Peripheral- located in the carotid bodies and
  aortic bodies
• Central- located on the ventral surface of the
  medulla
• Controls breathing via nerve fibers to the
  respiratory control centers

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Peripheral chemoreceptors
(Sherwood, Fig. 13-35)
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III. Gas exchange in air

• Peripheral chemoreceptors
• Sense changes in arterial O2, CO2 and H
• ?PCO2 ? chemoreceptor ?sensory neurons ?
• respiratory control ctr ?motor neurons ?
  respiratory muscle ??ventilation (CO2 blown off)
  ??PCO2
• ?H (keto or lactic acids) ? chemoreceptor ? resp
  control ctr ? ?ventilation ? ?PCO2 ??H

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III. Gas exchange in air

• Control of respiration in mammals is regulated by
  changes in PCO2 (not PO2)
• Peripheral O2 chemoreceptors do not contribute in
  regulating normal ventilation unless arterial PO2
  falls below 60 mm Hg
• Peripheral O2, CO2 and H chemoreceptors are
  weakly responsive and play a minor role in
  controlling respiration

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III. Gas exchange in air

• Central chemoreceptors
• Most important regulator of ventilation
• Do not monitor changes in PCO2 directly
• Respond to changes in CO2-induced production of
  H in cerebrospinal fluid (brain interstitial
  fluid)
• Blood-brain barrier allows the diffusion of CO2
  but is impermeable to H

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Central chemoreceptor
(Silverthorn, Fig. 17-31)
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Control of Breathing in Humans

• The main breathing control centers
• Are located in two regions of the brain, the
  medulla oblongata and the pons

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Regulation of respiration
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Hering Breuer reflex

• ?? Mediated by vagus nerve
• ?? Hering-Breuer Reflex. Slowly adapting stretch
• receptors (SARs) in bronchial airways send
• sensory information to medulla respiratory
• centers through vagus.
• ?? If vagus is severed on both sides, lungs will
• inflate maximally and use IRV
• ?? Hering-Breuer reflex is important in adults
• during exercise when tidal volume is increased

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Central chemoreceptors

• ?? Change in PaCO2 alters CSF pH
• ?? Increase PaCO2 will decrease CSF pH
• ?? Decrease PaCO2 will increase CSF pH
• ?? Decreased pH (Increased H) in CSF
• ?? Located on the ventral surface of medulla,
• bathed by Cerebrospinal fluid
• ?? CSF CO2 combines with water to form
• carbonic acid which dissociates to form
• hydrogen ions and bicarbonate.

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Central chemoreceptors

• ?? The CSF H diffuse into brain tissue to
• stimulate medullary chemoreceptors.
• ?? Increased arterial H may also stimulate
• central chemoreceptors slightly, but it
• does not diffuse into CSF as easily as CO2.
• ?? Stimulates receptors to increase
• ventilation

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Peripheral chemoreceptors

• ?? Located in carotid bodies at bifurcation of
• common carotid
• ?? Carotid body afferents in glossopharyngeal
• nerve.
• ?? Neural impulses from the carotid body
• increase as PaO2 falls below about 60
• mmHg
• ?? Also responds to pH

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Peripheral chemoreceptors

• ?? Aortic bodies, afferents in vagus nerve.
• ?? Respond to PaCO2 and PO2 but not pH

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Pneumotaxic center

• Located in the upper pons
• Turns off inspiratory activity
• Controls tidal volume and respiratory rate
• Normal breathing can persist without this
• center

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Dorsal respiratory group

• Inspiration
• ?? Controls basic rhythm of breathing
• ?? Oscillations in activity are due to multiple
• inputs /- pacemaker cells
• ?? Crescendo of activity leads to inspiration
• and decreases in expiration

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Dorsal respiratory group

• ?? Input from IXth and Xth nerves that
• terminate in nucleus of the solitary tract
• (NTS)
• ?? Output to inspiratory muscles

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Ventral respiratory group

• ?? Expiration
• ?? Inactive in normal, quiet breathing
• ?? Inspiration (DRG) is active, and expiration
• is passive without need for VRG output to
• expiratory muscles
• ?? Increases activity with exercise