1. 3- mammals : Why co2 yes but o2 no !!!!!!!!!!!!! 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 !!!!!!!!!!!!!

2. 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

3. 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

4. Lung volume
In mammals about 5% of body weight

7. 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

8. 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

9. Tidal Ventilation Inhalation: Exhalation:
One of the distinguishing characteristics of mammals is the presence of the diaphragm, a muscular bit of tissue that seals off the thoracic cavity from the abdomen…when it contracts, along with intercostal muscles between the ribs, the thoracic cavity and the lungs expand, producing negative pressure relative to the outside and air rushes in
the lungs are very elastic, so under normal breathing when these muscles relax, the lung will go back to its original size, increasing pressure in the lung and releasing the air…in addition the contraction of the diaphragm will compress some of the abdominal organs and they will also recoil
the alveoli are dead-ends, so there’s no possibility of unidirectional flow as in fish gills, it’s simply an in and out movement with the air passing through the same pathways, just in opposite directions…and capillaries are arranged failry randomly around each alveolus
Inhalation:
diaphragm, intercostals contract
negative pressure
Exhalation:
muscles relax
elastic recoil pushes air out

10. 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%

12. Respiratory Membrane
Figure 22.9b

13. Respiratory Membrane
Figure 22.9c ,d

14. 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.

15. 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.

16. 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.

17. 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.

18. (Silverthorn, Fig ) 13

19. 14

20. 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, surfactant’s ability to lower surface tension increases.
Insert fig

21. Respiratory Distress Syndrome (RDS)
Leading cause of death and illness in infants, especially premature infants
2 surfactant production pathways
One develops 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

22. Respiratory control centers
1- Medullary respiratory center
2- Pons respiratory center
(Sherwood, Fig )

23. 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?)

24. 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

25. 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

26. Peripheral chemoreceptors
(Sherwood, Fig )

27. 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+

28. 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

29. 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+

30. Central chemoreceptor
(Silverthorn, Fig )

31. Control of Breathing in Humans
The main breathing control centers
Are located in two regions of the brain, the medulla oblongata and the pons
Figure 42.26
Pons
Breathing control centers
Medulla oblongata
Diaphragm
Carotid arteries
Aorta
Cerebrospinal fluid
Rib muscles
In a person at rest, these nerve impulses result in about 10 to 14 inhalations per minute. Between inhalations, the muscles relax and the person exhales.
The medulla’s control center
also helps regulate blood CO2 level.
Sensors in the medulla detect changes
in the pH (reflecting CO2 concentration)
of the blood and cerebrospinal fluid
bathing the surface of the brain.
Nerve impulses relay changes in CO2 and O2 concentrations. Other sensors in the walls of the aorta and carotid arteries in the neck detect changes in blood pH and send nerve impulses to the medulla. In response, the medulla’s breathing control center alters the rate and depth of breathing, increasing both to dispose of excess CO2 or decreasing both if CO2 levels are depressed.
The control center in the
medulla sets the basic rhythm, and a control center in the pons moderates it, smoothing out the transitions between
inhalations and exhalations. 1
Nerve impulses trigger muscle contraction. Nerves from a breathing control center in the medulla oblongata of the brain send impulses to the diaphragm and rib muscles, stimulating them to contract and causing inhalation. 2
The sensors in the aorta and carotid arteries also detect changes in O2 levels in the blood and signal the medulla to increase the breathing rate when levels become very low. 6 5 4 3

33. Regulation of respiration

34. 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

35. 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.

36. 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

38. 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

39. Peripheral chemoreceptors
􀂄 Aortic bodies, afferents in vagus nerve.
􀂄 Respond to PaCO2 and PO2 but not pH

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

44. 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

45. Dorsal respiratory group
􀂄 Input from IXth and Xth nerves that
terminate in nucleus of the solitary tract
(NTS)
􀂄 Output to inspiratory muscles

46. 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