Transcript GENERAL AND COMPARATIVE ANIMAL PHYSIOLOGY Biology 556

3- mammals :
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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,
Exhalation:
•muscles
relax
intercostals contract •elastic recoil pushes
•negative pressure 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
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Figure 22.9b
Respiratory Membrane
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Figure 22.9c ,d
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.
Insert fig. 16.12
– 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.
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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 cente
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
1) Medullary respiratory center
• Controls inspiration and expiration
• Consists of dorsal respiratory group (DRG) and
ventral respiratory group (VRG)
• DRG contain mostly inspiratory neurons (Ineurons)
• 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 ” Ineurons (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+
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Achieved via chemoreceptors (2 types)
1) Peripheral- located in the carotid bodies and
aortic bodies
2) Central- located on the ventral surface of the
medulla
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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
1) 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
2) Central chemoreceptors
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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
Cerebrospinal
fluid
1 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.
Pons
2 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.
Breathing
control
centers
Medulla
oblongata
4 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.
5 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.
Carotid
arteries
Aorta
Figure 42.26
3 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.
Diaphragm
Rib muscles
6 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.
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Regulation of respiration
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Hering Breuer reflex
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􀂄 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
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􀂄 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
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􀂄 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
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􀂄 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
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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
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􀂄 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
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