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GASEOUS EXCHANGE AND ITS CONTROL

Gaseous exchange and its control in aals.

Structure of an alveolus

Structure & characteristics of haemoglobin

Transport of O2 & CO2 by haemoglobin

O2 dissociation curves of haemoglobin & myoglobin.

O2 dissociation curves of haemoglobin as in fetus and adult

Bohr effect

Role o! cheorece"tors in controling #reathing

Gaseous exchange and control in "lants

Structure and functions of guard cells

egulation of the stomatal opening and closing

Starch!sugar hyphothesis

"otassium ion hyphothesis



O$%ECTI&ES
describe ho# gaseous e$change occurs in lungs
describe the structure of haemoglobin and its affinity for o$ygen by using
the o$ygen dissociation curves
e$plain roles of haemoglobin in o$ygen and carbon dio$ide transportation in
blood
e$plain the control of ventilation
describe lung volumes and capacities
describe the mechanism of stomatal opening and closing

'()() * GASEOUS EXCHANGE

+icrosco"ic structure o! the al,eolus as
the #asic unit o! lung
consists o! tin- air sacs .here
gaseous exchange occurs
each lung "ac/ed .ith )(012(0
illion al,eoli
diaeter is 3(2 illieter each
eneshed in ca"illaries
.all o! each al,eolus is onl-
one cell thic/
thin la-er o! .ater- !luid
lining each al,eolus

%daptation of the lung for gaseous
e$change

consists o! illions al,eoli to


axii4e res"irator- sur!ace area

thin1.alled al,eoli rese#le tin-


#u##les5 there!ore "ro,ided
enorous sur!ace areas o!
di!!usion

al,eoli6s sur!ace reains oist5


thus gasses can easil- dissol,e in
thin !luid and di!!use through the
al,eolar and ca"illar- e#ranes

#oth al,eolar .all and the


ad7acent ca"illar- .alls are onl-
one cell thic/5 the air is extreel-
close to the #lood in the ca"illaries

Structure of heamoglobin

the ox-gen1carr-ing "rotein in


red #lood cells

consists o! t.o "airs o! ,er-


siilar "e"tides5 held together
#- h-drogen #onds

each "e"tide holds an iron1


containing organic olecule
called a hae that can #ind
one olecule o! ox-gen

there!ore5 one haeoglo#in


8H#9 olecule #inds u" to !our
ox-gen olecules

Hb + 4O2 Hb(O2)4
Oxyhaemoglobin
HHbNH2 + CO2 HHbNH2CO2
Carbamino-haemoglobin
Hb + CO COHb
carboxyhaemoglobin

Characteristics o! haeoglo#in as
res"irator- "igent
an effective respiration
pigment due to its high
affinity to O2 although
the partial pressure of
O2 is belo# 2&mm'g
release O2 easily #hen
the partial pressure of
O2 is lo#


O2 dissociation curve of 'b

an S! shaped curve
obtained #hen the
percentage O
2
saturation of
blood is plotted against the
partial pressure of O
2
an S!shaped curve is
obtained due to the #ay
that 'b binds to O
2
the first O
2
molecules that
combines #ith the 'b
alters the shape of the
molecule in such a #ay that
it is easier for the ne$t O
2

molecule to (oin

conversely) #hen one
molecule of O
2
dissociates
from the ox-haeoglo#in)
the 'b shape is ad(usted to
ma*e release of successive
molecules of O
2
increasingly
easy
at a partial pressure of +ero)
no O
2
is attached to the 'b
molecule
this is due to the ability of
'b to release O
2
easily
#hen the partial pressure of
O
2
is lo#

at an O
2
partial pressure of
appro$imately ,& mm 'g)
-& . of the 'b is present
as 'bO
8

this is caused by the high


affinity 'b to O
2
at partial
pressure of /, mm 'g)
the 'b is completely
saturated #ith O
2
this point
is called loading tension

at higher partial pressures


of O
2
) further upta*e of O
2

can occur) but 0&&.
saturation of 'b is rarely
achieved

O
2
dissociation curve of 'b and myoglobin
in comparison

-oglo#in molecule is #idely distributed in animals and is


particularly common in s*eletal muscle tissues of mammals

very similar to the 'b subunits #ith respect to both amino


acid se1uence and three dimensional structure
this pigment may also bind to O
2
) but since there is only one
haem group there can be no cooperative binding


displays great affinity for O
2

its O
2
dissociation curve is displaced #ell to the left of 'b it only
begins to release O
2
#hen the partial pressure of O
2
is belo# 2& mm
'g

in this #ay) it acts as a store of O
2
in resting muscle) only releasing it
#hen supplies of 'bO
8
have been e$hausted

the myoglobin!o$ygen dissociation curve is hyperbolic rather than


sigmoidal

Ox-gen dissociation cur,es o! haeoglo#in in !etus and
other
the fetus has a very high O
2

demand
the fetal 'b is of a type
#hich has a higher affinity
for O
2
than the mother2s 'b
O
2
is therefore readily
unloaded from the mother2s
blood to the fetal blood
a graph for fetal 'b sho#s a
shift to the left from the
curve for adult 'b
O
2
dissociation cur,es o! H# in !etus
and other
"
O2
3mm'g4
O
2

s
a
t
u
r
a
t
i
o
n

o
f

'
b

3
.
4
5etus
6other

E!!ect o! "artial "ressure o! car#on dioxide
to.ards O
2
dissociation
8$ohr6s e!!ect9
once blood has travelled
to the body tissues) O
2
is
released
this is due to the drop in
the partial pressure of the
O
2
and a rise in the partial
pressure of carbon dio$ide
in respiring cells

a rise in the partial


pressure of the carbon
dio$ide lo#ers the
affinity of 'b for O
2

#hich is therefore
released

this is called the Bohr


effect or the Bohr shift

an increase in the
"artial "resure o!
CO
2
shi!ts the O
2

dissociation cur,e to
the right

CO
2

T%7S"OT%T8O7
87 B9OO:

CO
2
T%7S"OT%T8O7 87 B9OO:

the red blood cell and 'b both


play a significant part in this
process as #ell as in the
transport of O
2
CO
2
is carried by the blood in
three different #ays

in a1ueous solution 3-.4

combined #ith protein


30&!2&.4

as hydrogencarbonate
3;-.4

CO
2
is carried by the blood in three
different #ays
i9 in a:ueous solution 80;9

most of the CO
2
carried in
this #ay is transported in
physical solution

a very small amount is


carried as carbonic acid
3'
2
CO
,
4

ii9 co#ined .ith "rotein 8)31
23;9
CO
2
combines #ith the amine 37'
2
4 group
of 'b to form a neutral car#aino1
haeoglo#in compound
HH#NH
2
< CO
2
HH#NH
2
CO
2
Car#aino1haeoglo#in
the amount of CO
2
that is able to combine
#ith 'b depends on the amount of O
2

already being carried by the 'b
the less the amount of O
2
being carried by
the 'b molecule) the more CO
2
that can be
carried by the 'b

CO
2
produced by the tissues
diffuses passively into the
bloodstream and passes into the
erythrocytes #here it combines
#ith #ater to form car#onic
acid

this process is catalysed by the


en4-e car#onic anh-drase
found in the erythrocytes and
ta*e less than one second to
occur

carbonic acid then proceeds to


dissociate into h-drogen and
h-rogen#icar#onate ions<
iii9 as hydrogenbicarbonate ion) 'CO
,!
3;-.4

#hen the erythrocytes leave the
lungs their o$yhaemoglobin is
#ea*ly acidic and associated #ith
"otassiu ions 3='bO
2
4

in areas of high CO
2

concentrations 3as at the tissue4)
O
2
is easily given up by
o$yhaemoglobin

#hen this happen) the 'b becomes


strongly asidic

it dissociates from the carbonic


acid forming haeoglo#inic acid
3''b4
the potassium ions associate #ith
hydrogencarbonate ions to form
"otassiu h-drogencar#onate

by accepting hydrogen
ions) H# acts as a #u!!er
olecule

this ena#les large


:uantities o! car#onic
acid to #e carried to the
lungs .ithout an- a7or
alteration in #lood "H
='bO
2
='b > O
2

'
>
> 'CO
,!
> ='b ''b > ='CO
,

the cell surface membrane of an


erythrocytes is relatively
impermeable to the passage of
sodium and potassium ions

ho#ever a cation pump


operates and e$pels large
numbers of sodium ions into
the plasma

the ma(ority of
hydrogenbicarbonate ions
formed #ithin the erythrocytes
diffuse out into the plasma
along a concentration gradient
and combine #ith sodium to
form sodium
hydrogencarbonate

the loss o!
h-drogen#icar#onate ions
!ro the er-throc-tes is
#alanced #- chloride ions
di!!using into er-throc-tes
!ro the "lasa

electrochemical neutrality is
maintained

this is called chloride shi!t



potassium
hydrogencarbonate #hich
formed in the erythrocytes
is also capable of
dissociating
some of the chloride ions
#hich enter the erythrocytes
combine #ith potassium
ions to form potassium
chloride) #hile the
hydrogencarbonate ions
diffuse out
#hen hydrogencarbonate
leaves the erythrocytes) the
e$cess '
>
ions #hich
remain decrease the p'
#ithin the erythrocyte

this caused the


dissociation of
potassium
o$yhaemoglobin
3='bO
2
4 into O
2
and
potassium 'b

#hen the erythrocytes


reach the lungs) the
reverse process occurs

9?7@ AO9?6B %7: C%"%C8T8BS

lung ca"acit- o! an a,erage an is a""roxiatel- 0 d=

during :uiet #reathing he .ill #reathe in and out a#out >03 c= o! air

this is called tidal volume



i! a!ter a noral tidal ins"iration he continues to inhale5 he can ta/e in a !urther )033 c=
o! air
this is called inspiratory reserve volume
i! a!ter a tidal ex"iration the an continues to exhale5 he can !orce out a !urther )033 c=
o! air
this is tered as expiratory reserve volume

the aount o! air exchanged a!ter a !orced ins"iration !ollo.ed


iediatel- #- a !orced ex"iration is tered the ,ital ca"acit-
e,en a!ter !orced ex"iration5 )033 c= o! air reain in the lungs

this cannot #e ex"elled and is called residual air


during ins"iration a#out =33 c= o! the tidal ,olue reaches the


lungs5 .hile the reaining )03c= reains in the res"irator-
tu#es5 .here gaseous exchange does not occur

.hen ex"iration !ollo.s5 this air is ex"elled !ro the #od- as


unchanged roo air and is called dead space air

the air that reaches the lungs mi$es #ith the 0-&& cm, of air already present in the
alveoli

its volume is small compared to that of the alveolar air and complete rene#al of air
in lungs is therefore a necessarily slo# process

the air that comes into close contact #ith the blood is alveolar air
it contains less O
2
than inspired air) but more CO
2

9?7@ AO9?6B %7: C%"%C8T8BS

Tidal volume

The volume of air that is moved in and out #ith each breath during normal rhythmic
breathing

8nspiratory reserve volume

The additional volume of air that can be forced out after a normal tidal inspiration

B$piratory reserve volume

The additional volume of air e$changed after a forced inspiration follo#ed immediately
by a forced e$piration

esidual air
The volume of air #hich remains in the lungs and cannot be e$pelled even after forced
e$piration

:ead space

The tidal volume #hich remains in the respiratory tubes during inspiration and gaseous
e$change does not occur

Aital capacities
The volume of air e$changed after a forced inspiration follo#ed immediately by a forced
e$piration

'()(2 CONTROL

Control o! ,entilation

7ervous system usually controls respirations automatically to meet body2s demands


#ithout our conscious concern

espiratory centre is the area from #hich nerve impulses are sent

8t is located in the brain stem

8t consists of groups of neurons in the brain stem

8t can be divided into three areasC


i. The medullary rhythmicity area in medulla oblongata
ii. The pneumota$ic area in the pons
iii. The apneustic area in the pons

+edullar- rh-thicit- area

8t controls the basic rhythm of respiration

both inspiratory and e$piratory areas are located here

the basic rhythm of respiration is determined by nerve impulses generated in the


inspiratory area

nerve impulses from the active inspiratory area travel via nerves to the muscles of inspiration
3diaphragm and e$ternal intercostal muscles4

these muscles contract and inspiration occurs


the e$piratory neurons remain inactive during normal 1uiet respiration

#hen the inspiratory neurons become inactive again) the muscles rela$) e$piration occurs and
the cycle repeat itself over and over

24 "neuotaxic area

located in the upper pons

transmits inhibitory impulses


to the inspiratory area

it help turn off the inspiratory


area before the lungs become
too full of air

,4 the a"neustic area
located in the lo#er pons
stimulates the inspiratory
area to prolong
inspiration) thus inhibiting
e$piration

The main stimulus that controls


the breathing rate is the
concentration of CO
2
in blood

#hen CO
2
levels increase)
cheorece"tors in the carotid
and aortic #odies of the blood
system are stimulated to
discharged nerve impulses #hich
pass to the inspiratory centre

the inspiratory centre sends
out impulses via the phrenic
and thoracic nerves to the
diaphragm and intercostal
musles
these muscles increase the
rate at #hich they contract
this automatically increases
the rate at #hich inspiration
ta*es place

ins"irator- acti,it- in!lates the


al,eoli5 and stretch rece"tors
located here and in the
#ronchial the- are stiulated to
discharge i"ulses to the
ex"irator- centre .hich
autoaticall- cuts o!!
ins"irator- acti,it-

the respiratory muscles therefore


rela$ and e$piration ta*es place

after this had occurred) the alveoli
are no longer stretched and the
stretch receptors no longer
stimulated
the e$piratory centre becomes
inactive and inspiration can begin
again
the #hole cycle is repeated
rhythmically throughout the life of
the organism

That2s all
for
today

GASEOUS EXCHANGE
AND CONTROL IN
?LANT

Stomata
Structure and !unction o!
guard cells in the stoatal
o"ening and closing
echaniss

stoa is a icro "ore


that located #et.een a
s"ecialised e"ideral cells
called guard cells

the guard cells occur in


"airs side #- side

guard cells ha,e a


distincti,e sha"e

the onl- e"ideral
cells that contain
chloro"lasts
Guard cell has a
thinner outer .all and
a thic/er5 less elastic5
inner .all
the si4e o! stoa is
ad7usted #- the
turgidit- o! the guard
cells

egulation of stomatal opening and closing
due to the guard cells turgidit-

three echaniss
i( Starch1sugar h-"othesis 8"hotos-nthesis in the guards cells and
accuulation o! sugar9
ii( CO
2
concentration in the lea! 8related to starch1sugar
h-"hothesis9
iii( ?otassiu ion concentration o! the guard cells


i( Starch1sugar h-"othesis 8"hotos-nthesis in the
guards cells and accuulation o! sugar9

an increase in sugar concentration 8!ro


"hothos-nthesis9 in guard cells during the da- lead to

the decrease in their solute potential and

entry of #ater by osmosis

cells become turgid



The outer #all of guard cell is thinner and more elastic than the inner
#all.
The increase in turgor pressure causes the guard cells to curve
out#ard
Stoma open

The decrease in sugar concentration 8light de"endent reaction
not occur9 in guard cells during the night lead to
the increase in their solute potential and
outflo# of #ater by osmosis
cells become flaccid
causes the closing of stoma

ii( CO
2
concentration in the lea! 8related to
starch1sugar h-"hothesis9
at night5 car#onic acid is accuulated in the interstitial
cells
car#onic acid is dissociate into h-drogen and
h-drogencar#onate ions
H
2
CO
=
HCO
=1
< H
<

this .ill increase the concentration o! H


<

en4-e catal-se the trans!oration o!


glucose1)1"hos"hate into starch

this decrease the turgidit- o! guard cells5


thus the "ore is close

da- tie5 CO
2
is used during "hotos-nthesis5 the
concentration o! H
<
is decreased
"hos"horilase catal-se the trans!oration o! starch into
glucose1)1"hos"hate in the guard cells
the turgidit- o! the guard cells increase5 the entr- o! .ater
#- ososis
the "ore is o"en

iii( ?otassiu ion concentration o! the guard cells

during the da-5 "hotos-nthesis occurs in the guard cells 5


AT?s are s-nthesi4es

the AT?s acti,ate the ions "u"5 increasing the


concentration o! "otassiu ions in the guard cells

this leads to the decreasing in the solute "otential o! the


ad7acent cells and the entr- o! .ater #- ososis

the "ore is o"en


during the night5 "hotos-nthesis 8light de"endent


reaction9 not occurs5

AT?s are not s-nthesi4es

The ions "u" #ecoe inacti,e5

The "otassiu ion di!!use out o! the guard cell

The concentration o! "otassiu ions in the guard cells


decrease(

this leads to the increasing in the solute "otential o! the


ad7acent cells and the out!lo. o! .ater #- ososis

the "ore is close



T'B B7:

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