TRANSPORT IN ANIMALS

INTRODUCTION
same as plants

WHY DIFFUSION ONLY IS NOT FOR US

Since diffusion is effective over 25µm only and being multicellular there is
great
distance that diffusing molecule will have to travel

SO WHAT DO WE HAVE
complex transport mechanism Diffusion

COMPLEX TRANSPORT MECHANISM

CARDIOVASCULAR SYSTEM
Components
i Heart
pumping device
2 Blood circulatory fluid
3 Blood vessels tubes in whichbloodflows
 TYPES OF CUS

OPEN BLOOD SYSTEM CLOSED BLOOD SYSTEM

DRAWBACKS GOODNESS
Bloodpressure is decreased distribution is well controlled
no
regulation of BP no mixing of oxy deoxy blood
distribution of nutrients and materials is regulation of the blood pressure
not well controlled BP is never completely lost
mixing of oxy deoxy blood efficient exchange of nutrients and
Present in frogs materials
Why are the insects fine with it
since they are
metabolically less active

If rate of diff 1 provision of nutrients t

TYPES OF CIRCULATORY SYSTEM

Single Circulation Double Circulation

the blood passes once through the heart in the blood passes through the heart twice
one complete circulation in one complete circulation

DRAWBACKS PULMONARY CIRCULATION

BP low as it's pumped to the the heart pumpsthe deoxy blood to the lungs
gets v gills
this low BP blood is carried to all parts at a lower BP bl lungs are at a close
of the body distance higherpressure would damage
exchange of nutrients material will be the delicate capillaries oflungs exchange
less efficient of rasp gases would be affected BP
decreases further this oxy blood is
IS THE FISH HAPPY carried back to the heart in order to
it's cold blooded regenerate the BP
it's metabolically less active
So it can survive with a compromised a
lung close distance
lesser exchange of nutrients materials
SYSTEMIC CIRCULATION
the
oxy blood is pumped by the heart at a
high pressure 1120 mm Hgl so that
the blood ran reach diff parts of the
body at a great distance for efficient
 g f e s

the deoxy blood is returned back to the

Smt
bodyparts greatdistance

BLOOD VESSELS
ARTERY

Tunica Intima Intern a

Tunica media
Tunica externa
Tunica Adventitia
MYp
lumen
Is mall and regularshaped
wall
regulate the BP
TUNICA INTIMA
inner most
layer
faces the lumen
cvinck led
 made up ofsingle layer of squamous epithelium thinnest

TUNICA MEDIA
2nd
layer
thickest layer
it has elastic fibres smooth muscles and few collagen
it has neurone endings too

TUNICA ADVENTITIA
outermost layer
thinner than tunica media
it has few elastic fibres and a lot of collagen

TYPES OF ARTERIES

ELASTIC MUSCULAR
closer to the heart away from the heart
v Bp Less
 g 9 I
withstand the BP regulate the bp
T EF in TM PSM in TM

CONTINUOUS BLOOD FLOW EVEN OUT BLOOD FLOW

Systole contraction of the car dial muscles blood is pumped at a high bp into the aorta
Diastole relaxation of the cardiac muscles bloodpressure is decreased

During the systole the elastic fibres stretch out decreasing the BP 120mm Hg
During the diastole the elastic fibres recoil increasing the BP 80 mmHg

ARTERIOLES
last resort for the regulation of BP ble they to form capillaries which are
the final exchange destination
same composition as that of the muscular arteries
they have Tsm in their Tm
hence they can do
a vasoconstriction

b vasodilation
 CAPILLARIES
extracellularspace
exchange destination
tissuefluid
formation of tissue fluid to mmHg

STRUCTURE
a thin walled
and

10mm
to
KÉÉ
venousend arterialend
arteriole

35mmits
a
single layer of endothelium
endothelial cells have gaps in bw
8
ADAPTATIONS
1 single layer of endothelium 125pm diffusion
t distance of diffusion rate of diff 9

2 numerous microscopic a
huge network
PSA to volume ratio rate ofdiffusionT

3
gaps in
b w the endothelial cell
fluid leaks out tissue fluid formation 9

4 capillaries are very close to the tells

is
 say y e ay f y
cell
t distance of diffusion rate of diff increases

5 the internal diameter of cap is 7mm

RBCs also have 7pm diameter RBCs squeezethrough the capillaries
acquiring
an umbrella shape distance of diff of Oz t rate of diffusion of 024

VEIN
BP 5mm Hg

tunica intima
smooth

tunica media
thinnerthan TE
mm
widerthan TM

Problem 7
Bc low the return the blood to the heart
 1

Adaptation
I hemen is
large more blood can flow per unit time
2 positioned in b w the skeletal muscles

TISSUE FLUID FORMATION

 totena

3LÉ__gggg
nm
Sad 35mm ng sava

bloodvessels By J
1001

why nottoo high

b c of water's mout
th
skin Yes ski ftp.sptoiteins
net outward
movement
y money
ut of the sap
venous en'd arterial end 1001 TF formation

TISSUE FLUID FORMATION AT ARTERIAL BED

In the arterial bed of the capillary the Hydrostatic Pressure is too high since the
bp 35mmHg the blood is contained within the capillary The HP in the extracellular
space is too low
Moreover in the arterial bed the solute conc is just high since since the blood has
small solutes and plasma proteins but as H2o is present so the sc is not very high
As the S C is high in cap the Y is low in capillaries and Y is high in Ecs
so we ran see that there are two forces existing but as the HP is a
huge for ie
so the net movement would be from inside of capillaries to the Ecs i.e tissue

fluid formation occurs

Remember plasmaproteins and blood cells don't leak out as their Mr is too high
TISSUE FLUID RETURN AT THE VENOUS BED
At the venous bed HP is still
high since the bp 10mmHg but now the magnitude
has reduced as much of the H2o of the blood has moved out in the Ecs during
TF formation
But Sc now has become a hugeforce as due to the presence of the plasma
proteins I due to lass H2o left in the cap in the venous bed the plasma pro
lone t a lot So the Y in the venous bed is too low and Y in the Ecs is too high
so now the TF return occurs from Ecs Npr to venous bed 4th

WHAT MAY HAPPEN IF TISSUE FLUID RETURN DOES N'T OCCUR

Extra accumulation of fluid in the ECS edema
H2O H2O
Y in the ECS will t dangerously
yo Y TM water will enter the cells a lot the
cell cells will swell and may burst
Yutt tissue dies

ECS

CUS no tissue fluid return

water blood
 t blood volume
t BP
stress on cardiac muscle failure
IF THE DIET LACKS IN PROTEINS WHAT ARE THE CONSEQUENCES ON TF
less proteins less plasma protein these deer eases in the venous bed
I would not be high anymore so the steep Y gradient which was responsible
TF return wouldn't be established so TF return won't occur
for the resulting
in edema osmotic prop in the tissue would be affected the H2O enters the
calls a lot they eventually burst cell dies tissue dies

901 OF THE TISSUE FLUID RETURNS TO THE VENOUS BED

Lymphatic system returns the leftover lot TF t proteins the lymphatic vessels
later join up with the vena cava

HAEMOGLOBIN
Haemoglobin Hb RBC
2d chains haem prostheticgroup
chain
 B
gas partialpressure
Hh 402 HbOa
oxyhaemoglobin
saturation of Hb T
association lungs
oxygen carrying pigment pp 02T affinity for 029
µ
dissociation muscles etc post affinity Oct
oxygen releasing pigment p
saturation of Hb t

If same amount of Hb is subjected to different pp or the saturation of Hb will be affected

The graph of the results is called as Hb dissociation curve
independent pp or
dependant saturation of Hb
constant no of Hb

i saturation
of Hh s shaped
sigmoid
i
 ppl 2
DESCRIPTION
bottom of graph less steep a small change in the pp or doesn't t the saturation of Hb
steeply
middle part verysteep a small change in the ppo and a steepT in the saturation
of Hb
last part plateau now Hb is maximally saturated and there is no effect of inc
the pp02

EXPLANATION
the graph is s shaped ble of cooperative binding property of Hb positive cooperativity
1st O mot to the 1st Hb chain is a little difficult as
According to this the binding of
the binding site of O on the Hb chain is not fully exposed This is evident on the bottom
less steep partof the graph
But somehow when the 1stOz molecule joins up with the 1st Hb chain the Hb mo l undergoe
conformational change shapechanged and the binding of the 2nd0 molecule to the 2nd
chain gets easier as the binding sitegetsexposedl
When the 2ndOz mo l binds the conf change occurs again and it becomes progressively
3rd and 4th to bind as the the
 f y y i 1 I g f

Hb dissociation curve can also be read to know about the position of Hb in the body

i saturation 17
of Hh lungs
readfromtop to bottom
f
normally

T ppo

A small change in the ppo and the Hb's

affinity for Oz decreases a lot and hence it gets
unsaturated very steeply This is amazing as the Hb's release of Oz is a lot and
immediate even if a small change in ppOz so we can say that cells muscles which
are not
respiring much can also get the Oz they require because of Hb's steepdrop
in affinity for Oz when the is
pp Or low
 Fetal Hb maternal Hb

i saturation
of Hh
fatal itb
30 t

10
2 pp02
Because at saturated than the maternal Hb that
any ppOz fetal Hb is more means the

affinity forOz is more This is what is required since fetus is dependant on the mother's
blood for the provision of nutrients and in this case 02 so it can take the Ozfrom
maternal Hb Imove saturation more affinity

Myoglobin It b

i saturation
 of Hh

pp02

Myoglobin is a pigmentfound in muscles has only one polypep chain and carries only one
Oz its affinity for Oz is massive and it remains saturated until the ppo getstoo low
i when Hh has become almost unsaturated then only myoglobin will release Oz The
e

graph is on extreme left and this could be taken as a last attempt to delay anaerobic
respiration

Factors affecting Itb Dissociation curve

1
pp 02
2
ppCO2
3 temperature

TEMPERATURE
High
i saturation
bindingof Oz to ha em prosthetic of Hh
group breaks down
ed
Hb's affinity for Oct
Yhitemperature
saturation of Hbt

Affinity app Oz a saturation

PPO2

EFFECT OF PpCO2
x
pp Con Affinity
pp Con a saturation

At higher ppcoz the Hb dissociation curve shifts to the right this shift is called as
Bohr shift
effect of ppcoz on Hb dissociation curve is called as Bohr effect

i saturation
of Hh
 no
EXPLANATION

Elite

lil Coz F H2coz

H2O

Iii H 21037 Htt HCO5

iii HbOf Htt Hhb 402
 caubghnifydrase

Allow

the CO2 produced in the respiring cells diffuses out of the cells into the tissue fluid and
then it diffuses throughthe endothelial wall of the cap into the bloodplasma then it
diffuses into the RBCs Carbonic Anhydrase enzyme is present in the RBCs which
catalyses the conversion of H2o and Co2 into carbonic acid which immediately
dissociates into H and it coz Now Hh has more affinity
for it than for oz so it
releases the Oz to bind to the H and hence it becomes Hit b ie Haemoglobinic Acid
The oxygen that is released diffuse out of the RBCs into the blood plasma then
diffuses across the endothelial wall ofthe capillariesinto tu TF and thenfinally into the
respiring cells

There are 2 advantages

the release of oxygen by oxyhaemoglobin which is later usedby the respiring cells
Hb mops up the protons and hence it resists the decrease in pH if these protons
had leaked out of the RBCs into the plasma we can say that the Hb acts as a
WAYS OF TRANSPORT OF CO2
as Hydrogencarbonate ion it 05 851
as carb amino haemoglobin 101
travels in dissolved form in blood plasma 51

CHLORIDE SHIFT
the movement ofchloride ions into red blood cells from bloodplasma to balance the
movement of H 105 into the bloodplasmafrom the RBCs The influx of CL helps to prevent
the overall charge inside the cell from becomingtoopositive

THE HEART
to Lungs
pulmonary vein

pulmonaryartery fromlungs

ofpressure
 deoxy t left atrium
valve i
i 11 tendons

rightatrium left ventricle

tricuspid valve septum

right ventricle
conical shaped tendons hold the Av valves during
the ventricularsystole when
papillarymuscles press r
too much they hold th valves firmly

DIFFERENCE IN THICKNESS DIW THE ATRIAL WALL VENTRICULAR WALL

Atrial wall is thinner vent wall is thicker
Atrial wall is less muscular vent wall is more muscular
Atrias don't have a lot of muscles b c they have to pushthe blood to just the lower
lying ventricles which are at a close distance so they don't need to generate a lot
of pressure
ventricle thick muscular generate a lot of BP

distance the blood to

 9 i dy

DIFFERENCE B W THE RIGHT AND LEFT VENTRICLES

RV is thin less muscular b c it has to pump the blood to the lungs which are at a
close distance if it were v muscular cap of the lungs would rupture 135mm itg
LV is thick more muscular ble it has to generate a lot ofpressure has to pump the
blood to diff parts of the body at a great distance If it were not muscular B Pt
adequate pressure in the cap won't be generated 135mm itg in eff exchange of
nutrients and materials

cap BP TT damage blood passes tooquickly

is not eff
cap BP It inadequatepress exchange of mat

CARDIAC CYCLE
The sequence of events that take place during a complete heart beat

SYSTOLE contraction
DIASTOLE relaxation
1 Atrial diastole ventricular diastole
2 Atrial systole
3 Ventricular systole
4 Ventricular diastole atrial diastole

ATRIAL DIASTOLE
Atria are relaxing

pressure
Iff
man

AT An time

MYOGENIC STIMULATION OF CARDIAC MUSCLES

muscles are i their or
 e
yog y y
relaxations

wave of excitation
wave of ex citation
after purkyne
tissue

Purkynetissue

There is a patch of specialised cardiac muscles called as SAN sino atrial node
found in the wall of right atrium Soduring atrial diastole when the deoxygenated
blood enters the RA the SAN gets stimulated and it generates a wave of
excitation and that rapidly travels throughout the two atrias and they show atrial
systole The wave of ex iitation does not travel down to the ventricles at the same
time since the atrioventricular septum is made of non conducting tissues except
AUN Aun is a it
 g il
the wave of excitation But the AVN creates a delay of 0 Is in transmitting
the impulse to make sure that the atrial systole occurs first and ventricular
systole occurs after the atrial systole has ended Hence the backflow of the blood
from the ventricles to the atrias is prevented If there was no delay and ventricles
had done the systole together with the atrial systole so the backflow of blood
would occur as the pressure in ventricle is
higher than that in the atria

Now after O is the AVN transmits theimpulse to the Purkyne tissue The Punky ne
tissue goes till the apex of the ventricle and then into the wall of the ventricles
so this means that the wave of excitation travels down to the apex of ventricles
and then up the ventricles Hencethe contraction of ventricles occurs from bottom
to the top of ventricle This results in effective emptying of the ventricles and
the blood hence enters to the aorta from left ventricle and to the pulmonary
artery from the right ventricle

If the contraction of ventricles would have occurred from top to bottom it would
have resulted in trapping of blood in the bottom of ventricles and bursting of the
ventricle might occur due to the abnormal increase in pressure