Transport in Animals 

• Formation of Tissue Fluid from Plasma:

  • -  Artery reaches the tissue and branches into smaller arterioles and capillary

    networks which eventually link up with venules to carry blood back to the veins

  • -  Arterial End: Blood has a high hydrostatic pressure which leads to blood being

    pushed out of small gaps in the capillary wall.

  • -  The leaving fluid has high levels of dissolved nutrients and oxygen but has no

    platelets, red blood cells and very few white blood cells as these remain in the

    blood as they are too large to fit though the small gaps in the capillary wall

  • -  Tissue fluid surrounds the body cells so gaseous exchange with the cells can

    occur and nutrients in the tissue fluid cna dissolve into the cells. This occurs by a mixture of facilitated diffusion, simple diffusion and active transport. CO2 is also actively transported out.

• -  Tissue fluid returning to the blood:

  • -  Venous End: Blood pressure very low so some tissue fluid renters the blood by

    diffusion down the pressure gradient and hydrostatic pressure of tissue fluid is

    high so further causes movement

  • -  The remaining tissue fluid enters the lymph system, excess tissue fluid is drained

    out of the tissue and reuters it to the blood in the subclavian vein in the chest

  • -  Lymph fluid is similar in composition to the tissue fluid and will have more

    lymphocytes as produced by the lymph nodes

• -  Oncotic Pressure:

  • -  Hydrostatic pressure is not the only influence oncotic pressure is the pressure of the solutes and dissolved substances of the blood on the walls and environment

  • -  Oncotic pressure of the blood plays a role in pulling the water back into the blood

  • -  Oncotic pressure of the tissue fluid has a role in pulling the water into the tissue

    fluid

• -  Cardiac Cycle:

  • -  Atrial systole, ventricular systole diastole

  • -  Atrial systole moves blood into the ventricles when the ventricles are full the atrial

    systole will stop and ventricular systole will occur from the apex of the ventricle upwards through the walls, thick muscle so strong contraction and blood pushed around respective circuits

  • -  Valves: atri-ventricular

    • -  Systole the ventricular walls relax and recoil anign pressure drops to

      below pressure in atria

    • -  Blood in the atria pushes atrioventricular valves open

    • -  Atrial systole causes blood to enter the ventricles though the atria

    • -  Blood continues to enter the atria so pressure of both atria and ventricles

      increases

    • -  Valves remain open and close when atrial diastole begins

    • -  Caused by swirling in the blood around the valves when the ventricle is

      full

• -  As ventricular systole occurs the pressure in the ventricles increases

• -  Pressure rises above the atrial pressure

• -  Swirling and pressure increase act to close the valves

• -  Blood moves upwards and the movement fills the valve pockets

  preventing the, from opening and blood flowing backwards into the atria.

- Valves: Semilunar valves

• -  Before ventricular contraction the pressure in the major arteries is higher than the pressure in the ventricles

• -  Semilunar valves are closed as a result

• -  Ventricular systole raises blood pressure in the ventricles

• -  When the pressure rises above above the major arteries the semilunar

  valves are pushed open

• -  Blood is under very high pressure so is forced out of the ventricles in a

  very powerful spurt

• -  Diastole occurs after ventricular systole is over

• -  Elastic tissue recoils in the ventricles and the pressure drops as the

  muscle is returned to its original size

• -  As the pressure drops below the pressure in the arteries blood flows back

  to the ventricles

• -  At this point the semilunar valves close as a result of blood collecting in

  the valve pocket

• -  The pressure wave created when the semilunar valves close is the pulse

- Control of the Cardiac Cycle:

• -  Heart muscle is myogenic as it introduces its own contraction

• -  If it is not controlled it may be inefficient and lead to issues in the amount of blood

  delivered to cells

• -  Initiation: at the top right atrium there is the Sino-Atrial Node and this leads to the

  generation of electrical activity

• -  The SAN generates a wave of excitation at regular intervals (this is the heart

  rate)

• -  The SAN is thus the pacemaker

• -  Atria:

  • -  Wave of excitation spreads over the walls of both atria travels across the membranes of the muscle tissue as the wave of excitation passes it causes cardiac muscle to contract, this is systole

  • -  Top of the node is the atrioventricular node (AVN) this is responsible for conduct the wave of excitation through the ventricles this causes a delay which is allows time for the atria to finish systole

• -  Ventricular:

  • -  After the delay the wave of excitation passes down and is carried by the

    Purkyne tissue

  • -  Runs down the interventricular septum

  • -  Base of the septum the excitation spreads over the ventricular walls

  • -  This causes muscular contraction

- Pushes blood towards the major arteries at the top of the heart

• -  Haemoglobin action:

  • -  Ability of oxygen to bind to haemoglobin is based on oxygen partial pressure, the partial pressure of oxygen is the effect that oxygen has as a relative pressure out a mixture of gases and may be called oxygen tension

  • -  Produces an S shaped curve as the partial pressure of oxygen increases the percentage saturation generally increases in an S curve (called haemoglobin dissociation curve)

  • -  At low partial pressure haemoglobin does not readily associate with oxygen molecules

  • -  This is as a result of the haem being in the centre of the molecule and somewhat covered

  • -  As partial pressure increases the diffusion gradient increases and eventually an oxygen molecule will neter and bind ot the haemoglobin and associates with one of the haem groups

  • -  This causes a conformational change in the shape (tertiary) of the haemoglobin molecule which leads to the ease of other oxygen molecules increasing and so there is a steep increase in the curve

  • -  Forms oxyhaemoglobin when o2 bonded

  • -  As the saturation nears 100% the curve flattens

  • -  This can all be explained as: when the initial oxygen molecule bonds the affinity

    of haemoglobin for oxygen increases

  • -  Additionally the partial pressure in respiring tissue is low enough to case oxygen

    to dissociate readily

  • -  Foetal Haemoglobin: slightly different as has a higher initial oxygen and so the

    curve lies to the right of normal haemoglobin

    • -  This is because the haemoglobin must be able to associate with oxygen

      in an environment where the oxygen tension is low enough that

      haemoglobin releases oxygen

    • -  As the oxygen tension in the placenta is low from the foetal blood

      absorbing oxygen and nutrients from surrounding fluid the mothers blood

      fluid can diffuse into the placenta

• -  Oxygen Dissociation:

  • -  Only 5% of oxygen is dissolved in the plasma itself

  • -  10% combines with haemoglobin to form carbaminohemoglobin

  • -  Majority (85%) forms hydrogencarbonate ions

  • -  Formation of hydrogencarbonate ions:

    • -  Carbon dioxide diffuses into the red blood cells

    • -  Combines with water to form carbonic acid and the reaction is catalysed

      with carbonic anhydrase

    • -  CO2 + H2O → H2CO3

    • -  This carbonic acid dissociates to give H+ ions and HCO3-, H2CO3 →

      HCO3- + H+

    • -  Hydrogencarbonate ions diffuse out of the red blood cell into the plasma

• -  The charge within the cells is maintained by a chloride shift where Cl- (chloride) ions from the plasma diffuse into the red blood cell

• -  As hydrogen ions build up the red blood cell pH decreases and becomes v acidic this is prevented as the H+ is taken out of solution by haemoglobin binding with H+ to form haemoglobinic acid (HHb) as a result the haemoglobin is described to act as a buffer as it maintains a roughly constant pH

• -  As blood nears respiring tissues the partial pressure fo oxygen int he tissues is lower so oxygen will dissociate and releases oxygen for the tissue thus the haemoglobin is available to take up H+

• -  This leads to the Bohr Effect:
  - Increasing concentration of CO2 means more CO2 can enter the

  red blood cells forming more carbonic acid which dissociates to

  form H+ ions
  - This reduces pH of the cytoplasm making it more acidic
  - The change in pH affects the tertiary structure of haemoglobin and

  reduces affinity for oxygen and thus the oxygen is all released

  from the oxyhaemoglobin to the tissue
  - In more respiring tissue there will be more carbon dioxide and so

  there is more oxygen released as a result the higher respiring the

  tissue
  - Therefore, More CO2 leads to haemoglobin being less saturated

  so the dissociation curve shits down to the right the more CO2 is present and the more activity there is and this is the Bohr shift