Mass Transport In Animals

• What is haemoglobin?

  Group of chemically similar molecules adapted for O2 transport, found in a wide variety of organisms.

  
• Describe the structure of haemoglobin

  Haemoglobin has a quaternary structure with 4 polypeptide chains linked together, with each chain associated with a prosthetic Fe2+ group.

  
  

  Each Fe2+ can combine with a single O2 molecule ---> 4xO2 molecules can be carried by each human haemoglobin molecule in humans.
• Hb reversible equation

  Hb + 4O2 -> HbO8 ( oxyhaemoglobin)
• What is the role of Haemoglobin in the transport of oxygen?

  1. Readily associate with O2 at gas exchange surface ( high oxygen partial pressures).

  
  

  2. Readily dissociate from O2 at respiring tissues ( low oxygen partial pressures) .

  
  

  => seems contradictory - Hb can change its affinity (chemical attraction) for O2 under different conditions ---> shape changes due to the presence of CO2.

  
  

  ---> in the presence of CO2, the new shape of the Hb molecule binds more loosely to O2 ---> Hb releases its O2.
• Bohr effect

  Higher CO2 partial pressures cause oxyhaemoglobin to dissociate into Hb + O2, therefore increases rate of oxygen unloading
• Is oxygen loaded/unloaded at the gas exchange surface? Explain why.

  O2 loaded, because:

  
  

  High [O2], low [CO2] ---> high affinity for O2.
• Is oxygen loaded/unloaded at the respiring tissues? Explain why.

  O2 unloaded, because:

  
  

  Low [O2], high [CO2] ---> low affinity for O2.
• Why is the oxygen dissociation curve shaped like an S?


  - O2 does not bind evenly to Hb across different partial pressures of O2.

  
  

  1. Closely packed polypeptide subunits, so hard for O2 to bind ---> low [O2], little binds ---> shallow gradient.

  
  

  2.Binding of 1st O2 molecule changes the 4 structure of Hb molecule ---> changes shape so that it is easier for other O2 molecules to bind to each subunit.

  
  

  => takes a smaller increase in PO2 to bind 2nd O2 molecule than it did to bind 1st O2 => positive cooperativity ---> binding of 1st facilitates binding of 2nd ---> steeper gradient of curve.

  
  

  3. After 3rd O2 molecule binds ---> more difficulty due to decreased probability of a single O2 molecule finding a free binding site ---> graph flattens off.

  
  

  NB=> Curve to left = higher affinity for O2.

  => Curve to right = lower affinity for O2.

  
• Describe the Bohr effect

  = Increasing [CO2], the more readily the Hb releases its O2 (+ less likely to load O2) due to a reduced Hb affinity for O2.

  
  

  Curve shifts to right.

  
  

  Always ensures enough for O2 for respiring tissues:

  
  

  - Increased respiration rate ---> more CO2 ---> lower pH ---> greater change in shape of Hb ---> O2 more readily unloaded ---> more O2 for respiration.
• Outline the continuous process of oxygen loading and unloading in the body

  1. Gas exchange surface, CO2 constantly removed.

  
  

  2. Slightly higher pH due to low [CO2].

  
  

  3. Higher in pH changes shape of Hb ---> loads O2 readily.

  
  

  4. Increase in affinity for O2 ---> O2 not released when being transported in blood to tissues.

  
  

  5. CO2 produced by respiring cells in tissues.

  
  

  6. CO2 acidic in solution so pH of blood falls.

  
  

  7. Lower pH changes Hb shape ---> decreased affinity for O2.

  
  

  8. Hb releases its O2 into respiring tissues.
• Describe cooperative binding

  Binding of first oxygen to haemoglobin causes change in shape

  Shape change allows more oxygen to bind
• Describe the structure of the human heart

  
• Describe the pressure and volume changes during the cardiac cycle that maintain a unidirectional flow of blood

  1. Ventricles relax, atria contracts

  - Decrease volume of chambers

  - Increase pressure inside chambers

  - Forces blood into ventricles

  
  

  2. Ventricles contract, atria relax

  - Increase pressure in ventricles compared to atria

  - Forces AV valves shut

  - Forces SL valves open

  - Blood forced into arteries

  
  

  3. Ventricles relax, atria relax

  - Blood returns to heart

  - Atria fill again

  - Increase pressure in atria

  - Ventricles relax, decreases pressure in atria

  - AV valves open

  - Blood flows passively into ventricles from atria

  - Atria contract, cycle begins again
• Name the valves present in the heart

  Atrioventricular (AV): link atria to ventricles

  - prevents blood flowing back intro atria

  
  

  Semi-Lunar (SL): link ventricles to pulmonary artery

  - stops blood flowing back into the heart
• Structure of arteries

  Thick muscle tissue

  Thick elastic tissue

  Folded endothelium

  
• Adaptions of arteries

  1. Elastic tissue allows stretching which maintains blood pressure as it stretches when ventricles contract - folded endothelium allows stretching

  2. Muscle for vasoconstriction

  3. Thick wall withstands bursting

  4. Smooth endothelium reduces pressure

  5. Aortic valve prevents back flow
• Structure of arterioles

  Tiny branches of arteries that lead to capillaries. These are also under the control of the sympathetic nervous system, and constrict and dialate, to regulate blood flow.
• Structure of veins

  Thin muscle wall

  Less elastic tissue

  Wide lumen

  Valves

  Blood flow helped by contraction of body muscles around them

  
• Function of veins.

  Veins carry deoxygenated blood to the heart [except pulmonary veins] where these will be processed through the lungs and given oxygen again.
• Adaptions of capillaries

  1. Near cells in exchange tissues ( therefore short diffusion path)

  2. One cell thick ( shortens diffusion path)

  3. Large number increases surface area
• Describe the formation of tissue fluid

  1. At start of capillary bed, HYDROSTATIC PRESSURE inside capillaries is greater than in tissue fluid

  2. Difference in hydrostatic pressure means overall outward pressure forces fluid out of capillaries into space around cells forming tissue fluid
• Describe how tissue fluid returns to the circulatory system

  1. At the start of the capillary bed, nearest the arteries, the pressure inside the capillaries is greater than the pressure in the tissue fluid.

  
  

  2. This difference in pressure forces fluid out of the capillaries and into the spaces around the cells, forming tissue fluid.

  
  

  3. As fluid leaves, the pressure reduces In the capillaries- so the pressure is much lower at the end of the capillary bed that's nearest to the veins.

  
  

  4. Due to the fluid loss, the water potential at the end of the capillaries nearest the veins is lower than the water potential in the tissue fluid - so some water re-enters the capillaries from the tissue fluid at the vein end by osmosis.

  
  

  XS tissue fluid drained into lymphatic system
• Describe atheroma formation

  1. Damage occurs to endothelium ( e.g. by high blood pressure)

  2. WBCs and lipids clump together under the lining forming fatty streaks

  3. Over time more WBCs, lipids and connective tissue build up and harden to form a fibrous plaque called an atheroma.

  4. Plaque partially blocks lumen, restricting blood flow, causing blood pressure to increase.
• Cause of CHD

  Having lots of atheromas in coronary arteres, restricting blood flow to heart muscle, leading to a myocardial infarction
• What is an aneurysm

  Balloon-like swelling of the artery
• Explain the cause of an aneurysm

  1. Atheroma plaques damage and weaken arteries, narrowing arteries and increasing pressure

  2. Blood travelling down weakened artery at high pressure pushes inner layers of artery through the outer elastic layer, forming a balloon like swelling

  3. Aneurysm may burst, causing haemorrhage
• Thrombosis

  Formation of a blood clot
• Describe the formation of thrombosis

  1. Artheroma ruptures endothelium of an artery

  2. This damages artery wall leaving a rough surface

  3. Platelets and fibrin accumulate at site of damage and form a blood clot ( thrombosis)

  4. Blod clot can cause complete blockage of the artery or become dislodged and block a vessel elswhere in body
• Describe the formation of a myocardial infarction

  1. Coronary arteries become blocked due to thrombosis

  2. Heart muscle receives no oxygen

  3. No aerobic respiration can occur

  4. Death + damage to cardiac muscle
• Which factors increase risk of cardiovascular disease?

  High blood cholesterol + Poor diet

  Cigarette smoking

  High blood pressure
• How does high blood cholesterol + poor diet cause cardiovascular disease?

  1.) Cholesterol is one of the main constituents of the fatty deposits that form artheromas

  2.) Atheromas lead to increased blood pressure and blood clots

  3.) These could block blood supply to coronary arteries, causing myocardial infarction

  Diet high in saturated fat associated with high blood cholesterol levels + Diet high in salt increases risk due to high blood pressure
• How does cigarette smoking increase cardiovascular disease risk?

  1. Nicotine increases high blood pressure

  2. Carbon monoxide combines with Hb, reducing amount of oxygen transported in blood, therefore less O2 available for tissues. If cardiac muscles don't have enough O2 = HA

  3. Smoking decreases amount of antioxidants in blood, therefore cell damage of coronary arteries more likely = atheroma formation
• How does high blood pressure increase risk of cardiovascular disease

  Increased risk of damage to artery walls

  Increased risk of atheroma formation

  Causing increased risk of blood clots

  Which could cause myocardial infarction