5.1. Gas exchange Flashcards
Adaptations of gas exchange surfaces to ensure a rapid exchange
permeable, large, thin (short diffusion distance) and moist (to dissolve the gases)
Cell respiration, gas exchange and ventilation (define and how are they connected)
Cell respiration – controlled release of E from organic compounds (uses up O2, releases CO2, creates a constant gradient of gases between tissue and blood
Gas exchange – diffusion of O2 and CO2 down their concentration gradients across the alveoli and capillary wall
Ventilation (breathing)– maintains the concentration gradient between lungs (alveoli) and blood (O2 goes into blood, CO2 into lungs)
These three processes maintain each other (if an organism dies, first goes CR>gas exchange>ventilation, because of accumulation of both gases in the body).
The human respiratory system consists of:
Nasal and oral cavities, palate, larynx, trachea, bronchi, bronchioles, lung, alveoli, diaphragm and intercostal muscles (external and internal)
Muscles used in breathing (antagonistic pairs)
Diaphragm (smooth muscle, autonomic nerve control) and muscle in the front wall of the abdomen, intercostal muscle between ribs (internal and external)
Inhalation vs exhalation muscle activity, rib cage, lung volume and pressure
Inhalation – external IM contract, internal IM relax, diaphragm contracts, AM relax, rib cage goes up, lung V is increased, lung p drops below atmospheric so air passively flows in
Exhalation – opposite (internal and abdominal contract)
Adaptations of lungs for efficient gas exchange
- Airways for ventilation – bronchioles, ending in alveolar ducts, leading to alveoli
- Large surface area (many tiny alveoli)
- Extensive capillary beds surrounding alveoli
- Short distance for diffusion – alveoli and capillary walls are both single layers of flattened cells (pneumocyte type I and endothelial cells)
- Moist surface with surfactant – fluid is secreted by pneumocytes type II, they also secrete pulmonary surfactant which reduces the surface tension and prevents water from sticking sides of alveolus together
Pneumocyte type I vs type II
Pneumocyte type I – flat, permeable to gases and responsible for gas exchange
Pneumocyte type II – rounded, bigger, secretes mucus for gas dissolution and surfactants
Cooperative bonding, O2 saturation
Binding or dissociating of a O2 from any haem group in Hb causes conformational changes to it that increase or decrease Hb’s affinity for oxygen. Because of cooperative bonding, the correlation between p(O2) and % saturation is positive but not proportional.
Hb is 100% saturated with eight oxygen atoms. The most stable forms of O2 are 0% and 100% saturated.
How does Hb O2 affinity change with p(O2)?. Why is it good that Hb is already completely saturated at 10 kPa?
When in contact with an area of high p(O2), Hb has high affinity for oxygen (oxygenated blood) and vice versa.
Allows Hb to provide O2 even to extremely active respiring tissue (3-5 kPa, normal tissue is 5-10 kPa)
Myoglobin
Pigment in muscles that stores one O2 molecule and acts as a reserve because it has higher affinity for O2 than Hb so it won’t release it easily and only if it’s really needed to postpone the onset of anaerobic CR. Its O2 affinity doesn’t change with pH (unlike Hb’s)
Foetal Hb (how does foetus obtain O2, O2 affinity of HbF, why?)
A foetus obtains oxygen via placenta; O2 dissociates from HbA in the maternal blood and binds to HbF in foetal. This can only happen because HbF has a higher O2 affinity than HbA (has a slightly different a-a sequence). At any p(O2) HbF is more saturated with O2 than HbA. Intensely growing foetus = rapid cell respiration, fast metabolism, a lot of O2 required and pO2 is constantly low. If HbF had the same affinity for O2 as HbA, it would not accept oxygens as readily as it does which would cause an insufficient amount of O2 provided to the respiring cells
What can rapid replacement of RBC after birth cause?
Massive breakdown of foetal RBC in combination with immature liver can cause physiological jaundice of a newborn (caused by overproduction of bilirubin (end product of Hb breakdown) increased levels can damage the brain, UV light speeds up its breakdown)
Why does O2 affinity decrease as p(CO2) increases?
- Increased p(CO2) = decreased pH, and Hb’s affinity for O2 drops with a decrease in pH – so when respiring tissue has high p(CO2), O2 tend to dissociate
- CO2 binds to Hb, creating carbaminohaemoglobin whose affinity for O2 is lower than that of Hb
Bohr shift
Shifting of the O2 dissociation curve to the left due to Hb’s reduced O2 affinity. It promotes the release of O2 in actively respiring tissue where CO2 is mass produced. It allows blood to be fully oxygenated in the lungs where p(CO2) is low so pH is high and carbaminoHb has been converted back to Hb.
Leaf adaptations to gas exchange:
- Waxy cuticle – upper and lower leaf surfaces covered in waterproof wax secreted by epidermal cells, restricts transpiration (water loss), prevents movement of CO2 and O2
- Guard cells – can change their shape to open or close a stroma (controlling passing of gases), usually closed at night and during water stress
- Air spaces – the stromata connect the air outside to a network of air space sin the leaf, CO2 and O2 can diffuse through them, saturated with water vapor.
- Spongy mesophyll – contains loosely packed, round cells, provides large SA of permanently moist cell walls for gas exchange (CO2 into cels, O2 from cells), photosynthesis maintains the concentration gradients
- Palisade mesophyll – contains tightly packed cells with chloroplast that perform photosynthesis.
- Vascular bundles (veins) – two types: xylem (transports H2O and minerals, upper half) and phloem (transports sugar and a-a, that is nutrients and end products of photosynthesis, lower half of leaf), they run in parallel and transport things at the opposite direction- veins replace the water lost by evaporation
