Microvascular Exchange Flashcards
What is a microcirculatory unit?
- Decreasing size: arteries–> terminal arterioles–> capillaries
- Small capillaries; low press, RBC width
- Arterioles, capillaries bed, post-capillary venules
Describe the surface area of capillaries?
- Thin walls and large SA
- Many present
Describe the structure of capillaries
- All have single endothelial layer with some pericytes (contractile abilities, no smooth muscle)
- Relationship between endothelial cells: continuous, fenestrated, sinusoidal/ discontinuous
Describe the sinusoidal capillary structure
- Huge gaps for red cells
- Liver, GI tract
- Large lipophobic molecules can move out
- Very specialised type
Describe the fenestrated capillary structure
- Less leaky (renal)
- Quite large openings
- Small lipophobic molecules and small proteins
- Quite specialised
Describe the continuous capillary structure
- Diffusion of lipophilic, slow diffusion for lipophobic (Pino/phagocytosis)
- Ubiquitous
- Fused invaginations
- Standard for most capillaries
- Tight junctions prevent paracellular transport- proteins anchor and orientate cells
- A lot of unwanted movement- especially in BBB
Describe transport at the endothelium
- Discontinuous- between cells (no membrane crossing, transporters not needed, similar in fenestrated)
- Continuous- transporters required (cell packed, more substances need to cross membrane, active transport, facilitated diffusion etc.)
What is Fick’s Law of diffusion?
- Rate of diffusion dependent on :
- Proportoional to conc gradient (∆C)
- Inversely proportional to distance (∆x)
- Proportional to SA (A)
- Proportional to solute diffusivity (D)
What is the equation of rate of diffusion (Fick’s Law)?
- Js = -D A ∆C/∆x
Describe capillary diffusion
- Js = -P (permeability)A∆C
- Lipid soluble- diffuse
- Water soluble, non-lipid soluble- intracellular pores (gaps or channels)
- Large solutes- large pore
- Gases diffuse easily
- Exchangeable proteins- pinocytosis and exocytosis
- Plasma proteins stuck- exert oncotic pressure
What are other forms of solute exchange?
- Some water-soluble solutes ‘swept’ along with fluid exchange- convective transport
- Other mechaniss: pinocytosis, GLUTs, true active transport generally limited to brain
- Water moves freely- small and sufficient pores
What are the limitations of diffusion?
- Relate to Fick’s law
- Solute properties and conc grads unlikely to change, temp unlikely to change- stable
- Increased capillary recruitment increases SA and decreases diffusion distance
- Muscle fibres- single capillaries- 2 fibres, with exercise demand for oxygen rises, increased SA with capillary recruitment
How are capillaries recruited?
- Terminal arteriole initially constricted, smooth muscle contracted, module not perfused
- During exercise, dilated, VSM relaxed, module becomes perfused
Describe fluid compartments
- Water 60% total body mass
- ~42L- 60% intracellular, 40% extracellular
- Fluid movement from vascular to interstitium and into cell
- 2/3 intracellular
- 1/9 total body fluid- vascular space
- 2/9 in extracellular interstitial space
How does fluid move into capillaries?
- Starling’s capillaries
- Flow out capillary depends on oncotic pressure in cap + interstium + hydrostatic press in capillary and tissue
- Net filtration pressure=
(Pc-Pi)-(πc-πi) - Oncotic press holds fluid in
- Plasma protein cannot leave vascular compartment
- Protein in interstitial space- opposes hydrostatic press holds fluid in that space
- Fluid does not re-enter- slow loss of fluid across capillary
How does filtration drop across the capillary?
- Interstitial press does not change
- Capillary press tends to drop because press drops across capillary
- Filtration drops towards venous end- no resorption from interstitium
Describe lymphatics and drainage
- Fluid leaving caps cleared by lymphatic circulation
- ~50% returns to circulation at subclav veins and remainder returns to lymph nodes
- Capillary flow of 4000L/day (8 into interstitial space)
What are the underlying causes of oedema?
- Increased hydrostatic pressure
- Decreased oncotic pressure
- Increased capillary membrane permeability
- Lymphatic obstruction
How could inflammation lead to oedema?
- Uncreased hydrostatic pressure- dilation
- Increased capillary permeability
Describe inflammatory swelling
- Classic inflam symptoms- rubor, calor, dolor and tumour
- Inflammation caused by local release of a wide range of mediators in response to pathogen/injury
