Capillary Circulation Flashcards
Capillary functions
- Nutrient Exchange: • Glucose • Oxygen • Free Fatty Acids • Other Nutrients
- Waste Exchange: • CO2 • Lactate & Ammonia • Other metabolic byproducts
Characteristics of capillaries that facilitate simple diffusion:
- Capillaries have thin walls - one cell thick
- Therefore, the distance traveled by diffusion particles (i.e. O2 & CO2) is short
- Capillaries have a high total surface area
- Flow velocity through capillaries is slow because of the large cross sectional area of capillary beds in the circulation. This will facilitate diffusion.
major factor that dictates open/closed precapillary sphincters
-metabolites generated in local tissues/environment
Primary local factors that affect precapillary shincters in skeletal muscle?
- dec P_O2 ***( hypoxia)
- inc P_CO2
- metabolic acids
Primary local factors that affect precapillary shincters in brain?
- P_CO2 and O2
- adenosine
Primary local factors that affect precapillary shincters in heart?
- *adenosine
- pH
- P_O2 and CO2
The effect of epinephrine contraction vs. dilation
will depend on the relative concentration of alpha1 and beta2 receptors within a given capillary bed.
The primary response of norepinephrine will be to (on capillaries)
cause a constriction since it will activate predominantly alpha1 receptors.
Dopaminergic receptors are abundant in the kidney & gut. At low doses, dopamine will cause a (on periperal resistance and kidney). At higher doses, dopamine will (on receptors and effect)
- will cause a drop in peripheral resistance and a selective perfusion of the kidney.
- dopamine will activate alpha1 receptors causing vasoconstriction.
Angiotensin II is a physiologically important
vasoconstrictor
Kinins, such as Bradykinin, are all
vasodialators
In the heart and most other places, adenosine acts to
vasodilate (A2 receptors) while in the kidney, adenosine acts to vasoconstrict (A1 receptors).
Hypoxia, Increased CO2, K+ & H+ : when present systemically, all tend to produce
vasodialation
Krebs Cycle Intermediates: presence of these indicate increased metabolism will cause
vasodialation
Endothelin (constriction) & Endothelium Derived Relaxing Factor do what?
vasodialation - all released from endothelium
Starling Forces that Favor Filtration:
- Capillary Hydrostatic Pressure: is simply the force that occurs due to blood pressure within the capillary that tends to drive fluid outward and through the endothelial pores.
- Interstitial Fluid Oncotic Pressure: The word oncotic is used to describe the osmotic effect due to capillary protein. Oncotic pressure, then is simply a colligative property. In this case - we are describing the influence of proteins which are present in the interstitium - their osmotic tendency to pull fluid out to the interstitium from within the capillaries.
Starling Forces that Favor Reabsorption:
- Capillary Oncotic Pressure: capillary oncotic pressure is the osmotic driving force - due to the presence of proteins inside the capillary - and tends to draw fluids from outside the capillary to the inside of the capillary.
- Interstitial Fluid Hydrostatic Pressure: This force tends to drive fluid back into the capillary. (For this discussion, we are assuming that interstitial fluid pressure is positive.)
conditions that may lead to edema and reasons
1) Liver disease=low serum production - not enough stuff in the blood= net effect more filtration out of capillary and less reabsorption
2) Elevated Capillary Blood Pressure: This can occur via two mechanisms - vasodilation & obstruction in the circulation. —>Increase in capillary hydrostatic pressure - will give rise to tendency towards edema.
3) Vasodilation - recall that in vasodilation, blood will enter the capillary at higher pressure. This will create a situation in which capillary blood pressure is excessively elevated with resultant edema. —> perhaps due to vasodilator drugs (i.e. some antihypertensives) - may produce edema.
4) Obstruction - such as a venous blood clot will cause the back up of pressure and hence an increase in pressure.—> will effectively increase capillary blood pressure due to the backing up of blood.
8) Congestive Heart Failure - Since the left ventricle is not efficiently pumping blood out of the heart, pulmonary pressure will increase and pulmonary capillaries will tend to leak due to elevated hydrostatic pressure. There will be potential towards pulmonary congestion and possibly pulmonary edema.
10) Post Capillary Venule permeability to proteins is increased. Proteins leaking out from venules will create an imbalance of Starlings Forces. Again, increased filtration and decreased absorption will be favored.
Effective Capillary Blood Pressure represents:
line that represents the forces that favor filtration.
Function of Lymph Capillaries:
- Removes excess fluid from interstitial space.
2. Removes excess protein from interstitial space.
bulk flow:
- Through the wall of Capillary
- movement of an ultrafiltrate of plasma through the capillary wall
normal flow:
down the lumen of capillary
exchange process is dependent on:
diffusion
pre-capillary sphincters are only from:
- arteries and metarteriole
- capillaries dont have bc they have no SM.
Explain why in increasing blood flow to a tissue it is more advantageous to open additional capillaries rather than to force more blood through the same number of capillaries.
- In order to get the perfusion that you need as during exericise… youd need to get some amount of flow more.
- Instead by opening more capillaries you increase the surface area and get the increased blood flow without too much more work
- high speeds would make for nutrient exchange difficult
Endocrine Catechoalmine effect on BV: epineprine
- constrictor (alpha 1) and dialator (beta2)
- effect on Beta1 also inc contractility and HR
- why both? depends on the RECEPTOR!
Endocrine Catechoalmine effect on BV: norepinephrine
-constrictor (alpha1)
Endocrine Catechoalmine effect on BV: dopamine
- at high dose activates alpha1 = vasoconstriction and activates Beta 1 = inc contractility
- at at low dose = dialation in renal and gut systems
- why both? depends on how much released/dosage
Endocine amine effect on BV: Histamine
dialator
Endocine amine effect on BV: Ach
dialator
Endocine polypeptide: angiotensin II effect on BV:
constrictor
Endocine polypeptide: kinins effect on BV:
dialator
Endocine polypeptide: vasopressin (ADH) effect on BV:
constrictor
Endocine polypeptide: vasoactive intestinal peptide effect on BV:
dialator
Locally produces chemicals effect on BV: adenosine
Constrictor = Alpha1 dialator = alpha2
Locally produces chemicals effect on BV: hypoxemia
dialator
Locally produces chemicals effect on BV: H+ and K+
dialator
Locally produces chemicals effect on BV: hypercapnia (CO2)
dialator
Locally produces chemicals effect on BV: krebs cycle intermediates
dialator
Locally produces chemicals effect on BV: endothelin
constrictor
Locally produces chemicals effect on BV: endothelium derived relaxing factor
dialator
Filtration is when:
fluid from capillary to interstitial fluid
reabsorption is when:
interstitial fluid to capillary fluid
why are proteins excluded from filtrate?
size and charge! too big and too negative to pass
What exerts an osmotic force (oncotic pressure) across capillary wall? What is the primary component of oncotic pressure?
- PROTEINS
- major=albumin
bleeding effect on riltration/reabsorption
decrease capillary hydrostatic pressure (by regulating BP) = decrease filtration = increase reabsorption (TO GET COLUME BACK– youll still need to make more RBC
donate blood and check Blood pressure before and after and its the same? Main reason for this?
Mainly vasoconstriction
Secondly inc HR
Tendency for edema increase when:
- Plasma protein levels decreased( inc Filtration, –> dec Reabsorption)
- Capillary hydrostatic P increased: venous clot; congestive heart failure - pulmonary edema; vasodilation
Edema only results when the build up of interstitial fluid exceeds
the capacity of lymphatics to remove the fluid.
Post capillary venule permeability to protein increased – effect?
dec reabsorption = inc filtration
