B4.064 Prework 1: Microcirculation Flashcards
components of the microcirculation
arterioles precapillary sphincters capillaries venules arteriovenous shunts lymphatics
discuss the morphology of microcirculation vessels
all vessels contain a single layer of epithelial cells
smooth muscle surrounds all vessels except capillaries and post capillary venules
effect of arteriole dilation
increase arteriolar radius within an organ
decrease vascular resistance in the organ
increase blood flow to the organ
increase capillary pressure
increase filtration of fluid
what do arterioles help regulate
organ blood flow
filtration by altering capillary pressure
function of precapillary sphincters
open and close # open determines # of perfused capillaries determines total surface area for exchange
do precapillary sphincters affect vascular resistance within an organ?
no
determined by arterioles
function of capillaries
single layer of endothelial cells with no overlying vascular smooth muscle
sit of exchange of nutrients and fluid between blood and tissue
filtration/reabsorption: capillary pressure, oncotic pressure of plasma
function of post capillary venules
single layer of endothelial cells with no overlying vascular smooth muscle
important site of inflammation induced: leukocyte trafficking, increased vascular permeability
describe arteriovenous shunts
blood flows from an arteriole directly to a venule, skipping capillaries
flow through AV shunts is termed non-nutritional blood flow since no exchange of nutrients occurs with the tissue
importance of AV shunts
temperature regulation
primarily located in skin
function of lymphatics
under normal conditions, filtration of fluid slightly exceeds reabsorption
lymphatics remove this excess fluid and also small amount of plasma proteins which enters tissue
net filtration force
(Pc-Pi) - (Op-Oi)
hydrostatic pressure gradient - oncotic pressure gradient
c=capillary
i=interstitial
pressures under normal conditions
interstitial pressure (Pi) about 0 interstitial protein concentration is nearly zero so the interstitial oncotic pressure (Oi) is about 0
what controls filtration under normal conditions
Pc, capillary pressure
what controls reabsorption under normal conditions
Op, plasma oncotic pressure
discuss the pressure gradients along a capillary
in first half Pc > Op so net filtration
in second half Op > Pc so net absorption
what is the effect of local dilation on arterioles within one organ?
less pressure drop across arterioles increases rate of inflow of blood into capillaries increases capillary blood volume increases capillary pressure filtration increased
what is the effect of local constriction on arterioles within one organ?
greater pressure drop across arterioles decreases rate of inflow of blood into the capillaries decreases capillary blood volume decreases capillary pressure filtration decreased
effect of venous pressure on capillary pressure
when venous pressure increases, rate of blood flow out of a capillary decreases
volume of blood in the capillary increases and capillary pressure increases
increased filtration of fluid out of the capillary into the tissue
what are 3 causes of decreased oncotic pressure
liver disease: impaired production of plasma proteins
kidney disease: can increase excretion of plasma proteins in urine
protein malnutrition: impaired plasma protein production
result of decreased oncotic pressure
force for reabsorption of fluid into capillaries is reduced
volume of interstitial fluid will be increased (edema)
what is an example of an event that would increase vascular permeability?
exposure to an allergen
what controls the opening of precapillary sphincters
open in response to locally produced dilators which accumulate in tissue when blood flow is not sufficient to meet metabolic demands of the organ
what is the result of the opening of precapillary sphincters
increased capillaries perfused
increased total surface area for exchange
increased filtration
give an overview of the lymphatic system
one way system that returns excess interstitial fluid to the cardio system
all lymphatic vessels converge into larger lymphatic vessels which empty into the systemic circulation via the systemic veins
what factors influence the contractile activity of vascular smooth muscle
stretch of vessels sympathetic vasoconstrictor nerves hormones local factors endothelin derived factors
how does cytosolic calcium influence muscle activity
cytosolic Ca2+ concentration control cross bridging and thus vasoconstriction
what factors regulate cytosolic Ca2+ levels
influx of Ca2+ through membrane channels
release of Ca2+ from sarcoplasmic reticulum
removal by Ca2+ ATPase pumps in sarcoplasmic reticulum and plasma membrane
how does vascular smooth muscle differ from cardiac or skeletal muscle?
rate of cross bridge cycling is much slower due to a lower ATPase activity
vascular smooth muscle to maintain sustained tension
changes in cytosolic Ca2+ are more dependent on the influx of extracellular Ca2+ rather than release from intracellular stores
how is NO produced in endothelial cells?
increases Ca2+ entry activates NO synthase
NO forms from L-arginine
vasodilation mechanism of NO
highly permeable
diffuses into underlying vascular smooth muscle
decreases intracellular Ca2+ levels
causes relaxation
continuously produced in nearly all organs
how is NO production inhibited
local infusion of L-name
competitive inhibitor
functions of NO
vasodilator
inhibits leukocyte and platelet adherence
maintains normal low vascular permeability
antioxidant
what is endothelin 1
21 AA peptide that is not stored but is synthesized in response to various stimuli slow process (1 hour) formation increased following endothelial cell damage
what is the function of endothelin 1
acts through membrane receptors on vascular smooth muscle cells to cause vasoconstriction by:
- release of intracellular Ca2+
- influx of Ca2+
what is unusual about the effects of endothelin 1
prolonged vasoconstriction
significantly augments organ injury in conditions where endothelin 1 formation is increased
what is ischemia
decreased blood flow
what is reperfusion
restoration of blood flow after ischemic period
what happens with reintroduction of O2 during reperfusion
generation of ROS
inactivation of NO
promotes microvascular injury
3 primary effects of ROS
damage to endothelial cells > increased permeability
inactivation of NO > leukocyte adherence, constriction
increased endothelin formation > constriction and decreased flow
