micocirculation Flashcards
using starlings equation, determine the flow of fluid into or out of the capillaries.
Pc=20
Pif=-2
Oc=25
Oif=2
NFP=Kf[(Pc-Pif)-(Oc-Oif)]
hydrostatic increase=
oncotic pressure=
You can assume thePif and Oc to be constant… the biggest variable is going to be Pc
(20-2)-(25-2)= -5, fluid moves in to the vessels
describe the histology of the vascular bed involved in regulating capillary resistance.
what is the regulation site?
- flow volume is not equual through capillaries
- regulation sites
- arterioles
- metarterioles- shunt
- capillary bypass and regulate flow into capillary
- closing off the capillary, the blood will flow through here.
- circular smooth muscle
- alters radius, therefore changing the resistance = less flow
- located
- arterioles
- precapillary sphincter
describe the mechanisms of mypgenic response
myogenic reponse
- VSMC respon
- sac opening-> increase na and Ca in ->depolarization ->increase calcium->VSMC contract
describe VSMC
- what makes them pulsatile? what are the consequences of this?
- what overides this pulsatility?
vascular smooth muscle cells
- undergo spontaneous alteration in tone due to intrinsic slow wave
- spontaneous depolarization due to Ca cauing depolarization
- blood flow through a given capillary is intermittent as blood is shunted between capillaries
- overiding pacemaker-based pulsility are local** and **global regulators
- local
- myogenic
- paracrine
- metabolic
- global
- hormones and autonomics
- playa minor role in regulating microcirculation
- operate largely on arteries and veins
- hormones and autonomics
- local
what are the VSMC local regulation via paracrine?
- NO
- major paracrine vasodilator
- response to a variety of events
- sheer
- pathogens
- injury
- induced by
- ACh
- ATP
- bradykinin
- serotonin
- substance P
- histamine
- action
- acttivation of guanylyl cyclase->increase cGMP->increase cGMP dependent protein kinase ->phophorylation of MLCK and SERCA
- MLCK is inhibited
- SERCA is inactivated
- acttivation of guanylyl cyclase->increase cGMP->increase cGMP dependent protein kinase ->phophorylation of MLCK and SERCA
- endothelin
- vasoconstrictor
- released by
- sheer
- hypoxia
- acts
- phospholipase C pathway
what are the local hyperimic factors inducing vascular smooth muscle cells for vasodilation?
Hyperemia= regulation of blood flow based on metabolic activity
- tissue dependent
-
pH
- mediated through indirect and direct pathways
- indirect
- contributes to NO production
- direct
- extracellular acidosis reducs intracellular calcium concentrations
- indirect
- maint contributors
- CO2
- lactic acid
- mediated through indirect and direct pathways
- decrease in PO2
- releases
- adenosin
- binds to the A2 receptor
- increases cAMP->vasodilation
- binds to the A2 receptor
- prostaglandin 2
- NO release
- induces cGMP
- adenosin
- releases
- ATP
- decrease in atp opens K channels (ATP dependent K channels)
- similar to pancreatic beta cells
- increases in K closes voltage gated calcium channels.
- decrease in atp opens K channels (ATP dependent K channels)
How does the vasular bed (VSMC) resond to changin systemic pressure?
autoregulation- response by vascular beds altering resistance in reponse to changing systemic pressure to stabilize tissue perfusion.
increasing tissue perfusion = decrease in
expalin the systems involved in global regulation of VSMC
sympathetic regulation, very little parasympathetic, is at the level of arteriole and small arteries and veins
- brain regions regulating sympatheti tone aretonically active with frequency of activity varying and varying the vascular tone
- respirationg make a contribution at lower frequencies
- majority of vascular smooth muscles adrenergic receptors are
-
a1
- induces constriction
- in higher concentration and require high concentration of E,
- overpower b2 b/c of higher amounts compared to B2
- prefers NE
-
b2
- induces dilation
- in lower concentration and receptors are high affinity, need very little to cause dilation
- prefers E
- postganglionic sympathetic neurons also release
- NE,ATP, NY- all leading to 3 phases of contraction
- medullar releases E
-
a1
compare regulation of veins and arteries by the sympathetic nervous system
- veins
- conttain ONLY a1
- can only contrict, NOT DILATE
- constriction is dependent on sympathetic tone, acting on veins before arteries
- also repond to
- paracrine and hormones
- not really influenced by hyperimic factors (metabolic)
- important for venous constriction during hemorrage and arterial dialtion
- conttain ONLY a1
- arteries
- Regultes the blood flow from one organ to another by changing total peripheral resistance (TPR)
- much of the body blood volume is in skeletal muscles
- TPR change is heavily targeted to skeletal vasculature
TPR change is heavily targeted to which organ?
TPR change is heavily targeted to skeletal muscle vasculature.
hyperimic factors contribut greatly to this
pH being the most effective, causing dilation of the blood vessels
Larger substances are most likely to move through which process through the cell?
trancellular, via endocytosis
movement across the cell requires ATP. does this obey ficks law
No, ficks law operates off of diffusion. and requires no ATP
NFP facors filtration in the ____ and reabsorption in the _____
NFP favors filtration in the first 2/3 of the capillary and reabsorption in the last 1/3
- hydrostatic pressure is greater in the first 2/3 and oncotic pressure is greater in the last 1/3
how does water move in the interstitium
diffusion
Lymph channels are found every where except ___(4). What is there instead?
how could head injury or broken bone play into question of lymph system?
lymph channels are found every where except: skin endomysium of muscle, bone and CNS
- skin, endomysium of muscle and bones
- have small prelymphatic channels that join lymph vessels
- CNS
- drain into CSF and then into the vessels
Head injury and broken bones are not conscerned with lymph flow?