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Cardiopulmonary I > Microcirculation > Flashcards

Flashcards in Microcirculation Deck (22):

What determines the number of perfused capillaries

The number of open pre capillary sphincter


Does sphincter affect TPR

TPR or resistance to blood flow by an organ is not influenced by the opening or closing of precapillary sphincters, the only thing that determines TPR or resistance to blood flow are the arterioles


Site of inflammation

Post capillary venules, this is the site of leukocyte traficking and increased vascular permeability


What are the places in the body where there are no capillaries

Arteriovenous shunts, there are no capillaries as blood from the arteries goes directly to the venules, they have a role in temperature regulation, no nutritional significance.

These are called AV shunts or metarterioles


Net infilteration fluid


What does vasodilation and vasoconstriction do to the pressure drop across the arterioles


How does vascular permeability of endothelial cells change with Ca

Increase in Ca causes the endothelial cells to contract, increasing the gaps between the endothelial cells and increasing the diffusion of plasma proteins into the tissues during inflammation

The radius of the capillaries remian the same.

Histamine can also do this by increasing the Ca inside the endothelial cells


What is vasomotion of precapillary sphincters

Within an organ when O2 is low precapillary sphincters open to increase blood flow to the organ to compensate for the low O2 levels. Capillary pressure also increases, number of perfused capillaries increases and hence the surface area for exchange of O2 increases.

As a result filteration increases


Explain the physics behind nutrient exchnage in edema

There is increased diffusion distance for one.

The interstitial pressure is increased that actually causes closing of venular resistance and hence blood flow decreases


4 factors that determine Ca levels

1. Na-Ca pump that is activated when Na is high inside the cell

2. Influx of Ca into the cell

3. Ca coming out of the SR or ER

4. Removal of Ca from the cytosol and back to the ER or SR


Which of the previosuly mentioned factors are the most important for Ca concentration in endothelial cells and their subsequent contraction

Extracellular Ca levels or the influx of Ca into the endothelial cells


Define a characteristic of vascular tone

The smooth muscles in endothelial cells are much slower in developing cross bridges and producing a power stroke than the smooth muscles in skeletal muscles


What does norepi do to endothelial cells

Increases Ca influx into the endothelial cells, causing the smooth muscles in the vessels to constrict (I just realized we're not only talking about endothelial cells here but vascular smooth muscles that are found in the arterioles as well)


What does EPI do to the blood flow to the skeletal muscles

Epi works on beta2 receptors which in the arterioles are only found in the arterioles going to the skeletal muscles, hence epi will cause relaxation of smooth muscles by decreasing Ca levels.

This increases blood flow to the skeletal muscles


What does hyperkalemia do to SA node MDP 

It makes it more negative and takes it further away from the threshold potential

I do not know what will be the concequence for this. I think the excitability will decrease or the rate of SA node firing will decrease


Explain the phenomena of hyperpolarization mediation vasodilation

Natural phenomena: When there is hypoxia, ATP generation is impaired in a cell, which causes increase in K efflux from that cell. The greater K efflux causes localized hyperkalemia around the smooth muscles of vessels which impairs flow of Ca into the smooth muscle cells and hence the cells relax. This causes vasodilation. 

Drugs such as diazoxide are vasodilators that act bu opening the K-ATP channels and causes vasodilation through the same effect


What does an increase in Ca do in endothelial cells and smooth muscle cells of the arterioles

Causes constriction of vessels since smooth muscle cells contract and in endothelial cells it causes production of NO which causes vasodilation


L Name

It is a drug that inhibit NO synthase, causing constriction of vessels in tha organ and reducing blood flow


What is the role of NO in inflammation

It is anti inflammatory. We know this fact since if L Name when given will reduce [NO] and it will result in inflammation and damage to the endothelial cells by releasing proteolytic enzymes and ROS


What is the function of NO in coagulation

NO inhibits platelet aggregation and so does prostacyclin.

This is the mechanism where when the endothelial cells are damaged they reduce the production of NO and prostacyclin which causes platelet aggregation and causes thrombosis or even DIC


Endothelian 1

It is another important endothelial derived factor. 

1. Not stored but synthesized when endothelial cells are damaged, it is a 21 aa peptide

2. Most potent vasoconstrictors,  by increasing the extracellular Ca levels and increasing the influx of Ca into the smooth muscles


Reperfusion injury

Tissue with prolonged ischemia when it starts receiving O2 causes reperfusion injury by generating ROS. ROS damages endothelial cells, reduces NO levels and causes the production of endothelian 1

All of this causes decreased blood flow and imapired O2 delivery.

This is a major problem in organ transplant