Microvascular Hypercoagulability Model for MS

A forum to discuss Chronic Cerebrospinal Venous Insufficiency and its relationship to Multiple Sclerosis.

Microvascular Hypercoagulability Model for MS

Postby North52 » Fri Nov 05, 2010 2:57 pm

I would like to propose a model for MS and CCSVI that implicates fibrin/fibrinogen as a mediator of the inflammary reaction. The first 8 points describe the hypothesis and the following text provides some supporting evidence for it. It gets quite technical.

Microvascular Hypercoagulability Model for MS:

1) MS is a result of the stenosis or obstruction of the larger veins (internal jugulars, vertebrals, azygous) that drain the central nervous system.
2) This obstruction of the larger veins in turn results in reduced rate and velocity of flow in the microvasculature (capillaries and post capillary venules) upstream from the stenosis or obstruction. This deduction is supported by simple hemodynamic principals.
3) Reduced blood flow and stasis results in ischemia and activation of the coagulation cascade at the micro-vascular level.
4) This activation of the coagulation cascade is of a continuous low grade nature that results in the production of fibrin strands in the microvasculature and increases blood viscosity, reducing blood flow further. It does not result in the formation of clot.
5) In this setting of stasis and ischemia, there is breakdown of the blood brain barrier with entry of fibrin strands into the central nervous system. The stasis of blood, as well, results in capillary and venular dilatation that facilitates breaching of the blood brain barrier.
6) Fibrin strands deposit on the axon myelin sheath, impair its functioning and therefore the transmission of neuronal impulses. If fibrin could be removed before death of the nerve cell, nerve function could be restored. If myelin damage progresses to cell death, nerve function cannot be restored. The entry of fibrin into the tissues stimulates the production of cytokines by the cells, stimulating the immune response.
7) An inflammatory reaction ensues and results in the infiltration of T lymphocytes into the CNS that proceed to remove myelin debris, dead tissue and fibrin degradation products. Demyelinating plaques then result.
8) With the breakdown of the blood brain barrier, erythrocytes enter the CNS tissue as well, and their breakdown results in the deposition of iron, as is seenin histologic specimens of MS demyelinating lesions and MRI images of the brains of MS patients.

If this theory is true, then following four points can be deduced and their validation would provide very strong evidence to this theory’s validity. Below each point is some scientific evidence for it.

1) Fibrin and fibrin degradation products such as D-dimer should be visible around the nerve axon prior to the arrival of T and B lymphocytes and d-dimer levels should be increased in the multiple sclerosis population:

“The detection of an apparent increase in tPA-PAI-1 complex formation and fibrin degradation peptides in both normal appearing white matter and normal appearing grey matter (in EAE mice brains) is the most striking observation of the study. With increasing evidence of axonal damage at the earliest stages of the inflammatory demyelinating reaction in multiple sclerosis, deposition of fibrin and an imbalance in the tPA-PAI1 ratio in apparently normal tissue would produce a situation in which axonal integrity is compromised.”

“ There is MRI evidence of fibrin deposition prior to clinical signs of multiple sclerosis (Kermode et al., 1990) and immunochemically, it precedes the cerebral parenchymal reactions and demyelination (Wakefield et al 1994)”

“Persistent blood-brain barrier damage and fibrin exudation are prominent features of demyelinating lesions (Claudio et al., 1995) and similarly precede the clinical manifestations of experimental allergic encephalomyelitis (EAE) an animal model for multiple sclerosis (Inoue et al., 1996)”

“In the white matter tissue sections from control and multiple sclerosis cases, D-dimer was confined to the lumen and walls of blood vessels whilst in acute multiple sclerosis lesions, it was immunocolonized on foamy macrophages and large diameter axons. Immunostaining of serial sections with antibody directed against neuromonofilament protein confirmed axonal localization of fibrin D-dimer.”

Homocysteine and D-dimer levels were significantly higher in both male and female MS patients when compared to the control group. Plasma D-dimer levels, in males, were approximately twice as high (p = 0.001) while in female subjects they were approximately three times higher (p = 0.001) (Aksungar et al., 2007)

2) Fibrin deposition around axons may be responsible for impaired neuronal transmission and if fibrin could be removed before cell death occurs, then nerve conductivity should be improved or restored. Removal of fibrin strands can be accomplished by mechanisms that optimize fibrinolytic activity:

“Studies in peripheral nerve injury have shown that fibrin deposition is a factor impeding axonal regeneration whilst removal of fibrin is associated with restoration of axonal function (Akassoglou et al., 2000). Plasminogen activators are central to degrading fibrin and extracellular matrix proteins in the CNS, dissolving adhesive contacts to promote synaptic contact and axonal outgrowth (Lo et al 2002)”

“Downstream damaged axons (covered with fibrin) would be restricted in their ability to penetrate the altered extracellular matrix environment and adherent inflammatory cells to attain synaptic contact.

“In experimental models of peripheral nerve damage, mice deficient for tPA or plasminogen display aggravated axonal degeneration and delayed functional regeneration, which can be rescued by fibrinogen deficiency (Akassoglou and Strickland, 2002). Fibrin is co-localized on the denuded multiple sclerosis axon with tPA and there is accumulation of high molecular weight fibrin peptides, products of tPA proteolysis. In the chronic inflammatory state, this could be seen as an attempt to reduce fibrin accumulating on the demyelinated axon and interfering with axonal function. However, the decrease in fibrinolytic potential in multiple sclerosis tissue is not due to a descrease in tPA, but to formation of complexes with inhibitors, most likely PAI1, as observed in samples and in preformed complexes of tPA and PAI-1 standards electrophoresed without reduction”

“In the chronic inflammation characteristic of multiple sclerosis, co-localization of tPA to demyelinated axons with non-phosphoylated neurofilament and fibrin(ogen) suggest an association with axonal damage (Gveric et al., et al). Alternatively, it may represent a protective mechanism to remove fibrin deposits, which exacerbate axonal injury as reported in the model of sciatic nerve damage (Akassouglou et al., 2000) and promote regeneration by activation of growth factors (Siconolfi and Seeds, 2001).”

“Tissue plasminogen activator(tPA) is the key fibrinolytic enzyme, the activation rate of which is greatly enhanced in the presence of fibrin (chandler et al., 2000). tPA is also present at a high concentration in neurons, where upon activation, it has been found to have a role in neuronal development and synaptic remodeling (Calabresi et al., 2000). In neurodegenerative diseases, disruption of neuronal cell links with the extracellular matrix by tPA-generated plasmin is a mechanism of cell death (Strickland 2001). “

“The evident dependence of peripheral nerve regeneration on the plasminogen activator system has important implications for neuroprotection in the CNS and specifically for therapeutic approaches in multiple sclerosis to minimize fibrin deposition in the earliest stages of lesion formation.”

3) Tissue samples of active demyelinating lesions should demonstrate decreased fibrinolytic activity. As fibrin is being produced at a rapid rate in the microvasculature, so is the action of to breaking it down with TPA. As TPA is being used up rapidly, fibrinolytic activity (fibrinolysis) will therefore be decreased locally at the tissue level:

“The data reported in this study demonstrate the fibrinolytic potential in demyelinating multiple sclerosis lesions to be markedly diminished- the result of a documented reduction in tPA enzyme activity and increase in PA-1inhibitor levels (Gveric et al 2001). “

4) This reduction in fibrinolytic activity should be even greater in active lesions as stasis as well as fibrin production would be greater:

“In contrast, all multiple sclerosis tissue samples were characterized by markedly decreased fibrinolytic activity. The lowest fibrinolytic activity was observed in acute multiple sclerosis lesions with t1/2 of 255.8 +/- 79.54 min and only 13 +/- 17% of the clot degraded.”

Please note that all the material above in quotation marks was taken from the following paper:

Impaired Fibrinolysis in Multiple Sclerosis: a role for tissue plasminogen activator inhibitors. Gveric et al. Brain(2003), 126, 1590-1598
All the references mentioned above can be found in the reference section of this paper.

Another reference:

Coagulation status and biochemical and inflammatory markers in multiple sclerosis. Aksungar et al., 2007. Journal of Clinical Neuroscience Volume 15, issue 4, April 2008.

North
Last edited by North52 on Sat Nov 06, 2010 6:29 pm, edited 2 times in total.
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Postby Merlyn » Sat Nov 06, 2010 5:05 pm

When I have had my fibrin levels tested, they have been close to 900... Dr. Paul Cheney says they should never be over 400. He recommended using turmeric to lower fibrin, but I never found it effective. Fibrin levels seem to be related to the lack of enzymes, specifically plasmin... I am now taking pancreatic enzymes and will hopefully tolerate some broad-spectrum enzyme concoctions. I have had trouble with enzymes causing abdominal pain, but I am hoping that by eliminating lactose I will eventually tolerate them as the gut inflammation decreases. There is something in the blood that is causing my spasticity, because when I have phlebotomy, the reduced spasticity is wonderful.

http://tinyurl.com/2fys48r


Their anti-inflammatory action works on all circulating immune complexes, not just the ones in the myelin. This action reduces inflammation in all soft and connective tissues of the body such as internal organs, eyes, skin, muscles, tendons, fascia, joint capsules, blood vessels, etc. All of these various tissues benefit from the reduction of inflammation.
They are anti-fibrotic, meaning that they break down hard, fibrotic tissue, and in so doing, help prevent atherosclerotic plaqueing, hypertension and other cardiovascular diseases, thrombosis, blood clots, uterine fibroids and other fibromas, fibrocystic breasts and other fibrous degeneration.
They are blood-thinning. Like aspirin, proteolytic enzymes lower blood viscosity. Unlike aspirin, enzymes present no risk of hemorrhage (the blood becoming too thin) and cause no complications from gastrointestinal bleeding. The mechanisms by which the thinning occurs involves the breaking down and cleaning up of waste products, cellular debris, circulating immune complexes, and white blood cells. By cleaning up the blood, more white blood cells are made available to protect the body from new intruders.


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Postby Cece » Sat Nov 06, 2010 5:09 pm

great post, North52
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Postby charlie656 » Sat Nov 06, 2010 7:31 pm

Im not sure if an experience I had last year supports your theory but.

This was a few weeks before I went and got steroids for a relapse, I was worsening. I went home one evening feeling normal but a couple of hours after my betaferon injection I started to feel ill. I dont usually react to the interferon so I don't know if that was just coincidence. I started to feel generally unwell and ended up just going to bed. I began feeling increasingly cold even though I was buried under the covers. My extremities became ice cold and I couldn't warm them up. I started shivering quite badly.

The result was that my legs became really useless to the point that although i managed to stand up I just couldnt use them. I was trying to get to the toilet but ended up falling and having to drag myself there and had to use my upper body strength to get on the seat and the same to get back into bed.

It was quite dramatic for me as at the time I could walk for about 10minutes before I would start getting into trouble. However after taking paracetemol I began to recover over the next few hours, and warmed up again. I was able to function normally the next day as if nothing had happened.

The MS nurse I spoke to suggested that I had had a temperature.

I wonder what happened to me. It just seems to me that the way my body had shut down the blood flow to my extremities was related to the dramatic loss of function. I wonder if the way the body regulates flow is playing a role in MS rather than simply mechanical blockages.

Im have absolutely no medical expertise, but that is something I have been pondering. Though I would it out there.
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Postby North52 » Sun Nov 07, 2010 9:08 am

charlie656 wrote:Im not sure if an experience I had last year supports your theory but.

This was a few weeks before I went and got steroids for a relapse, I was worsening. I went home one evening feeling normal but a couple of hours after my betaferon injection I started to feel ill. I dont usually react to the interferon so I don't know if that was just coincidence. I started to feel generally unwell and ended up just going to bed. I began feeling increasingly cold even though I was buried under the covers. My extremities became ice cold and I couldn't warm them up. I started shivering quite badly.

The result was that my legs became really useless to the point that although i managed to stand up I just couldnt use them. I was trying to get to the toilet but ended up falling and having to drag myself there and had to use my upper body strength to get on the seat and the same to get back into bed.

It was quite dramatic for me as at the time I could walk for about 10minutes before I would start getting into trouble. However after taking paracetemol I began to recover over the next few hours, and warmed up again. I was able to function normally the next day as if nothing had happened.

The MS nurse I spoke to suggested that I had had a temperature.

I wonder what happened to me. It just seems to me that the way my body had shut down the blood flow to my extremities was related to the dramatic loss of function. I wonder if the way the body regulates flow is playing a role in MS rather than simply mechanical blockages.

Im have absolutely no medical expertise, but that is something I have been pondering. Though I would it out there.


Dear Charlie656,

It sounds to me like you developed a fever. Feeling cold and shivering happens when a fever is developing. In MS, fever is known to worsen symtoms and cause pseudo-exacerbations. I suspect the paracetamol took away your fever and that is why you started to feel better and regain your strength.

I do think this all fits in with my theory of hypercoagulability. If this theory is correct, anything that makes blood more coagulable, should worsen symptoms by thickening the blood and reducing flow more. It is well known that blood becomes more coagulable when its temperature is raised. I suspect this is why you got worse.

Interestingly, by the same reasoning, this theory also predicts why MS symptoms get worse with heat (heat intolerance).

It also explains why PWMS can get exacerbations with certain infections. Infections (even without fever), like heat are well known to increase coagulability of blood.

North
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Postby LR1234 » Sun Nov 07, 2010 9:20 am

Hi North,
I do agree that hypercoagulation has an effect on MS (as mentioned I feel better from being on heparin) but I do not feel free of MS and there are many people on Warfarin for years with MS that continue to deteriorate.

I think inflammation is creating slow flow through the veins and whilst blood thinning meds can help this if the stenosis created by the inflammation is so bad thinners alone will not improve the situation. I also agree with Cheer's theory of addressing endothilium health as this obviously has an impact on the veins.

What drugs increase blood flow? I know fludrocortisone raises BP (which might be an option) but is there another drug that increases volume too?
Thyroxine has helped my fatigue as its raised my heart rate and I suppose increased my blood flow too.
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Postby North52 » Sun Nov 07, 2010 9:32 am

Dear LR1234,

I agree with you and do not believe heparin will solve all problems. Relieving stenosis, however, might. I think drugs like heparin can partially help in those with existing outflow obstruction.

One supplement that I think might help is nattokinase. This is a fibrinolytic that assists in the breakdown of fibrin. I tried it out of curiousity in the setting of an exacerbation and the results were immediate, remarkable and unmistakable. My gait improved tremendously. The results, however were short lived, about 3-4 hours. I cannot however be sure how safe it is. I suspect there may be an increased risk of bleeding. I also suspect there may be a risk of rebound worsening. I was alway a big skeptic of supplements but this changed my view on them.

North
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Postby LR1234 » Sun Nov 07, 2010 10:19 am

I am/have been taking nattokinase....in fact I ran out of it about 2 weeks ago and haven't bought anymore as I am about to embark on IVF treatment.
Strangly enough some of that vertigo and lightheaded feeling has returned in the evenings but the heparin is still doing a good job of keeping the MS in check.

I was taking 400mgof natto a day along with heparin (which i know is risky but I was being monitored carefully) and it def had its benefits.
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Postby Merlyn » Sun Nov 07, 2010 1:46 pm

I am presently reading Enzymes and Enzyme Therapy by Dr. Cichoke and it says many things in here that make a lot of sense concerning fibrin and systemic disease... I am using pancreatin because I seem to be sensitive to Aspergillus, and thus far am tolerating proteolytic component. Usually I have had trouble with abdominal pain from these proteolytic enzymes but this is okay. I've been taking Nattokinase but haven't noticed anything from it... so far however I have been taking the pancreatin with food and I am learning from this book that you have to take them on an empty stomach, so I will be my next experiment.

Kulvis.com is where I picked up the pointer to this book. Dr. Cichoke gives very detailed explanations as to why the lack of enzymes affect microcirculatory functioning in the vascular system in general. And how as we age we produce less and less pancreatic enzymes and how this leads to arteriosclerosis. This is really worth reading.
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Re: Microvascular Hypercoagulability Model for MS

Postby malden » Sun Nov 07, 2010 2:16 pm

North52 wrote:I would like to propose a model for MS and CCSVI that implicates fibrin/fibrinogen as a mediator of the inflammary reaction. The first 8 points describe the hypothesis and the following text provides some supporting evidence for it. It gets quite technical.

Microvascular Hypercoagulability Model for MS:

1) MS is a result of the stenosis or obstruction of the larger veins (internal jugulars, vertebrals, azygous) that drain the central nervous system.
2) This obstruction of the larger veins in turn results in reduced rate and velocity of flow in the microvasculature (capillaries and post capillary venules) upstream from the stenosis or obstruction. This deduction is supported by simple hemodynamic principals.
...

In read the whole following text and I did not find any supporting evidence for those two first hypothesis.
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Postby North52 » Sun Nov 07, 2010 2:31 pm

Malden,

You are correct. Perhaps I should have specified the supporting evidence was just for points 3-8.

North
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Postby malden » Sun Nov 07, 2010 3:07 pm

North52 wrote:M,

You are correct. Perhaps I should have specified the supporting evidence was just for points 3-8.

North

Tx. North52, then let me present some unsuporting evidence for point no. 2:
2) This obstruction of the larger veins in turn results in reduced rate and velocity of flow in the microvasculature (capillaries and post capillary venules) upstream from the stenosis or obstruction. This deduction is supported by simple hemodynamic principals.

http://nobelprize.org/nobel_prizes/medicine/articles/krogh/index.html

"...When the body performs work, this greatly increases its need for oxygen, especially in the muscles, but the question was where this increased oxygen supply came from. The capillaries had been known for 250 years. The conventional view was that they all stood open. It was assumed that the speed of blood flow increased during work. Krogh's mathematical calculations indicated that this could not be true. Faster blood flow through the capillaries hardly increased the potential for more oxygen supply, because the time for diffusion meanwhile decreased. Instead, Krogh elegantly and clearly demonstrated (by measurements of the oxygen content in capillaries and muscle fibers, direct observations and histological sections) that a relatively small number of capillaries are open during rest. In fact, capillaries are opening and closing all the time. During work, however, more capillaries are open. He also found that capillaries can vary in diameter and are thus independently contractile. Although the speed of blood flow through the capillaries is the same during rest and work, the oxygen supply increases because so many capillaries are open and each capillary can hold more blood...."

Thats from:

"Schack August Steenberg Krogh - A Versatile Genius"
The Nobel Prize in Physiology or Medicine 1920

and his

"A Monumental Contribution to Research in Integrative Physiology"

Nobel Lecture, December 11, 1920:
"A Contribution to the Physiology of the Capillaries"

August Krogh was awarded the Nobel Prize in Physiology or Medicine in 1920 "for his discovery of the capillary motor regulating mechanism." During the 1939-40 Winter War between the Soviet uni0n and Finland, when the Danes began collecting money in support of Finland, August Krogh was urged to donate his Nobel medal, which was made of solid gold, for this purpose. He did so, but first he had his daughter Bodil Schmidt-Nielsen make a copy of the medal in silver, which was then gold-plated.
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Postby Sotiris » Mon Nov 08, 2010 7:43 am

@malden
According to my understanding the excerpt you provided should have been coloured as follows:
...When the body performs work, this greatly increases its need for oxygen, especially in the muscles, but the question was where this increased oxygen supply came from. The capillaries had been known for 250 years. The conventional view was that they all stood open. It was assumed that the speed of blood flow increased during work. Krogh's mathematical calculations indicated that this could not be true. Faster blood flow through the capillaries hardly increased the potential for more oxygen supply, because the time for diffusion meanwhile decreased. Instead, Krogh elegantly and clearly demonstrated (by measurements of the oxygen content in capillaries and muscle fibers, direct observations and histological sections) that a relatively small number of capillaries are open during rest. In fact, capillaries are opening and closing all the time. During work, however, more capillaries are open. He also found that capillaries can vary in diameter and are thus independently contractile. Although the speed of blood flow through the capillaries is the same during rest and work, the oxygen supply increases because so many capillaries are open and each capillary can hold more blood....

In other words, Krogh is not arguing that the blood flow has a constant speed during work (he knows its speed is increased, since the heart is pumping at a higher rate), but he shows that this is not enough and consequently the capillaries can not be always open. As regards the blood speed at the capillary level I do not think that his work can give as a strict answer.
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Postby North52 » Mon Nov 08, 2010 7:59 am

Malden wrote:
North52 wrote:Malden,

You are correct. Perhaps I should have specified the supporting evidence was just for points 3-8.

North

Tx. North52, then let me present some unsuporting evidence for point no. 2:
2) This obstruction of the larger veins in turn results in reduced rate and velocity of flow in the microvasculature (capillaries and post capillary venules) upstream from the stenosis or obstruction. This deduction is supported by simple hemodynamic principals.

http://nobelprize.org/nobel_prizes/medicine/articles/krogh/index.html

"...When the body performs work, this greatly increases its need for oxygen, especially in the muscles, but the question was where this increased oxygen supply came from. The capillaries had been known for 250 years. The conventional view was that they all stood open. It was assumed that the speed of blood flow increased during work. Krogh's mathematical calculations indicated that this could not be true. Faster blood flow through the capillaries hardly increased the potential for more oxygen supply, because the time for diffusion meanwhile decreased. Instead, Krogh elegantly and clearly demonstrated (by measurements of the oxygen content in capillaries and muscle fibers, direct observations and histological sections) that a relatively small number of capillaries are open during rest. In fact, capillaries are opening and closing all the time. During work, however, more capillaries are open. He also found that capillaries can vary in diameter and are thus independently contractile. Although the speed of blood flow through the capillaries is the same during rest and work, the oxygen supply increases because so many capillaries are open and each capillary can hold more blood...."

Thats from:

"Schack August Steenberg Krogh - A Versatile Genius"
The Nobel Prize in Physiology or Medicine 1920

and his

"A Monumental Contribution to Research in Integrative Physiology"

Nobel Lecture, December 11, 1920:
"A Contribution to the Physiology of the Capillaries"

August Krogh was awarded the Nobel Prize in Physiology or Medicine in 1920 "for his discovery of the capillary motor regulating mechanism." During the 1939-40 Winter War between the Soviet uni0n and Finland, when the Danes began collecting money in support of Finland, August Krogh was urged to donate his Nobel medal, which was made of solid gold, for this purpose. He did so, but first he had his daughter Bodil Schmidt-Nielsen make a copy of the medal in silver, which was then gold-plated.


Dear Mladen,

Your argument makes complete sense of what happens to the velocity of blood flow in capillaries during increased work, but I do not see how you can apply this same argument to the scenario of stenosed veins. Are you saying that blood flow will not be decreased because capillaries have the abililty to dilate and therefore increase blood flow in this setting? If this is your conclusion, I do not fell that you are correct.

To try and explain this, I would like to make an analogy. Imagine the arterial and venous system as streets and highways with various numbers of lanes. Let us assume the major inflow and outflow routes of arteries and veins (eg carotid artery and jugular veins) have a capacity of 5 lanes. Let us also assume that the smaller routes (capillaries) can only allow one car to pass at a time. Lets also assume that under normal conditions the there are 5 capillary routes available for the cars to use, but they have the capacty to open up to 10 capillary routes in times of "increased work". Assume also that each car is 1 cm long. Under normal conditions let us assume velocity of the cars in the artery is 5cm per second.This allow a total of 25 cars to pass/second. In this scenario the velocity of passage of cars in the larger route will be the same in the smaller route as they both have a capacity for 5 cars. If now you increase the velocity in the larger route to 10 cm/second (or passage of 50 cars/second), the capillaries have two options to accomodate this. The cars can either speed up to 10 cm per second and use 5 lanes or increase the number of lanes to 10 and continue to travel at 5 cars per second. Both scenarios allow the passage of 50 cars per second.Your argument proposes the latter and I believe this is correct.

Now look at the scenario of a stenosed vein or reduced outflow route. Assume a rate of passage of 25 cars per second or 5 lanes with cars traveling at 5cm per second in the artery. Let's assume an 80% obstruction in the vein, so that the outflow highway is reduced to 1 lane. In this scenario we can try to open up the capillary routes from 5 to 10 lanes but this will not have much impact on how much blood goes though the narrowed vein portion. To increase flow to 25 cars/second, the only way to do this would be to increase the inflow pressure significanty. This might happen to a certain degree but not likely to the point of increasing flow back to 25 cars/sec through the narrowed portion. The velocity of flow in the capillaries will therefore be decreased if you maintain the number of capillary routes to 5. Ironically, if you increase the number of capillary routes to 10, you will actually be reducting flow even further. To maintain velocity of flow in the capillaries, the number of capillaries will have to be decreased. I doubt this is an adaptive mechnism that the body uses. This would result in absent perfusion in much tissue. In this scenario, although velocity could be maintained, overall perfusion would still be decreased

I also want to say that there is ample evidence that there is decreased perfusion in ms brains.

North
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Postby malden » Mon Nov 08, 2010 10:07 am

North, Tx for your comment. I will try to explain my point of view using your analogy (This bring me back in my youth and I remember my Matchbox small car models colection and plastic roads we build all over the floor ;) )

... the capillaries have two options to accomodate this. The cars can either speed up to 10 cm per second and use 5 lanes or increase the number of lanes to 10 and continue to travel at 5 cars per second. Both scenarios allow the passage of 50 cars per second.Your argument proposes the latter and I believe this is correct...

- This is corect because there is a speed limit in the town (brain), and the only way to manage increased input trafic is to open new roads/pathways.

...Let's assume an 80% obstruction in the vein, so that the outflow highway is reduced to 1 lane. In this scenario we can try to open up the capillary routes from 5 to 10 lanes but this will not have much impact on how much blood goes though the narrowed vein portion. To increase flow to 25 cars/second, the only way to do this would be to increase the inflow pressure significanty...

- This is not the only way. To keep flow on 25 cars/second in one line, you can speed up trafic in that one line five times! The trafic in the town remain the same.
malden
 

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