Veins and smooth muscle tissue. Why?

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Veins and smooth muscle tissue. Why?

Postby CureOrBust » Sun Jul 10, 2011 4:23 am

I guess the title says it all. Why in the body are the veins surrounded by smooth muscle tissue? ie what is their function in the anatomy?

and how strong / ability to affect the shape / flow are these muscles?
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Postby 1eye » Sun Jul 10, 2011 8:43 am

Curious and I and others have been talking about this. To cool us, for one. To distribute what oxygen and sugar is left by the time the blood reaches the veins. Those are the big ones I can think of. The temperature and more generally blood flow control is done in large part by the constriction and relaxation of these smooth muscles under the direct control of the endothelium and the signals from the autonomic nervous system, I think. That causes the diameters of the vessels to instantaneously grow and shrink to perform these functions.

It is very precise control due to the 4th exponent relationship between resistance and diameter of the vessel.

The other one which goes with cooling is conservation of heat, which coincidentally is only necessary above a certain latitude.

The influence of Starling Resistors on lesions and the like is the other nifty property of veins we have been thinking about. The eyeball must be considered as a whole lot of Starling Resistors too!

If they are having this much effect perhaps that may explain: why veins and not arteries? The arterial pressures are so much higher, and the artery walls so much stiffer, that there is no Starling resistance effect of any significance.
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Postby cheerleader » Sun Jul 10, 2011 9:14 am

Hi Cure--
Vascular smooth muscles communicate and modulate blood flow and resistance throughout the body. Areteries have more smooth muscle, that's why they're thicker. They need to pump, veins need to receive and return. Both arteries and veins have the same endothelial lining (directly over the smooth muscle cells) which communicate and signal the vascular smooth muscles to contract or expand...

Vascular smooth muscle contracts or relaxes to both change the volume of blood vessels and the local blood pressure, a mechanism that is responsible for the redistribution of the blood within the body to areas where it is needed (i.e. areas with temporarily enhanced oxygen consumption). Thus the main function of vascular smooth muscle tonus is to regulate the caliber of the blood vessels in the body. Excessive vasoconstriction leads to hypertension, while excessive vasodilation as in shock leads to hypotension.


Here's a great paper which looked at the differences between venous and arterial smooth muscle cells (SMC)-

The differentiation state of SMC has been implicated in various vascular pathologies such as atherosclerosis [9,17] and intimal hyperplasia [10,11]. The dedifferentiated phenotype for venous SMC reported in this study is consistent with the cellular behavior characterized by increased proliferation, migration, and synthetic capabilities. Our results show increased levels of collagen synthesis and gelatinase activity in venous SMC. Collagen synthesis and accumulation are integral aspects of vascular repair [14,18]. Previous studies have also shown that gelatinase activity is a critical component of SMC migration in vein graft disease [19] and the formation of intimal hyperplasia after arterial injury and in vein grafts [14,20,21].


We see this remodeling in vein graft surgeries, which tend to fail after time because of the SMC reaction. This is why surgeons aren't keen on replacing veins just yet....these grafts have a higher failure rate due to intimal hyperplasia from SMCs.

Although the saphenous vein remains a commonly utilized conduit in coronary artery bypass grafting, it is often plagued by vein graft diseases such as fibrointimal hyperplasia and accelerated atherosclerosis within 5–10 years after surgery [3]. The causes for vein graft diseases are multifold. Studies have shown that many factors such as surgical trauma [35] and hemodynamic changes [36,37] are important in the development of vein graft intimal hyperplasia. Furthermore, consistent with our in vitro results, venous SMC dedifferentiation and proliferation have been shown in vein graft intimal hyperplasia [10,11]. Based on our study, venous SMC have particular intrinsic characteristics that may contribute to the development of vein graft disease.

http://cardiovascres.oxfordjournals.org ... 3/702.full

hope this help explain....it's definitely part of CCSVI, as Dr. Gabbiani's studies into the collagen remodeling of the smooth muscle cells of CCSVI veins has shown us. CCSVI jugular veins have stiffer, less plient linings.
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Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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Postby cheerleader » Sun Jul 10, 2011 9:22 am

1eye wrote:If they are having this much effect perhaps that may explain: why veins and not arteries? The arterial pressures are so much higher, and the artery walls so much stiffer, that there is no Starling resistance effect of any significance.


good point, one eye...there is a definite Starling effect in cerebral blood return to the heart, but it hasn't been illucidated in CCSVI (yet)--you'll like this paper:
This investigation was undertaken to determine whether a Starling resistor or venous waterfall effect exists between the sagittal sinus and the cerebral veins such that increases in sagittal sinus pressure (Pss) do not abolish cerebral venous outflow and to examine two possible contributions of extracranial venous valves in regulating outflow.

http://jap.physiology.org/content/53/6/1496.abstract
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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Postby David1949 » Sun Jul 10, 2011 9:52 am

Interesting stuff! I've been wondering how the body manages to direct blood flow to where it is needed at the moment.

This furthers my belief that Dr. Zamboni is barking up the right tree but hasn't peeled the right banana yet. (Pardon me for mixing my metaphors.)
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Postby 1eye » Sun Jul 10, 2011 10:08 am

cheerleader wrote:
1eye wrote:If they are having this much effect perhaps that may explain: why veins and not arteries? The arterial pressures are so much higher, and the artery walls so much stiffer, that there is no Starling resistance effect of any significance.


good point, one eye...there is a definite Starling effect in cerebral blood return to the heart, but it hasn't been illucidated in CCSVI (yet)--you'll like this paper:
This investigation was undertaken to determine whether a Starling resistor or venous waterfall effect exists between the sagittal sinus and the cerebral veins such that increases in sagittal sinus pressure (Pss) do not abolish cerebral venous outflow and to examine two possible contributions of extracranial venous valves in regulating outflow.

http://jap.physiology.org/content/53/6/1496.abstract


Waall, I like the abstract but increasingly I am having to say no to publishers for pdfs because of a deficit in my pockets.

Wish I had one of those institutional subscriptions, but there's just me and the chair, here.
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Postby cheerleader » Sun Jul 10, 2011 10:22 am

David1949 wrote:Interesting stuff! I've been wondering how the body manages to direct blood flow to where it is needed at the moment.

This furthers my belief that Dr. Zamboni is barking up the right tree but hasn't peeled the right banana yet. (Pardon me for mixing my metaphors.)


David--my thought (or banana) has been that's it's also about the endothelial lining of blood vessels breaking-down, or endothelial dysfunction, complicating venous stenosis. I started on that path because of my husband's blood numbers at his diagnosis (high liver enzymes, hyper-coagulation, petechiae on his limbs and jaundice) It looked like a systemic breakdown of his endothelium. The blood brain barrier has an endothelial lining, and the endothelium communicates with the smooth muscle cells, controlling vasodilation and vasoconstriction. Here' the research I put together on this...
http://www.ccsvi.org/index.php/helping- ... ial-health
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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Postby 1eye » Sun Jul 10, 2011 12:36 pm

cheer wrote:....it's definitely part of CCSVI, as Dr. Gabbiani's studies into the collagen remodeling of the smooth muscle cells of CCSVI veins has shown us. CCSVI jugular veins have stiffer, less pliant linings.

Stiffer: cause or effect? You think there is this remodeling that thickens the smooth muscle? Why does that happen? Is it a genetic thing? The quote you gave seems to say it is an expected result of surgery: kind of scarring, in other words, But if it is part of a disease process, gosh darn and all that that entails.
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Postby 1eye » Sun Jul 10, 2011 1:44 pm

When trying to understand blood flow in veins, I found this short physics and chemistry thing useful. Thanks CurIous for telling me this stuff!
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Postby David1949 » Sun Jul 10, 2011 4:10 pm

cheerleader wrote:
David1949 wrote:Interesting stuff! I've been wondering how the body manages to direct blood flow to where it is needed at the moment.

This furthers my belief that Dr. Zamboni is barking up the right tree but hasn't peeled the right banana yet. (Pardon me for mixing my metaphors.)


David--my thought (or banana) has been that's it's also about the endothelial lining of blood vessels breaking-down, or endothelial dysfunction, complicating venous stenosis. I started on that path because of my husband's blood numbers at his diagnosis (high liver enzymes, hyper-coagulation, petechiae on his limbs and jaundice) It looked like a systemic breakdown of his endothelium. The blood brain barrier has an endothelial lining, and the endothelium communicates with the smooth muscle cells, controlling vasodilation and vasoconstriction. Here' the research I put together on this...
http://www.ccsvi.org/index.php/helping- ... ial-health


The Nitric Oxide promoting products claim a plethora of benefits. Has your husband tried them? If so did they produce any benefits with regard to MS symptoms?
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Postby 1eye » Sun Jul 10, 2011 4:48 pm

The first sentence I read at the Veins of The Brain was
The veins of the brain possess no valves, and their walls, owing to the absence of muscular tissue, are extremely thin.


Is there only an endothelium, and how do I get headaches? Only from arteries?
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