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Summary
Three types of vascular dysfunction have been described in multiple sclerosis (MS).

First, findings from epidemiological studies suggest that patients with MS have a higher risk for ischaemic stroke than people who do not have MS. The underlying mechanism is unknown, but might involve endothelial dysfunction secondary to inflammatory disease activity and increased plasma homocysteine concentrations. ... Read More - http://www.msrc.co.uk/index.cfm/fuseact ... ageid/2944

Found an interesting document describing the endothelium.

As I think I have noticed, the smooth muscle in blood vessels is a major user of energy in the human body...

"Thus, endothelial cells line the entire vascular system, from the heart to the smallest capillary, and control the passage of materials—and the transit of white blood cells—into and out of the bloodstream. A study of the embryo reveals, moreover, that arteries and veins develop from small vessels constructed solely of endothelial cells and a basal lamina: pericytes, connective tissue and smooth muscle are added later where required, under the influence of signals from the endothelial cells. The recruitment of pericytes in particular depends on PDGF-B secreted by the endothelial cells, and in mutants lacking this signal protein or its receptor, pericytes in many regions are missing. As a result, the embryonic blood vessels develop microaneurysms—microscopic pathological dilatations—that eventually rupture, as well as other abnormalities, reflecting the importance of signals exchanged in both directions between the pericytes and the endothelial cells.

Once a vessel has matured, signals from the endothelial cells to the surrounding connective tissue and smooth muscle continue to play a crucial part in regulating the vessel's function and structure. For example, the endothelial cells have mechanoreceptors that allow them to sense the shear stress due to flow of blood over their surface; by signaling this information to the surrounding cells, they enable the blood vessel to adapt its diameter and wall thickness to suit the blood flow. Endothelial cells also mediate rapid responses to neural signals for blood vessel dilation, by releasing the gas NO to make smooth muscle relax in the vessel wall..."**


That means that the sympathetic nervous system, while it controls directly some of the cardiovascular functions, especially in the arteries, does not have the same influence over the bloodflow when it comes to the smooth muscle and the endothelium. Control is automatic, both chemistry and physics-based, occurring, as described, as a result of on the one hand, shear stresses, and the other, neural signalling, chemicals which originate from the CNS.

The smooth muscle in blood vessels is directly under the control of the endothelium, which must be in good health for it to work. If it is not, the main background "tonic" use of energy by the smooth muscle all over the body can be in jeopardy. In the case of arteries this job is much easier, since the supply of oxygen is plentiful. However, the closer the blood is to the point of needing recharging with oxygen, the harder this job becomes. That is why the cerebro-spinal veins sometimes do not get enough oxygen. Their turn sometimes comes last.

**http://www.ncbi.nlm.nih.gov/books/NBK26848/

As this guy from up the Ottawa used to say at work: "Holy wick!"

I just typed something like smooth muscle endothelium shear stress into Google and got into Google scholar. You know how they always give you 80 million results and you only needed the first two? That's because Google uses the same scheme as academia, of counting up how many papers reference yours.

Well this one paper... If I were starting out figuring out what causes CCSVI I'd start there. I spent half the evening just reading the titles of the references! Am I a sophomore or what?

Google Scholar Result

Laminar Shear Stress
Mechanisms by Which Endothelial Cells Transduce an Atheroprotective Force
Oren Traub; ; Bradford C. Berk

From the Departments of Pathology (O.T.) and Medicine (B.C.B.), Division of Cardiology, The University of Washington, Seattle.

Abstract—Mechanical forces are important modulators of cellular function in many tissues and are particularly important in the cardiovascular system. The endothelium, by virtue of its unique location in the vessel wall, responds rapidly and sensitively to the mechanical conditions created by blood flow and the cardiac cycle. In this study, we examine data which suggest that steady laminar shear stress stimulates cellular responses that are essential for endothelial cell function and are atheroprotective. We explore the ability of shear stress to modulate atherogenesis via its effects on endothelial-mediated alterations in coagulation, leukocyte and monocyte migration, smooth muscle growth, lipoprotein uptake and metabolism, and endothelial cell survival. We also propose a model of signal transduction for the endothelial cell response to shear stress including possible mechanotransducers (integrins, caveolae, ion channels, and G proteins), intermediate signaling molecules (c-Src, ras, Raf, protein kinase C) and the mitogen activated protein kinases (ERK1/2, JNK, p38, BMK-1), and effector molecules (nitric oxide). The endothelial cell response to shear stress may also provide a mechanism by which risk factors such as hypertension, diabetes, hypercholesterolemia, and sedentary lifestyle act to promote atherosclerosis.

seems like another good one! I did not take anywhere near the biology and anatomy or pre-med courses I would've taken, had I known I'd develop this interest (and illness) ten years later.

Here's a mouse study on arteries. If you make several mental leaps you can imagine a similar mechanism of high venous blood pressure causing endothelial and/or smooth muscle oxidative damage in veins. You can also imagine a similar biochemical rescue using antioxidants.

mouse study

Wouldn't it be nifty if you could treat somebody by delivering an antioxidant in the form of a viral infection?

an oldie but goody?

oldie