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I have been doing a little light reading of internet-based (and therefore suspect) information on blood physics, hoping not to become a pseudo expert on vascular medicine but to have my own curiosity somewhat satisfied and to better understand my own blood. The mystery to me is: why is the effect of temperature on my nervous system so abrupt at around 73 degrees of air temperature (different water temperature in the shower, but similarly abrupt)?

Anyway, on my travels I have encountered a thread which throws some light, and others which intrigue. I thought maybe a thread featuring a progression of learning on theoretical topics will help some participants to understand the basic theory. It can get very complex. So to throw out some icebreaking, I give you the following tutorial discussion I found. An understanding of Ohm's Law helps:

http://www.cvphysiology.com/Hemodynamics/H004.htm

A suitable test question might be: If resistance to blood flow in a tubular structure like a vein or artery is proportional to the 4th power of the diameter (i.e., a twofold narrowing produces a 16-fold increase in resistance) why is a figure of 75% narrowing more likely to be used to describe a stenosis?

Future topics: viscosity, laminar versus turbulent flows, shear stress, hematocrit level, Reynold's number, etc...

-Chris Sullivan

P.S. I was just reading another thread at the top of today's discussions, and though it sounds unlikely, the discussion of Rici's experiences may be connected with this one.

This is a great idea, 1eye. Although your test question has me stumped already.

1eye wrote: An understanding of Ohm's Law helps:

http://www.cvphysiology.com/Hemodynamics/H004.htm

A suitable test question might be: If resistance to blood flow in a tubular structure like a vein or artery is proportional to the 4th power of the diameter (i.e., a twofold narrowing produces a 16-fold increase in resistance) why is a figure of 75% narrowing more likely to be used to describe a stenosis?

Future topics: viscosity, laminar versus turbulent flows, shear stress, hematocrit level, Reynold's number, etc...

-Chris Sullivan

I know this is somewhat crazy and futile, but there is a free simulation program for electronics http://www.linear.com/designtools/software/ltspice.jsp that I have been using for hobby projects that could be used to "simulate" veins and arteries as resistors, the heart as a signal generator, etc, maybe capacitors and inductors can be used to simulate... what?. This program shows graphically how every component behaves.

I know, I know, plain crazy, but intriguing nonetheless. At least it could be used for learning.

More links:

http://en.wikipedia.org/wiki/Blood_flow

That's good info 1eye. Thanks for posting it. Yeah the reported stenosis figure, wether it is based on diameter or area, doen't reveal the true extent to which flow is restricted.

The article leads one to believe that a stenosis in one vein would have little effect on total blood flow. That's probably true, but what happens when all of the major veins are stenosed, as is the case in many of the people who have been checked for ccsvi? Also what would happen in the case of a small vein which became stenosed? The total blood flow through the brain might not be altered much because other veins would pick up the difference. But would the small part of the brain which is serviced by that particular vein be deprived of blood? Are there enough redundant veins (in parallel with that one) to provide adequate blood flow locally?

BTW I've read some of Ricci's posts but haven't been able to determine what the situation is. Can someone enlighten me?

I think in mentioning Ricci I was referring to the problem of diameter reduction. As shown in the text, major organs are fed and drained by veins, many of which are in series-parallel networks, where a narrowing may have little effect. Parallel networks have the property that total resistance (to flow, in this case) is always lower than the lowest (least stenosed, largest) resistance. That means the flow in the largest vein has the most overall influence on the total. Because of parallel collaterals and normal veins, flow continues even when jugulars are blocked.

Depending very markedly on flow in jugulars, we can demonstrably live without their contribution to drainage. However, because they are the lowest resistance in a parallel circuit, their absolute capacity does have a major effect. Because they are always in series with the capillary beds, their total capacity affects brain perfusion.

Ricci experienced a reflux that was not swamped by the increased diameter where a valve was destroyed. That sounds to my very uneducated ears like a timing thing, possibly in his right heart, which is capable of driving reflux if it does it when the heart valve is open. This type of reflux is a known heart-problem, which is often asymptomatic, and has a high prevalence in otherwise normal people. When it is symptomatic, the symptoms can resemble MS.

My problem seems to be reflux that is happening when I am lying down. I want to find out more about the influences of temperature and viscosity. My problems seem very sensitive to temperature. I have now seen what I think is confirmation that this happens in other people with MS: the temperature/problem curve seems to have a sharp inflection, and possibly in my case anyway, at 73 degrees F, where past some point, I start to get really bad symptoms. I think reflux may be happening, and I'd like a physical explanation.

Viscosity of blood is very temperature-dependent: when it is measured, the temperature is often part of the data. Is my blood warming up enough to admit reflux, when I get warm enough?

I think medicine in general could use some kind of symbology and precise terminology like what is found in electronics, however, right now it is far too imprecise and not accurately described.

1eye, your statement "i know, i know sounds a little crazy". none the less your find is interesting. and, in the scheme of things "a little crazy" may help solve a lot of the unknowns. the whole ccsvi theory is deemed crazy by some. but, the ones that have been in charge of research and treatment for years have yet to prove to me that they are the sane bunch.

Blossom, it was not me who said that. It doesn't sound crazy at all to me. The thing that electronics resembles most of all in my life is plumbing. So the symbols and diagrams may be more directly applicable than we think. Both areas follow the same physical laws, and though the substance which is flowing is different, so all the components are different, nonetheless many of the same tricks may apply. Homeostasis: are there negative feedback loops, and can we change the gain, or phase?

sorry 1eye, i need to pay better attention.

this has less to do with blood and more to do with nerves, but for what it may or may not be worth:

Rutkove, S. B., Kothari, M. J. and Shefner, J. M. (1997), Nerve, muscle, and neuromuscular junction electrophysiology at high temperature.
Abstract
Although the effect of low temperature on the peripheral nervous system has been systematically studied, the effect of high temperature has not. We investigated the effect of elevating limb temperature from 32°C to 42°C [JL edit: 98.6 degF to 107.6 degF] by performing sequential motor studies, antidromic sensory studies, and 3-Hz repetitive stimulation in normal subjects. In addition, we recorded single motor units by using threshold stimulation. On average, motor amplitude and duration decreased by 27% and 19%, respectively, whereas sensory amplitude and duration decreased by 50% and 26%, respectively. Neuromuscular transmission remained normal at 42°C. Single motor unit recordings revealed a reduction in amplitude of 26%, similar to the overall reduction in compound motor amplitude. These findings demonstrate that significant reductions in sensory and motor amplitudes can occur in normal nerves at high temperature; we hypothesize that these changes are secondary to alterations in nerve and muscle ion channel function.

HTH

It might be good to study how long blood heating takes to have a measurable impact on nerve conduction and ditto with cooling.

more about nerve and muscle ion channel function:

http://www.answers.com/topic/action-potential
Nerve axons come in two varieties: myelinated and unmyelinated. Myelin is a fatty sheath that surrounds the myelinated fibres and allows faster transmission of nerve impulses. Action potentials race along myelinated nerve fibres at rates of up to 100 metres/second or more, but can barely manage 1 metre/second in many unmyelinated fibres. The rate at which action potentials are transmitted also depends on temperature, and conduction slows down when the nerve is cooled. [jl note: or excessively warmed]

http://en.wikipedia.org/wiki/Action_potential
In physiology, an action potential is a short-lasting event in which the electrical membrane potential of a cell rapidly rises and falls, following a stereotyped trajectory. Action potentials occur in several types of animal cells, called excitable cells, which include neurons, muscle cells, and endocrine cells, as well as in some plant cells. In neurons, they play a central role in cell-to-cell communication.

http://faculty.washington.edu/chudler/qa4.html
What is the effect of temperature on the shape of the action potential?
Answer: The effect of temperature is mainly on ionic permeability of the neuronal membrane. Specifically, sodium channels open and close faster at higher temperature. Reductions in temperature lengthen the action potential and slow conduction velocity...these are the classic experiments of Hodgkin and Katz (1949).

http://www.ncbi.nlm.nih.gov/pmc/article ... 2-0254.pdf
THE EFFECT OF TEMPERATURE ON THE ELECTRICAL ACTIVITY OF THE GIANT AXON OF THE SQUID (Hodgkin and Katz, 1949)
...effects on action and resting potential in sea water solution at different temperatures...
http://www.ncbi.nlm.nih.gov/pmc/article ... 77/?page=3
(link to results graphs p242)
from summary p249
The action potential diminished in amplitude as the temperature was
raised. This change was slight from 2 to 200 C., the mean value falling from 85 to 80 mV. The decrease in spike height became very rapid above 350 0., and a reversible 'heat block' occurred between 35 and 400 C.
The positive phase of the membrane action potential was diminished at
low and high temperatures and reached a maximum, of approximately
10-15 mV., at about 250 C.

excellent intro/exercises on action potential in nerves:
http://outreach.mcb.harvard.edu/animati ... ential.swf

sodium-potassium pump close-up video, showing ATP activity:
http://highered.mcgraw-hill.com/olc/dl/120068/bio03.swf