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Old 09-14-2007, 12:54 AM
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Vicc Vicc is offline
In Remembrance
 
Join Date: Nov 2006
Location: SE Kansas.
Posts: 374
15 yr Member
Vicc Vicc is offline
In Remembrance
Vicc's Avatar
 
Join Date: Nov 2006
Location: SE Kansas.
Posts: 374
15 yr Member
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You probably learned in high school that our cells combine oxygen (O2) with glucose (Gl), to generate the energy that keeps them alive: No Gl and no O2 = no energy. You probably also learned that our cells also create all of the heat necessary to keep the body at a constant 98.6 degrees. Heat is a by-product of cells transforming matter into energy.

Without any O2 or Gl, the cells would die, if enough cells die, the body temp would begin its drop to the temp of the air around it. There is a mid-range, however, when the cells aren’t getting enough 02 or Gl to function properly, but still survive. But the temperature will drop.

The only explanation I have found for our painful hyper-sensitivity to cold and lowered skin temperatures is that the cells aren’t getting enough O2, or Gl, or both. This is that mid-range I just talked about.

I’ll talk more about exactly why RSD falls into this mid-range in future posts, but my purpose here is to show how ischemic hypoxia: blood flow to cells and organs that is not sufficient to maintain their normal function.* explains these symptoms, while nerve injury does not.

The only way to stop or decrease cell metabolism is by reducing the amount of O2 or Gl reaching it.

We can know we suffer from tissue hypoxia simply by looking at our blue to purplish skin. That is the color defined as cyanosis: a bluish or purplish discoloration (as of skin) due to deficient oxygenation of the blood.*

Our skin is supposed to be a normal, healthy color; you know: “Skin color”, so why isn’t it? Cyanosis is a bluish or purplish discoloration (as of skin) due to deficient oxygenation of the blood.*It is visible proof of hypoxia. If our skin is cyanotic, our cells are hypoxic.


When we see cyanosis, we are actually looking at millions of microvascular systems (MVS) filled with oxygen depleted blood, and that blood isn’t moving. Our MVS are part of the circulatory system and blood is supposed to be constantly moving, never stopped. Those MVS are ischemic. A low oxygen state usually due to obstruction of the arterial blood supply or inadequate blood flow leading to hypoxia in the tissue.*

MVS are the arterioles, capillaries, and venules that deliver “fresh” arterial blood to the cells and return “used” blood to the veins. The blue color means that blood is not flowing through the arterioles and into the capillaries that supply everything the cells need. When this happens, our cells do what they are programmed to do to:

They switch from aerobic metabolism to glycolysis; generating energy without using O2, but glycolysis doesn’t generate any heat, and isn’t nearly as efficient as aerobic metabolism. It does provide enough energy for the cells to survive, but not enough for them to function properly.

They also release chemical neurotransmitters (Nts) that tell the brain that they aren’t getting enough 02; and they tell other nearby cells the same thing: Nearby cells may be served by functioning MVS, and if they are, they transfer some O2 and Gl to the needy ones. This helps keep those cells alive, but it also means the donor cells now don’t have enough of either to function properly. Now they aren’t able to generate enough heat to keep the limb warm.

This works pretty well during an emergency, but if crisis lasts very long, all of the cells suffer. In RSD, the crisis lasts too long. Many, if not most of the cells in the affected area are now dysfunctional and the temperature of the affected limb begins to fall.

The temp doesn’t need to drop much before the cells begin releasing Nts telling the brain they’re cold. Our bodies are designed to maintain a constant temp of about 98.6 degrees; a drop of one degree can cause the cells to begin complaining, 96.6 degrees feels bitterly cold, and a core temperature of 95.6 degrees will produce violent shivering.

When the air temp in my room drops to 68 degrees, it gets too cold for my feet: They start screaming that they’re freezing. Other things may be contributing to the cold pain I’m experiencing; my “pain nerves”, C-fibers (Cfs), aren’t getting enough 02 either, and they may be amplifying the cold messages from the cells.

The bottom line is that when cells don’t get enough O2 and Gl, they can’t generate enough heat to warm themselves, much less the tissue around them. They start sending out frantic signals because this is a real crisis.

They send signals telling the brain they aren’t getting enough O2, so the brain tells the sympathetic nerves to increase blood flow, and this aggravates things because one of the things the SNS does to increase blood flow is to stimulate the release of adrenalin. Adrenalin increases the burning pain of RSD.

We know that adrenalin does this because if you inject norepinephrine (artificial adrenalin) just below the site of a recent sympathetic block; the burning pain comes back. That is what sympathetically maintained pain (SMP) is, and it is why blocks work: They are blocking normal sympathetic release of adrenalin, NOT blocking some abnormal SNS activity.

Several things can cause the kind of cyanosis we see in RSD: In late stage diabetes, the disease has damaged small arteries so badly that they can’t carry enough arterial blood to supply the cells; in Raynaud’s Disease, spasming of the arterioles in the MVS prevent arterial blood from getting into the MVS. In both of these disorders, too many cells die and gangrene can develop, making amputations necessary.

RSD patients sometimes end up with an amputated limb, but not because of gangrene: When microcirculation is impaired, wounds can’t heal properly and infections can develop; antibiotics are delivered in arterial blood, so the amount that reaches the site where they’re needed is too little to do the job.

Something else causes the cyanosis in RSD, and after ten years of research the only explanation I’ve found that makes sense is ischemia-reperfusion injury (IRI). It begins with a physical trauma, followed by inflammation and then by ischemia in which some cells still get enough O2 and Gl.

I’ll explain more about IRI in future posts, but before I get to that I need to prove that ischemia can cause every sign and symptom of this disease. I hope that once I’ve done that, you will be more open to the idea that this disease is NOT caused by nerve damage. My next post will talk about those other signs and symptoms…Vic

* Online Medical Dictionary (OMD)
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Last edited by Vicc; 09-14-2007 at 06:32 AM.
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