Dr. Martin Pall is a pioneer in the study of ME/CFS and has looked closely at the role of nitric oxide. Some people with chronic health issues do well with low-dose LDN, which blocks sedatives. I keep thinking ME/CFS may be akin to a kind of “walking” general anesthesia where the person is too vasodilated, so I was wondering what drugs they use to bring a person up from general anesthesia. I found this:
“Vasodilators are used to control systemic hypertension; increase cardiac output by decreasing afterload, preload, or both; control pulmonary hypertension; and control cardiac shunting. Commonly used agents include nitroglycerin and hydralazine, with sodium nitroprusside less commonly used today. Nitroglycerin and sodium nitroprusside generate intracellular nitric oxide, which then augments cGMP in vascular smooth muscle, specifically in both arteries and veins, leading to vasodilation. Sodium nitroprusside also interacts with oxyhemoglobin and forms methemoglobin while releasing cyanide. Nitric oxide release is responsible for its vasodilating effects.”
Vasodilation is used to control hypertension because it takes the pressure off. Could ME/CFS involve a kind of “twin” dysfunction, where the person is both hypertensive and, as a result, hyper-vasodilated?
Vasodilation treats hypertension. I am wondering if vasodilation might also CAUSE hypertension. Let’s say a hose (so to speak) is working fine from its own perspective. If you open it wider, now it feels itself as experiencing HYPOTENSION, so it has to push harder and faster, to compensate. To re-establish the connection. When you force a vein open, have changed the degree of dilation, not the consciousness.
To us it looks as if my friend with extreme ME/CFS has severe hypertension. But to her own cardiovascular system, it may not.
When we give her vasodilators, from the perspective of her central nervous system, we are inducing HYPO-tension. To keep her arterial pressure stable and functioning, her body then has to use too much ARGININE. This, then, can contribute to the re-activation of latent viruses. And it perpetuates the problem.
Could what presents as hypertension actually be masking hypotension?
Could what presents as hypotension actually be masking hypertension?
Are we seeing what is fundamentally wrong—or are we seeing what the body is doing to correct for it?
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