Decreased Upright Cerebral Blood Flow And Cerebral Autoregulation In Normocapnic Postural Tachycardia Syndrome

[ramakentesh]

Another interesting study:

http://ajpheart.physiology.org/cgi/content...ct/00138.2009v1

[summer]

Thank you sooo much for posting this. I have been talking recently with my doctors about this but haven't been able to find anything very current! Can't get much more current than that! .....Got to go and email that link to someone now....

How do you find all the really current research?

MANY thanks!!

Summer

[MightyMouse]

Summer, to find current articles you can use google and search scholarly papers only:

http://scholar.google.com/

For example, I use the search term of Postural Orthostatic Tachycardia and here's the search result.

Then you can click "recent articles" on the masthead bar. I then tightened the search to just 2007 forward, and here's that result.

[summer]

Nina,

That's fantastic! I've always wondered how you guys found all the good stuff! Thanks a lot for letting me know how to use that. I'll have no more excuse for not being up to speed on new research now.

Summer

[Heiferly]

There's also PubMed:

http://www.ncbi.nlm.nih.gov/pubmed/

[ajw4790]

Thanks for posting!

[ramakentesh]

I dont know if this is related to how my head literally fills up like a balloon when i lean forward...

[summer]

I know what you mean. I was looking for something under my bed last night and thought my head would explode.

Ok... I'm going to ask the question that I have been avoiding in my mind for a long time. Is there anyway that this messed up brain blood flow is not putting us at risk for various problems. Hypoperfusion and vasocontriction..... doesn't sound like that would be too good for a person's brain. Any thoughts... or better yet, research?

Summer

[ramakentesh]

There was a study that suggested that people with low blood pressure or reduced blood flow to the brain resulted in an earlier onset of alzeimers. But this was actually in a newspaper so its creditibility might have been questionable.

Now days there is a medical study for every possibility. Many are really conjectural.

[firewatcher]

Hypoperfusion and cerebral vasoconstriction are very large research topics in Brazil and high altitude climates. There are many studies about the compensatory mechanisms of the human body to lack of oxygen and "air pressure." POTS is our compensation, so the body is adapting to whatever the "cause" is. There are several issues and common diseases among the indigenous peoples of these high regions and many are completely reversed by bringing them to sea level (I guess we'd have to live in a cave )

Since these disorders are so "new" in studies, there is no way to tell what the long term prognosis is yet.

[ramakentesh]

Do you mean that the compensatory mechanisms relating to nitric oxide at altitude? Well I guess so, but the compensatory mechanisms could be a little different as well. Although its an interesting concept - it seems unclear whether this poor head vascular regulation is a primary problem or just a result of poor perfusion, although this may indicate the former.

At altitude, a normal body re-regulates levels of nitric oxide to control periperhal resistance, blood pressure and circulation without undue difficulty. When there are sudden changes in altitude some people suffer altitude sickness.

POTS is possibly a mechanism to counteract blood pooling or blood flow abnormalities that are present at all altitudes. It may also be caused by primary excess sympathetic excitability or parasympathetic withdrawal (and thus hyperadrenergic).

In Low Flow POTS, a subset of patients were found to have low nitric oxide bioavailability. Whether the system that regulates nitric oxide in relation to altitude is functional in these patients has never been tested. The bioavailability problem is neuronal rather than endothelial and relates to elevation of angiotensin II.

I guess my point is that where nitric oxide is implicated in POTS, adaptions to atlitude would have an obvious similarity, whereas with other forms of POTS its an interesting investigatory option.

[firewatcher]

Do you mean that the compensatory mechanisms relating to nitric oxide at altitude? Well I guess so, but the compensatory mechanisms could be a little different as well. Although its an interesting concept - it seems unclear whether this poor head vascular regulation is a primary problem or just a result of poor perfusion, although this may indicate the former.

At altitude, a normal body re-regulates levels of nitric oxide to control periperhal resistance, blood pressure and circulation without undue difficulty. When there are sudden changes in altitude some people suffer altitude sickness.

POTS is possibly a mechanism to counteract blood pooling or blood flow abnormalities that are present at all altitudes. It may also be caused by primary excess sympathetic excitability or parasympathetic withdrawal (and thus hyperadrenergic).

In Low Flow POTS, a subset of patients were found to have low nitric oxide bioavailability. Whether the system that regulates nitric oxide in relation to altitude is functional in these patients has never been tested. The bioavailability problem is neuronal rather than endothelial and relates to elevation of angiotensin II.

I guess my point is that where nitric oxide is implicated in POTS, adaptions to atlitude would have an obvious similarity, whereas with other forms of POTS its an interesting investigatory option.

I am only saying that IN MY CASE, my labs and responses look like I live in the Andes: high hematocrit, high RBC, high serum osmolality, high lung perfusion/O2 absorption, slower breathing, low GFR, high creatinine...

[ramakentesh]

And I wonder what your nitric oxide levels are like...

[firewatcher]

Nitric oxide, histamine, prostaglandins, norepinephrine, epinephrine, dopamine, serotonin............

There are many neurochemicals and many have completely different functions inside the brain and then outside in the rest of the body. Histamine is an inflammatory inducer, immune system agent and the neurochemical that goes from the eyes to the hypothalamus to tell us to wake up...It also causes anaphylaxis and vasodilation. Oxytocin makes us feel all loving and bonded, but it also causes similar effects to ADH in the kidney's ability to reabsorb water...All the others have multiple jobs as well and many must work in conjunction with another to get it's "job" done, too much or too little of one and the whole system goes haywire! Dr. Robertson at Vanderbilt was on to one piece of the puzzle years ago with histamine being more than "an allergic reaction," just as Dr. Stewart is on to Nitric Oxide (which is also implicated in the induction of sleep and control of wakefulness---just like histamine!) What happens to Nitric oxide in low sodium level blood? or with too much dopamine, or histamine? Let's throw Estrogen into the mix, how does it make the reaction different? We are YEARS away from understanding this! I don't mean to discourage you from researching, honestly! Keep posting articles and thinking. There are many very good minds here (just as good, if not better than some of the doctors I've seen!) and I will not be surprised if it is not a PATIENT that makes the connection and figures this out...for some of us.

I just think that it is more than one faulty response to a molecule that causes all this.

[ramakentesh]

Yeah true - and then there are all the nerve-released inflammatory markers that cause nitric-oxide induced vasodilation, like substance P (which I think Low did a talk on in 2007 in relation its connection with POTS) and Calcitonin gene related peptide (which has been linked to migraines).

Its a complex one that is for sure.

Did you say that you had increased peripheral resistance?

[firewatcher]

Yes, when I got to substance P in my reading, I thought "these people truly have no idea what they are dealing with!" They have a thing, but they aren't sure what kind of thing it is, but they can see that it does this, but they don't know why or what produces it........

The human body...the final frontier...

[ramakentesh]

its so typical that the illness I get is the one that isnt a simple one to resolve. Still Im learning slowly.

[firewatcher]

its so typical that the illness I get is the one that isnt a simple one to resolve. Still Im learning slowly.

That's the thing though, there are no "simple" illnesses. We can't even cure or prevent the common cold! How much time, money and research has been thrown at more common diseases which still have no "cure." Ours is simply unexplored, not unknown. Since it encompasses so many other systems AND the system that controls the entire body, it will, by its nature, be complex. The human body is incredibly resilient and compensates in vast and unpredictable ways. Plus, the human gene pool itself is HUGE! Most of the lab animals have a single gene pool to play with, once you throw in the "wild type" all bets are off.

[ramakentesh]

I like it when they call it the POTS phenotype. Like our bodies chose to adopt this particular phenotypical genetic characteristic.

As an example my friend put this to me. What if NET reduction found in some POTS patients from hypermethylation of the NET gene promoter is actually an adaptive mechanism due to faulty norepinephrine release or to prevent syncope due to pooling?

Anyway Ill be interested when Dr Grubb releases his new study by the end of the year detailing his description of three subsets of hyperadrenergic POTS (which I assume would be NET deficiency, alpha 1 supersensitivity and beta-supersensitivity (although the relevance of beta venoconstrictive properties in orthostatic stress are still being debated).

Like you say, it appears that POTS is the final path for a myriad of bodily problems, some appearing to be caused by the OPPOSITE of others.

As two examples, some patients have reduced peripheral resistance and alpha1 agonists would be ideal, but other POTS patients have increased periperhal resistance either during orthostatic stress or at all times (with or without reduced blood flow) as part of the problem and the medication that helps one clearly wouldnt help those with already have this hyperadrenergic response.