Has anyone looked at baroreceptors role in M.E?

[BlahBlahBlah]

ive been on daily IV saline for 3.5 years now and it helps far more than just boosting my BP to help me sit up. My doctors theory is the sudden stretch on the baroreceptors changes the signals they sent. Reading about their role in the body makes a lot of sense but I never see it mentioned in M.E stuff. Has it been looked at?

 

[Hip]

My doctors theory is the sudden stretch on the baroreceptors changes the signals they sent.

Could you elaborate a bit on this: how are the baroreceptors being stretched? Is it the extra volume of fluid in the blood circulation resulting from the IV saline that stretches the blood vessels and baroreceptors?

 

[BlahBlahBlah]

Sorry, I did mean the sudden increase in blood volume (due to the saline) puts the stretch on the blood vessels and the receptors. We tried subcut fluids which didn’t make any difference and tried running iv fluids over long periods and that didn’t help much. 1litre over 4 hours seems to work best for me. Running in 500mls in an hour if I’ve crashed

 

[Research 1st]

ive been on daily IV saline for 3.5 years now and it helps far more than just boosting my BP to help me sit up. My doctors theory is the sudden stretch on the baroreceptors changes the signals they sent. Reading about their role in the body makes a lot of sense but I never see it mentioned in M.E stuff. Has it been looked at?

Hello. Well without trying to be clever, there isn't any ME research as no one has a test yet for ME, so we have to go with CFS and CFS is of course all over the place in terms of findings because diagnosing people with ME on the basis they feel exhausted is going to lasso in various different reasons people feel exhausted, with only subsets of having your issues. Ergo the research on ME is always spare, as it's 'stolen' into other areas of medical research, such as POTS, even if many PWME PWCFS have POTS, or more likely, undiagnosed POTS
and or hypovolemia etc. However...I'll stick with CFS and baroreceptor function:

The observed increase in the sympathetic component of the baroreceptor feedback with even mild orthostatic stress in CFS patients indicates early sympathetic activation and may reflect diminished baroreflex reserve for more severe stressors. These changes further suggest that the baroreflex may have a diminished ability to buffer a variety of internal and external influences on arterial pressure, but particularly those related to upright activity and ambulation, in line with our previous report on the combined effect of orthostatic stress and isometric exercise in CFS patients (Wyller et al. 2008b). The function of the baroreceptor reflex has been addressed in two previous CFS studies. In a group of adolescent CFS patients and controls, Stewart (2000) reported significantly lower α-gain in the HF as well as the LF range among CFS patients, both during rest and during 70° head-up tilt. In adult CFS patients, Peckerman et al. (2003) reported enhanced decline in baroreceptor sensitivity upon standing as compared to controls. However, the sequential method adopted in the latter study does not allow separate estimation of LF and HF gain, making it most sensitive for parasympathetic heart rate control. Differences from the current study might be explained by different inclusion criteria, experimental protocols and mathematical algorithms. Taken together, however, like this study, they indicate a sympathetic predominance of baroreflex heart rate control during orthostatic stress in CFS patients.
Blood pressure variability and closed-loop baroreflex assessment in adolescent chronic fatigue syndrome during supine rest and orthostatic stress.
Eur J Appl Physiol. 2011 Mar; 111(3): 497–507.
Published online 2010 Oct 2. doi: 10.1007/s00421-010-1670-9
Vegard Bruun Wyller,corresponding author1 Riccardo Barbieri, and J. Philip Saul
https://link.springer.com/article/10.1007/s00421-010-1670-9

Patients with CFS had a greater decline in baroreceptor reflex sensitivity (BRS) during standing, although only those with severe CFS were significantly different from the controls.
Source:
Psychosom Med. 2003 Sep-Oct;65(5):889-95.
Baroreceptor reflex and integrative stress responses in chronic fatigue syndrome.
Peckerman A1, LaManca JJ, Qureishi B, Dahl KA, Golfetti R, Yamamoto Y, Natelson BH.
https://insights.ovid.com/pubmed?pmid=14508037

By design, all CFS and POTS patients experienced orthostatic tachycardia, often associated with hypotension. R-R interval and heart rate variability were decreased in CFS and POTS patients compared with control subjects and remained decreased with head-up tilt. Low-frequency (0.05-0.15 Hz) blood pressure variability reflecting vasomotion was increased in CFS and POTS patients compared with control subjects and increased further with head-up tilt. This was associated with depressed baroreflex transfer indicating baroreceptor attenuation through defective vagal efferent response. Only the sympathetic response remained. Heart rate variability declined progressively from normal healthy control subjects through syncope to POTS to CFS patients. Timed breathing and Valsalva maneuver were most often normal in CFS and POTS patients, although abnormalities in select individuals were found. Heart rate and blood pressure regulation in POTS and CFS patients are similar and indicate attenuated efferent vagal baroreflex associated with increased vasomotor tone. Loss of beat-to-beat heart rate control may contribute to a destabilized blood pressure resulting in orthostatic intolerance. The dysautonomia of orthostatic intolerance in POTS and in chronic fatigue are similar.
Source:
Pediatr Res. 2000 Aug;48(2):218-26.
Autonomic nervous system dysfunction in adolescents with postural orthostatic tachycardia syndrome and chronic fatigue syndrome is characterized by attenuated vagal baroreflex and potentiated sympathetic vasomotion.
Stewart JM
https://www.nature.com/articles/pr2000180

This paper discusses the development of a system to measure continuous cardiac baroreceptor measurement during a 45-minute 70-degree head-up tilt (HUT) of five groups of subjects suffering the following: chronic fatigue syndrome (CFS), CFS with fibromyalgia (CFS-FM), CFS with postural orthostatic tachycardia syndrome (CFS-POTS), controls with POTS (CON-POTS), and controls (CON). The duration of the test was 56-minutes, which included a five-minute supine baseline, a 45-minute HUT and a six-minute recovery period. The system was developed in LabView, and can provide a comparative time analyses of weighted BRSI averages. Baroreflex effectiveness index (BEI) was also investigated over the course of lags 0, 1 and 2 as well as an assessment of overall BEI performance between groups.
Source:
Continuous measurement of BRSI in chronic fatigue syndrome
The 26th Annual International Conference of the IEEE Engineering in Medicine and Biology Society.
D.L. Donnelly New Jersey Inst. of Technol., Newark, NJ, USA; R.H. Rockland ; S.S. Reisman ; K.S. Quigley
2004
https://ieeexplore.ieee.org/document/1403306

That's all I can find with a quick search. What I would say is, if you're on daily saline I hope your doctor gave you a blood volume test and if they didn't they should as you may have a condition misdiagnosed as ME CFS.

If you don't have hypovolemia or Addison's disease (misdiagnosed as ME CFS) then they shouldn't just pump
you full of saline daily and leave it! Presumably you've have your antidiuretic hormone measured? (ADH/Vasopression). Also have they run a 24hr Aldosterone, 24hr sodium urine also?

If you have the possibility, I'd considering asking for medical input on having a pituitary 3T MRI brain scan with contrast if your pituitary hormones are out of whack but a standard head MRI shows nothing. Has anyone bothered measuring your hormones extensively? I ask as usually in ME CFS the answer is no! I'm always shocked at the amount of forum members who get useless tests (for ME CFS) like a full blood count, TSH/T4, LFT, U&E's and sent home....for life...with ''it's a mystery you're so sick'', or the old chestnut ''but all your tests are normal''. What doctors mean is, all the tests for the conditions you don't have, are normal - big difference.

 

[BlahBlahBlah]

I don’t have addisons and never had blood volume measured, just assumed it would be low. I’ve been diagnosed with pcos based on hormone results and hashimotosis but that was a long way into my M.E

 

[BlahBlahBlah]

They pumped me with saline and left it as it’s having good results for now (and for the past 3.5years)

 

[Hip]

I did mean the sudden increase in blood volume (due to the saline) puts the stretch on the blood vessels and the receptors.

There was a thread discussing IV saline, and how it is able to produce improvements in symptoms. Some on that thread discounted the benefits as placebo effect, but I am more inclined to believe it is a real effect (though I have never tried IV saline myself).

One point made on that thread was that when you drink water (or saline), it goes straight into the bloodstream, thus the argument was that there should be no difference between getting an IV saline infusion, or drinking the same amount of saline. Hence that was why it was discounted as placebo.

But I guess it is possible that drinking water might be different in some way to IV saline, and perhaps does not stretch the blood vessels as much as IV saline might.

I found this study which examined the changes in blood volume in humans as a result of drinking water.

 

[BlahBlahBlah]

I actually get annoyed with the people (not you) who say drink more. I was drinking over 6 litres a day (and another litre over night)on salt tablets and still dehydrated. I ended up in a&e last week and had a nurse who had a pots patient who totally understood it. If IV fluids didn’t have any more effect on the body’s response to things then any conscious patient seriously ill in resus would be handed a glass of water instead of IV.

My heart rate comes down a lot on it so they can see the difference in things like pulse, BP and my colour but the non visible symptoms that improve obviously aren’t able to be measured as some are such vague symptoms

 

[Hip]

I appreciate what you are saying @BlahBlahBlah, but the mystery for me is why do people find IV saline is different to drinking saline.

Normal saline (also called physiological solution) contains 9 grams of sodium chloride per liter, which is the same salt concentration as is found in the blood. So if you add 9 grams of salt (around 1 heaped teaspoon) to each liter of water you drink, that will have the same salt level as a liter of IV saline.

Are you saying that you have tried putting a heaped teaspoon of salt (9 grams) in each liter you drink to make normal saline, but it is still is not the same as IV saline?

 

[BlahBlahBlah]

I’ve never drunk 9grams of salt per litre. I have 1l of saline IV over 4 hours every 24 hours. We tried running a litre of saline in subcut every 24 hours (so exactly the same amount of saline every day as normal) and I went downhill, back to struggling to sit up or transfer and other symptoms going downhill. Also tried running the fluids in really slowly (can’t remember exactly how slow but almost continuous), again 1 litre every 24 hours and again went back downhill. Speed IV seems to be the key which both of my doctors involved expected to some extent, the one who used to prescribe it prescribed it over 2 hours but I find 4 suits me better

 

[Hip]

Also tried running the fluids in really slowly (can’t remember exactly how slow but almost continuous), again 1 litre every 24 hours and again went back downhill. Speed IV seems to be the key which both of my doctors involved expected to some extent, the one who used to prescribe it prescribed it over 2 hours but I find 4 suits me better

That's very interesting; it does suggest that there is something about the sudden impact of IV saline on the system — such as your doctor's theory that the extra fluid stretches the baroreceptors — which is fundamental to its benefits.

 

[Hip]

I’ve never drunk 9grams of salt per litre.

I might be interesting for you to try drinking 1 liter of water with the same salt content as the IV saline you get over 4 hours, and see if that has any effects or not.

When I was trying out salt plus water for my POTS, I found that the more salt I took, the more weight I put on (as measured by an accurate bathroom scales). Consuming more salt causes the body to retain water, leading to an increased in measure weight.

 

[alex3619]

But I guess it is possible that drinking water might be different in some way to IV saline, and perhaps does not stretch the blood vessels as much as IV saline might.

IV saline is not just water, its water and salt. The increased salt will have an impact too, possibly including lower water excretion, though I currently understand it can also increase water loss, depending on other factors. I have not investigated this much. One thing it might do temporarily is increase absorption of drinking water into the bloodstream, but again I am not sure about this.

In any case salt is often recommended to treat orthostatic intolerance.

I might be interesting for you to try drinking 1 liter of water with the same salt content as the IV saline you get over 4 hours, and see if that has any effects or not.

Yes, sounds like a potentially useful experiment. I do know that drinking one liter of water per hour will temporarily increase my blood volume, I use this trick to make my veins easier to find for phlebotomists.

it does suggest that there is something about the sudden impact of IV saline on the system

Another possibility is the sudden influx of fluid triggers a range of biochemical sensors, and baroreceptors might not be the only things implicated. It looks like an investigation into how the body handles water volume, including sensors and feedback loops, might be useful. It might be, for example, that a sudden influx of salt is the primary trigger. However its important to consider the impact of potassium, and include blood tests, if there is any radical change in salt intake. Regular electrolyte tests that are monitored by a doctor might be helpful.

 

[BlahBlahBlah]

Seeing you mention potassium reminded me I asked to try either ringers lactate or Hartman’s. I did a months this trial of a litre of ringers lactate which is closer to your blood chemistry (my dr was saying he used to give it a lot to patients in emergencies while waiting for blood to arrive). I felt no different to the saline so stopped after the month and went back to just saline.

I really don’t want to try it as I don’t want to mess up my sugars as it’s somethibg I rarely have issue with but I have wondered whether a bad of dextrose would have any effect seeing as some say we have issues moving it in and out of cells. I know our body breaks things down into it but curious as to whether it would make any difference.


Re drinking litre of water with that much salt. I don’t know how much salt I was having before, I was on 6 slow sodium tablets a day and had insane salt cravings so used to add salt to everything and occasionally gave in and would just put salt on my hand to lick. One night I did find myself looking up salt lick blocks for horses on amazon lol! I found fludrocortison, slow sodium and drinking lots reduced my heart rate by about 10bpm and reduced how breathless I got when sitting up or crawling but still could only manage trips to the bathroom

 

[BlahBlahBlah]

I have blood tests every few months to check ectrolytes and make sure my kidneys are handling the extra salt, so far so good

 

[Hip]

Another possibility is the sudden influx of fluid triggers a range of biochemical sensors,

Yes, that's one thought I had too. Given that the latest studies indicate POTS may be an autoimmune disease caused by autoantibodies to the adrenergic and muscarinic acetylcholine receptors (see this list of autoantibodies in ME/CFS), I was wondering whether the sudden influx of fluid might in some way disable these autoantibodies in the blood, and in that way improve POTS temporarily.