Low-level tragus stimulation improves autoantibody-induced hyperadrenergic postural tachycardia syndrome in rabbits 2023 Guo et al

Background
Recent studies have demonstrated that antiadrenergic autoantibodies are involved in the pathophysiology of postural orthostatic tachycardia syndrome (POTS).

Objective
The purpose of this study was to test the hypothesis that transcutaneous low-level tragus stimulation (LLTS) ameliorates autoantibody-induced autonomic dysfunction and inflammation in a rabbit model of autoimmune POTS.

Methods
Six New Zealand white rabbits were co-immunized with peptides from the α1-adrenergic and β1-adrenergic receptors to produce sympathomimetic antibodies. The tilt test was performed on conscious rabbits before immunization, 6 weeks after immunization, and 10 weeks after immunization with 4-week daily LLTS treatment. Each rabbit served as its own control.

Results
An enhanced postural heart rate increase in the absence of significant change in blood pressure was observed in immunized rabbits, confirming our previous report. Power spectral analysis of heart rate variability during the tilt test showed a predominance of sympathetic over parasympathetic activity in immunized rabbits as reflected by markedly increased low-frequency power, decreased high-frequency power, and increased low-to-high-frequency ratio. Serum inflammatory cytokines were also significantly increased in immunized rabbits. LLTS suppressed the postural tachycardia, improved the sympathovagal balance with increased acetylcholine secretion, and attenuated the inflammatory cytokine expression. Antibody production and activity were confirmed with in vitro assays, and no antibody suppression by LLTS was found in this short-term study.

Conclusion
LLTS improves cardiac autonomic imbalance and inflammation in a rabbit model of autoantibody-induced hyperadrenergic POTS, suggesting that LLTS may be used as a novel neuromodulation therapy for POTS.

Open access, https://www.heartrhythmopen.com/article/S2666-5018(22)00350-6/fulltext

 

Sorry I just hope these rabbits are okay x

 

Worth remembering that rabbit have very big ears and don't often stand up.

 

I see a lot of trials to "stimulate" this and that nerve, but there doesn't seem to be much basic knowledge about the general mechanism happening here.

Seems a bit Frankenstein, pour some electricity and see what happens. Except it's more add electricity, then look if it affects a specific thing.

 

Snakes on a plane? How about...rabbits on a tilt table!

 

If there is a mechanism.

I am increasingly sceptical that the tragus branch of the vagus nerve is anything other than some skin sensory fibres that at some point in embryogenesis got packaged with the stomach nerve.

The facial nerve includes fibres that move the face - smiling etc. and taste fibres. They really have nothing to do with each other except they pass through the same openings. For some reason the ear ends up with fibres doing various jobs being co-packaged in various nerve trunks - eighth, seventh, fifth, tenth.

There are reflexes that run in nerves like vagus - so stimulating input fibres can have effects through the output fibres. Stimulating the ear clearly does not directly stimulate vagal output fibres as a neck device could. But reflexes can also run in different nerves. Eating curry can make you sweat - seventh to tenth maybe. Smells can make you retch (first to tenth and more?). Tickling your tragus does not do much as far as I can see.

 

Link to a 2019 paper by the same department which explains why they used rabbits and describes the tilting process.

Adrenergic Autoantibody‐Induced Postural Tachycardia Syndrome in Rabbits

https://www.ahajournals.org/doi/10.1161/JAHA.119.013006