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H2S is cardioprotective but impairs sympathetic flow

Discussion in 'The Gut: De Meirleir & Maes; H2S; Leaky Gut' started by guest, Jul 11, 2010.

  1. guest

    guest Guest

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    Studies:


    Recent evidence indicates Down's Syndrome trisomy patients may
    overproduce amyloid beta but are also protected from cardiovascular
    disease. I think this may be due to the fact that Down's patients also
    have an extra copy of the H2S-producing cystathionine beta synthase.
    AND H2S is cardioprotective. Turns out, H2S can lower sympathetic tone.
    I think this might be a reason the cardiovascular system appears
    protected in Down's Syndrome. It's also suspicious that in colitis,
    patients can't detox H2S *and* they have impaired sympathetic flow into
    the gut.

    Neurochem Res. 2009 Mar;34(3):400-6. Epub 2008 Jul 16
    *
    Effect of hydrogen sulfide on sympathetic neurotransmission and
    catecholamine levels in isolated porcine iris-ciliary body.
    Kulkarni KH, Monjok EM, Zeyssig R, Kouamou G, Bongmba ON, Opere CA, Njie
    YF, Ohia SE.
    Department of Pharmacological and Pharmaceutical Sciences, College of
    Pharmacy, University of Houston, Houston, TX 77204, USA.

    In the present study, we investigated the pharmacological action of
    hydrogen sulfide (H2S, using sodium hydrosulfide, NaHS, and/or sodium
    sulfide, Na2S as donors) on sympathetic neurotransmission from isolated,
    superfused porcine iris-ciliary bodies. We also examined the effect of
    H2S on norepinephrine (NE), dopamine and epinephrine concentrations in
    isolated porcine anterior uvea. Release of [3H]NE was triggered by
    electrical field stimulation and basal catecholamine concentrations was
    measured by high performance liquid chromatography (HPLC). Both NaHS and
    Na2S caused a concentration-dependent inhibition of electrically evoked
    [3H]NE release from porcine iris-ciliary body without affecting basal
    [3H]NE efflux. The inhibitory action of H2S donors on NE release was
    attenuated by aminooxyacetic acid (AOA) and propargyglycine (PAG),
    inhibitors of cystathionine beta-synthase (CBS) and cystathionine
    gamma-lyase (CSE), respectively. With the exception of dopamine, NaHS
    caused a concentration-dependent reduction in endogenous NE and
    epinephrine concentrations in isolated iris-ciliary bodies. We conclude
    that H2S can inhibit sympathetic neurotransmission from isolated porcine
    anterior uvea, an effect that is dependent, at least in part, on
    intramural biosynthesis of this gas. Furthermore, the observed action of
    H2S donors on sympathetic transmission may be due to a direct action of
    this gas on neurotransmitter pools.

    Publication Types:
    * In Vitro

    PMID: 18629636

    The formation of H2S from cyst(e)ine is catalyzed by three enzymes,
    cystathionine beta synthase, cystathionase, and 3-mercaptopyruvate
    sulfurtransferase. In the liver, kidney, enterocytes and vascular smooth
    muscle cells, H2S is principally synthesized by cystathionase. In
    contrast, it is synthesized by cystathionine beta synthase in the brain
    and partially by 3-mercaptopyruvate sulfurtransferase in cardiac tissue.
    H2S is catabolized, essentially in mitochondria by thiosulfate
    reductase. The sulfite generated is then oxidized to sulfate by sulfite
    oxidase. The amount of thiosulfate excreted in the urine is the best
    indicator of H2S biosynthesis, together with sulfhemoglobin
    determination in erythrocytes. H2S acts as a neuromodulator in the
    brain, increasing responses mediated by NMDA receptors, facilitating the
    induction of long-term potentialization in the hippocampus. H2S also
    acts as a vasodilator, acting directly on ATP-dependent potassium
    channels in vascular smooth muscle cells. The concentration of H2S is
    abnormally low in the brains of subjects with Alzheimer's disease, due
    to changes in the concentration of the physiological activator of
    cystathionine beta synthase. The overproduction of H2S described in
    subjects with Down's syndrome probably results from the overproduction
    of cystathionine beta synthase, as the gene encoding this protein is
    located on chromosome 21 [PMID 15329822]
     
  2. Mark K

    Mark K

    Messages:
    26
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    0
    california
    good post diesel but its too much for my brain to help answer it :)
     
  3. richvank

    richvank Senior Member

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    Hi, Diesel.

    "Sympathetic flow" refers to the flow of nerve impulses in the sympathetic nervous system. Normally, there is a balance between the sympathetic and parasympathetic arms of the autonomic nervous system. The parasympathetic system promotes the"housekeeping" functions in the body that take place when it is not under stress, such as processing food in the digestive system. In CFS, there is a dominance of the sympathetic over the parasympathetic system, and that interferes with some of the things that need to be done in the body. H2S may actually help in this situation, but the problem is that many PWCs have a lot of sulfate-reducing bacteria in their guts, and these generate far too much H2S, so that toxic effects are produced.

    Dr. Kenny de Meirleir is at the forefront of treating this situation, and I am looking forward to his publications about this. As you probably know, his lab in Belgium offers a test for H2S in the urine, and he tests for and treats sulfate-reducing bacteria in the gut. He is reporting good results from this.

    Best regards,

    Rich
     
  4. mhj

    mhj

    Messages:
    21
    Likes:
    7
    Norway
    The positive effect is due to people with Downs syndrom, because of the extra chromocome.

    For us H2S is toxic and as it says:

    This lead to imbalance in the sympathetic and parasympathetic of the autonomic nervous system. A massive on:Retro mad: , and as Rich said sympathetic response is increased.

    Due to:

    is not surprising because of the autonomic imbalance and immunodysfunctional system.

    If you want to increase sympathical flow, you have to rest............

    Rich you said:
    What publications? Has he said so... when?
    -------------------------------------------------------------------------------------
    Increased D-Lactic Acid Intestinal Bacteria in Patients with Chronic Fatigue Syndrome

    http://iv.iiarjournals.org/content/23/4/621.abstract

    Regards for now ;)
     

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