Review: 'Through the Shadowlands’ describes Julie Rehmeyer's ME/CFS Odyssey
I should note at the outset that this review is based on an audio version of the galleys and the epilogue from the finished work. Julie Rehmeyer sent me the final version as a PDF, but for some reason my text to voice software (Kurzweil) had issues with it. I understand that it is...
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Blunted Cerebral Blood Flow Velocity, Nitric Oxide in POTS

Discussion in 'Other Health News and Research' started by redrachel76, Jun 12, 2014.

  1. redrachel76

    redrachel76 Senior Member

    Blunted Cerebral Blood Flow Velocity in Response to a Nitric Oxide
    Donor in Postural Tachycardia Syndrome (POTS)
    Andrew Thomas Del Pozzi, Akash Pandey, Marvin S. Medow, Zachary R.
    Messer, Julian M. Stewart
    American Journal of Physiology - Heart and Circulatory
    PhysiologyPublished 30 May 2014Vol. no. DOI:
    Cognitive deficits are characteristic of postural tachycardia syndrome
    (POTS). Intact nitrergic nitric oxide (NO) is important to cerebral
    blood flow (CBF) regulation, to neurovascular coupling, and to
    cognitive efficacy. POTS patients often experience defective (NO)
    mediated vasodilation caused by oxidative stress. We previously showed
    dilation of the middle cerebral artery (MCA) in response to a bolus
    administration of the NO donor sodium nitroprusside (SNP) in healthy
    volunteers. We hypothesized a blunted MCA response to SNP in POTS.
    Using combined transcranial-Doppler-ultrasound to measure CBF velocity
    (CBFv), and near-infrared spectroscopy (NIRS) to measure cerebral
    hemoglobin oxygenation while supine. The responses of 17 POTS patients
    were compared with 12 healthy controls (ages 14-28). CBFv in POTS and
    control were not different at baseline (75 ± 3 vs. 71 ±2 cm • s-1 P =
    0.31) and decreased to a lesser degree with SNP in POTS (to 71 ± 3 vs
    62 ± 2 cm • s-1; P = 0.02). The changes in total and oxygenated
    hemoglobin (8.83 ± 0.45 and 8.13 ± 0.48 µmol/kg tissue) were markedly
    reduced in POTS compared to control (14.2 ± 1.4 and 13.6 ± 1.6 µmol/kg
    tissue), primarily due to increased venous efflux. The data indicate
    reduced cerebral oxygenation, blunting of cerebral arterial
    vasodilation and heightened cerebral venodilation. We conclude based
    on the current study outcomes decreased bioavailability of NO is
    apparent in the vascular beds resulting in a down regulation of NO
    receptor sites, ultimately leading to blunted responses to exogenous
    taniaaust1 and merylg like this.

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