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Phenylephrine alteration of cerebral blood flow during orthostasis: effect on n-back performance in chronic fatigue syndrome, 2014, Medow et al

Discussion in 'ME/CFS research news' started by Hoopoe, Aug 1, 2022.

  1. Hoopoe

    Hoopoe Senior Member (Voting Rights)

    Messages:
    5,255
    My summary
    In CFS subjects, phenylephrine reduces the decrease in cerebral blood flow that occurs during head up tilt testing. This had a positive impact on performance in a cognitive test.

    The study might hint at how to treat ME/CFS and at the underlying mechanisms of reduced cerebral blood flow. I found this by looking for a relationship between myogenic vasoconstriction and ME/CFS.

    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4233252/
     
    Last edited: Aug 1, 2022
    ahimsa, mango, Mij and 3 others like this.
  2. Snow Leopard

    Snow Leopard Senior Member (Voting Rights)

    Messages:
    3,827
    Location:
    Australia
    The baroreceptor sensitivity effect has been known for decades in POTS - but not necessarily ME/CFS.

    A side note, but increased sensitivity to the baroreflex may explain why in some people the other normal cardiac reflexes are unable to raise their heart rate to near the age/sex predicted rate ('chronotropic incompetence')
     
    FMMM1 likes this.
  3. Andy

    Andy Committee Member

    Messages:
    21,963
    Location:
    Hampshire, UK
    Abstract

    Chronic fatigue syndrome (CFS) with orthostatic intolerance is characterized by neurocognitive deficits and impaired working memory, concentration, and information processing. In CFS, upright tilting [head-up tilt (HUT)] caused decreased cerebral blood flow velocity (CBFv) related to hyperventilation/hypocapnia and impaired cerebral autoregulation; increasing orthostatic stress resulted in decreased neurocognition. We loaded the baroreflex with phenylephrine to prevent hyperventilation and performed n-back neurocognition testing in 11 control subjects and 15 CFS patients. HUT caused a significant increase in heart rate (109.4 ± 3.9 vs. 77.2 ± 1.6 beats/min, P < 0.05) and respiratory rate (20.9 ± 1.7 vs. 14.2 ± 1.2 breaths/min, P < 0.05) and decrease in end-tidal CO2 (ETCO2; 42.8 ± 1.2 vs. 33.9 ± 1.1 Torr, P < 0.05) in CFS vs. control. HUT caused CBFv to decrease 8.7% in control subjects but fell 22.5% in CFS. In CFS, phenylephrine prevented the HUT-induced hyperventilation/hypocapnia and the significant drop in CBFv with HUT (−8.1% vs. −22.5% untreated). There was no difference in control subject n-back normalized response time (nRT) comparing supine to HUT (106.1 ± 6.9 vs. 97.6 ± 7.1 ms at n = 4), and no difference comparing control to CFS while supine (97.1 ± 7.1 vs 96.5 ± 3.9 ms at n = 4). However, HUT of CFS subjects caused a significant increase in nRT (148.0 ± 9.3 vs. 96.4 ± 6.0 ms at n = 4) compared with supine. Phenylephrine significantly reduced the HUT-induced increase in nRT in CFS to levels similar to supine (114.6 ± 7.1 vs. 114.6 ± 9.3 ms at n = 4). Compared with control subjects, CFS subjects are more sensitive both to orthostatic challenge and to baroreflex/chemoreflex-mediated interventions. Increasing blood pressure with phenylephrine can alter CBFv. In CFS subjects, mitigation of the HUT-induced CBFv decrease with phenylephrine has a beneficial effect on n-back outcome.
     

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