Prolonged acetylcholine-induced vasodilatation in the peripheral microcirculation of patients with chronic fatigue syndrome

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    Abstract

    Although the aetiology of chronic fatigue syndrome (CFS) is unknown, there have
    been a number of reports of blood flow abnormalities within the cerebral circulation and systemic blood pressure defects manifesting as orthostatic intolerance. Neither of these phenomena has been explained adequately, but recent reports have linked cerebral hypoperfusion to abnormalities in cholinergic metabolism. Our group has previously reported enhanced skin vasodilatation in response to cumulative doses of transdermally applied acetylcholine (ACh), implying an alteration of peripheral cholinergic function. To investigate this further, we studied the time course of ACh-induced vasodilatation following a single dose of ACh in 30 patients with CFS and 30 age- and gender-matched healthy control subjects. No differences in peak blood flow was seen between patients and controls, but the time taken for the ACh response to recover to baseline was significantly longer in the CFS patients than in control subjects. The time taken to decay to 75% of the peak response in patients and controls was 13.7 ± 11.3 versus 8.9 ± 3.7 min (P = 0.03), respectively, and time
    taken to decay to 50% of the peak response was 24.5 ± 18.8 versus 15.1 ± 8.9 min (P = 0.03), respectively. Prolongation of ACh-induced vasodilatation is suggestive of a disturbance to cholinergic pathways, perhaps within the vascular endothelium of patients with CFS, and might be related to some of the unusual vascular symptoms, such as hypotension and orthostatic intolerance, which are characteristic of the condition.
    Original languageEnglish
    Pages (from-to)282-285
    Number of pages4
    JournalClinical Physiology and Functional Imaging
    Volume23
    Issue number5
    DOIs
    Publication statusPublished - Sep 2003

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    Chronic Fatigue Syndrome
    Microcirculation
    Vasodilation
    Acetylcholine
    Orthostatic Intolerance
    Cholinergic Agents
    Cerebrovascular Circulation
    Vascular Endothelium
    Hypotension
    Blood Vessels
    Healthy Volunteers
    Blood Pressure
    Skin

    Cite this

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    title = "Prolonged acetylcholine-induced vasodilatation in the peripheral microcirculation of patients with chronic fatigue syndrome",
    abstract = "Although the aetiology of chronic fatigue syndrome (CFS) is unknown, there havebeen a number of reports of blood flow abnormalities within the cerebral circulation and systemic blood pressure defects manifesting as orthostatic intolerance. Neither of these phenomena has been explained adequately, but recent reports have linked cerebral hypoperfusion to abnormalities in cholinergic metabolism. Our group has previously reported enhanced skin vasodilatation in response to cumulative doses of transdermally applied acetylcholine (ACh), implying an alteration of peripheral cholinergic function. To investigate this further, we studied the time course of ACh-induced vasodilatation following a single dose of ACh in 30 patients with CFS and 30 age- and gender-matched healthy control subjects. No differences in peak blood flow was seen between patients and controls, but the time taken for the ACh response to recover to baseline was significantly longer in the CFS patients than in control subjects. The time taken to decay to 75{\%} of the peak response in patients and controls was 13.7 ± 11.3 versus 8.9 ± 3.7 min (P = 0.03), respectively, and timetaken to decay to 50{\%} of the peak response was 24.5 ± 18.8 versus 15.1 ± 8.9 min (P = 0.03), respectively. Prolongation of ACh-induced vasodilatation is suggestive of a disturbance to cholinergic pathways, perhaps within the vascular endothelium of patients with CFS, and might be related to some of the unusual vascular symptoms, such as hypotension and orthostatic intolerance, which are characteristic of the condition.",
    author = "Faisel Khan and Vance Spence and Gwen Kennedy and Belch, {Jill J. F.}",
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    T1 - Prolonged acetylcholine-induced vasodilatation in the peripheral microcirculation of patients with chronic fatigue syndrome

    AU - Khan, Faisel

    AU - Spence, Vance

    AU - Kennedy, Gwen

    AU - Belch, Jill J. F.

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    N2 - Although the aetiology of chronic fatigue syndrome (CFS) is unknown, there havebeen a number of reports of blood flow abnormalities within the cerebral circulation and systemic blood pressure defects manifesting as orthostatic intolerance. Neither of these phenomena has been explained adequately, but recent reports have linked cerebral hypoperfusion to abnormalities in cholinergic metabolism. Our group has previously reported enhanced skin vasodilatation in response to cumulative doses of transdermally applied acetylcholine (ACh), implying an alteration of peripheral cholinergic function. To investigate this further, we studied the time course of ACh-induced vasodilatation following a single dose of ACh in 30 patients with CFS and 30 age- and gender-matched healthy control subjects. No differences in peak blood flow was seen between patients and controls, but the time taken for the ACh response to recover to baseline was significantly longer in the CFS patients than in control subjects. The time taken to decay to 75% of the peak response in patients and controls was 13.7 ± 11.3 versus 8.9 ± 3.7 min (P = 0.03), respectively, and timetaken to decay to 50% of the peak response was 24.5 ± 18.8 versus 15.1 ± 8.9 min (P = 0.03), respectively. Prolongation of ACh-induced vasodilatation is suggestive of a disturbance to cholinergic pathways, perhaps within the vascular endothelium of patients with CFS, and might be related to some of the unusual vascular symptoms, such as hypotension and orthostatic intolerance, which are characteristic of the condition.

    AB - Although the aetiology of chronic fatigue syndrome (CFS) is unknown, there havebeen a number of reports of blood flow abnormalities within the cerebral circulation and systemic blood pressure defects manifesting as orthostatic intolerance. Neither of these phenomena has been explained adequately, but recent reports have linked cerebral hypoperfusion to abnormalities in cholinergic metabolism. Our group has previously reported enhanced skin vasodilatation in response to cumulative doses of transdermally applied acetylcholine (ACh), implying an alteration of peripheral cholinergic function. To investigate this further, we studied the time course of ACh-induced vasodilatation following a single dose of ACh in 30 patients with CFS and 30 age- and gender-matched healthy control subjects. No differences in peak blood flow was seen between patients and controls, but the time taken for the ACh response to recover to baseline was significantly longer in the CFS patients than in control subjects. The time taken to decay to 75% of the peak response in patients and controls was 13.7 ± 11.3 versus 8.9 ± 3.7 min (P = 0.03), respectively, and timetaken to decay to 50% of the peak response was 24.5 ± 18.8 versus 15.1 ± 8.9 min (P = 0.03), respectively. Prolongation of ACh-induced vasodilatation is suggestive of a disturbance to cholinergic pathways, perhaps within the vascular endothelium of patients with CFS, and might be related to some of the unusual vascular symptoms, such as hypotension and orthostatic intolerance, which are characteristic of the condition.

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