Tag: beta blockers

Challenges of memory enhancers

Abstract:

40 per cent of people over the age of 65 experience some form of memory loss, called as the age related memory impairment. This might be due to hormone and proteins (Growth factors) which repair the brain cells decline with age. Certain conditions such as age, stress, disease and excessive emotional response may lead to loss of memory, loss of learning ability and altered mood and behaviour. These conditions may be treated by using nootropic agents which can help to improve learning abilities and memory.

Source: Chaudhry, Sunil. Challenges of memory enhancers. Annals of Geriatric Education and Medical Sciences; 2020/08/22. https://www.agems.in/article-details/11990 (Full text)

IgG stimulated β2 adrenergic receptor activation is attenuated in patients with ME/CFS

Abstract:

Background: There is emerging evidence of a network of natural autoantibodies against GPCR which is dysregulated in various diseases. β2 adrenergic and M3 and M4 cholinergic receptor (β2 AdR and M3/4 mAChR) antibodies were found to be elevated in a subset of ME/CFS patients.

Methods: We comparatively analyzed the effects of polyclonal IgG on β2 AdR signaling and immune cell function in vitro. 16 IgG fractions were isolated from serum of 5 ME/CFS patients with elevated (CFS AABhigh) and 5 with normal levels (CFS AABnorm) of β2 AdR autoantibodies, and from 6 healthy controls (HC). The effect of each IgG on β-arrestin recruitment and cAMP production in β2 AdR and M3/4R reporter cell lines was studied. Further effect of each IgG on human monocyte cytokine production and on T cell proliferation in vitro was analyzed. In addition, studies on cytokine production in β2 AdR wild type and knockout mice splenocytes incubated with IgG fractions were performed.

Results: We found that IgGs from HC could stimulate β-arrestin recruitment and cAMP production in β2 AdR reporter cell lines whereas IgGs from CFS AABhigh had no effect. The IgG-mediated activation of β2 AdR was confirmed in β2 AdR wt and ko mice. In accordance with previous studies IgG fractions from HC inhibited LPS-induced TNFα and stimulated LPS-induced IL-10 production of monocytes. Further IgG fractions from HC enhanced proliferation of T-cells stimulated with anti-CD3/CD28. IgG fractions from CFS AABhigh patients had no significant effect on both cytokine production and T cell proliferation, while IgGs from CFS AABnorm had an intermediate effect. We could also observe that IgG can modulate the signaling of β2 AdR ligands isoprenline and propranolol.

Conclusions: We provide evidence that IgG can activate β2 AdR. The β2 AdR activation by IgG is attenuated in ME/CFS patients. A dysregulation of β2 AdR function could explain many symptoms of ME/CFS.

Source: Hartwig J et al. IgG stimulated β2 adrenergic receptor activation is attenuated in patients with ME/CFS. Brain, Behaviour and Immunity [Epub ahead of print]. https://www.sciencedirect.com/science/article/pii/S2666354620300120 (Full article)

Treatment of chronic fatigue and orthostatic intolerance with propranolol

Abstract:

We describe the effect of propranolol in an adolescent with chronic fatigue syndrome and orthostatic intolerance. Our observations suggest that the head-up tilt-test and beta-blocker treatment might be considered in patients with chronic fatigue syndrome and that enhanced sympathetic nervous activity might be part of the underlying pathophysiology.

 

Source: Wyller VB, Thaulow E, Amlie JP. Treatment of chronic fatigue and orthostatic intolerance with propranolol. J Pediatr. 2007 Jun;150(6):654-5. https://www.ncbi.nlm.nih.gov/pubmed/17517256

 

The relationship between neurally mediated hypotension and the chronic fatigue syndrome

Abstract:

OBJECTIVE: To compare the clinical symptoms and response evoked by upright tilt-table testing in healthy individuals and in a sample of those satisfying strict criteria for chronic fatigue syndrome.

DESIGN: Case-comparison study with mean (SD) follow-up of 24 (5) weeks.

SETTING: Tertiary care hospital.

PATIENTS AND OTHER PARTICIPANTS: A sample of 23 patients with chronic fatigue syndrome (five men and 18 women; mean age, 34 years), each of whom fulfilled the strict diagnostic criteria of the Centers for Disease Control and Prevention, was recruited from regional chronic fatigue support groups and from the investigators’ clinical practices. There were 14 healthy controls (four men and 10 women; mean age, 36 years).

INTERVENTIONS: Each subject completed a symptom questionnaire and underwent a three-stage upright tilt-table test (stage 1, 45 minutes at 70 degrees tilt; stage 2, 15 minutes at 70 degrees tilt with 1 to 2 micrograms/min of isoproterenol; and stage 3, 10 minutes at 70 degrees with 3 to 4 micrograms/min of isoproterenol). Patients were offered therapy with fludrocortisone, beta-adrenergic blocking agents, and disopyramide, alone or in combination, directed at neurally mediated hypotension.

MAIN OUTCOME MEASURES: Response to upright tilt and scores on symptom questionnaires prior to and during follow-up.

RESULTS: An abnormal response to upright tilt was observed in 22 of 23 patients with chronic fatigue syndrome vs four of 14 controls (P < .001). Seventy percent of chronic fatigue syndrome patients, but no controls, had an abnormal response during stage 1 (P < .001). Nine patients reported complete or nearly complete resolution of chronic fatigue syndrome symptoms after therapy directed at neurally mediated hypotension.

CONCLUSIONS: We conclude that chronic fatigue syndrome is associated with neurally mediated hypotension and that its symptoms may be improved in a subset of patients by therapy directed at this abnormal cardiovascular reflex.

Comment in:

Chronic fatigue syndrome and neurally mediated hypotension. [JAMA. 1996]

Orthostatic hypotension and chronic fatigue syndrome. [JAMA. 2001]

Chronic fatigue syndrome and neurally mediated hypotension. [JAMA. 1996]

Chronic fatigue syndrome and neurally mediated hypotension. [JAMA. 1996]

 

Source: Bou-Holaigah I, Rowe PC, Kan J, Calkins H. The relationship between neurally mediated hypotension and the chronic fatigue syndrome. JAMA. 1995 Sep 27;274(12):961-7. http://www.ncbi.nlm.nih.gov/pubmed/7674527