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Reduced Sympathetic Baroreflex Sensitivity in Individuals with Multiple Sclerosis During the Valsalva Maneuver

˜The œFASEB journal(2020)

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摘要
Multiple sclerosis (MS) is a neurodegenerative autoimmune disease characterized by demyelination in central nervous system leading to potential impairments in the autonomic control of cardiovascular function. We have previously demonstrated individuals with MS exhibit a diminished ability to increase blood pressure in response to a simulated hypotensive stimulus (carotid neck pressure) compared with healthy controls likely due to impaired sympathetic modulation of the vasculature. The aim of the current investigation was to test the hypothesis that individuals with MS have a blunted muscle sympathetic nerve response (MSNA) to drops in arterial blood pressure induced via a Valsalva maneuver compared to matched healthy controls. Four patients with relapsing‐remitting MS (2 females/2 males, EDSS < 4) and 4 sex‐, age‐ and mass‐matched healthy controls were instrumented for MSNA (peroneal nerve), arterial blood pressure (Finometer), and heart rate. Participants performed a Valsalva maneuver (VM) at 40 mmHg for a 15 s after a normal inspiration. Sympathetic baroreflex function was assessed by relating all sympathetic burst occurring during the 15 s straining period of the VM to the maximum fall in DBP measured from highest values (Phase I) to the nadir prior to the end of the VM (Phase III). Drops in diastolic pressure during the Valsalva were similar between groups (MS: −31 ± 10 mmHg: CON: −25 ± 15 mmHg; P = 0.30). Individuals with MS produced less total MSNA bursts during the 15 s VM compared to healthy controls (MS: 8.3 ± 4.1 bursts/15 s; CON: 15.0 ± 4.1 bursts/15 s; P = 0.003). Sympathetic baroreflex sensitivity was reduced in individuals with MS (MS: −0.32 ± 0.25 bursts/15 s/mmHg) vs. CON: −0.77 ± 0.43 bursts/15 s/mmHg; P = 0.048). Individuals with MS have a reduced ability to increase MSNA in response to decreases in blood pressure during the VM confirming previous speculations of abnormal sympathetic baroreflex control of arterial blood pressure in this clinical population.
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