Blunted cerebral blood flow velocity in response to a nitric oxide donor in postural tachycardia syndrome.

摘要: Cognitive deficits are characteristic of postural tachycardia syndrome (POTS). Intact nitrergic nitric oxide (NO) is important to cerebral blood flow (CBF) regulation, neurovascular coupling, and cognitive efficacy. POTS patients often experience defective NO-mediated vasodilation caused by oxidative stress. We have previously shown dilation the middle artery in response a bolus administration NO donor sodium nitroprusside (SNP) healthy volunteers. In present study, we hypothesized blunted SNP POTS. used combined transcranial Doppler-ultrasound measure CBF velocity near-infrared spectroscopy hemoglobin oxygenation while subjects were supine position. The responses 17 compared with 12 control (age: 14–28 yr). not different at baseline (75 ± 3 vs. 71 2 cm/s, P = 0.31) decreased lesser degree (to 62 0.02). Changes total oxygenated (8.83 0.45 8.13 0.48 μmol/kg tissue) markedly reduced (14.2 1.4 13.6 1.6 tissue), primarily due increased venous efflux. data indicate oxygenation, blunting arterial vasodilation, heightened venodilation. conclude, based on study outcomes, that bioavailability apparent vascular beds, resulting downregulation receptor sites, ultimately leading exogenous NO.