Blunted Cerebral Blood Flow Velocity in Response to a Nitric Oxide
Donor in Postural Tachycardia Syndrome (POTS)
Andrew Thomas Del Pozzi, Akash Pandey, Marvin S. Medow, Zachary R.
Messer, Julian M. Stewart
American Journal of Physiology - Heart and Circulatory
PhysiologyPublished 30 May 2014Vol. no. DOI:
10.1152/ajpheart.00194.2014
Abstract
Cognitive deficits are characteristic of postural tachycardia syndrome
(POTS). Intact nitrergic nitric oxide (NO) is important to cerebral
blood flow (CBF) regulation, to neurovascular coupling, and to
cognitive efficacy. POTS patients often experience defective (NO)
mediated vasodilation caused by oxidative stress. We previously showed
dilation of the middle cerebral artery (MCA) in response to a bolus
administration of the NO donor sodium nitroprusside (SNP) in healthy
volunteers. We hypothesized a blunted MCA response to SNP in POTS.
Using combined transcranial-Doppler-ultrasound to measure CBF velocity
(CBFv), and near-infrared spectroscopy (NIRS) to measure cerebral
hemoglobin oxygenation while supine. The responses of 17 POTS patients
were compared with 12 healthy controls (ages 14-28). CBFv in POTS and
control were not different at baseline (75 ± 3 vs. 71 ±2 cm • s-1 P =
0.31) and decreased to a lesser degree with SNP in POTS (to 71 ± 3 vs
62 ± 2 cm • s-1; P = 0.02). The changes in total and oxygenated
hemoglobin (8.83 ± 0.45 and 8.13 ± 0.48 µmol/kg tissue) were markedly
reduced in POTS compared to control (14.2 ± 1.4 and 13.6 ± 1.6 µmol/kg
tissue), primarily due to increased venous efflux. The data indicate
reduced cerebral oxygenation, blunting of cerebral arterial
vasodilation and heightened cerebral venodilation. We conclude based
on the current study outcomes decreased bioavailability of NO is
apparent in the vascular beds resulting in a down regulation of NO
receptor sites, ultimately leading to blunted responses to exogenous
NO.
Donor in Postural Tachycardia Syndrome (POTS)
Andrew Thomas Del Pozzi, Akash Pandey, Marvin S. Medow, Zachary R.
Messer, Julian M. Stewart
American Journal of Physiology - Heart and Circulatory
PhysiologyPublished 30 May 2014Vol. no. DOI:
10.1152/ajpheart.00194.2014
Abstract
Cognitive deficits are characteristic of postural tachycardia syndrome
(POTS). Intact nitrergic nitric oxide (NO) is important to cerebral
blood flow (CBF) regulation, to neurovascular coupling, and to
cognitive efficacy. POTS patients often experience defective (NO)
mediated vasodilation caused by oxidative stress. We previously showed
dilation of the middle cerebral artery (MCA) in response to a bolus
administration of the NO donor sodium nitroprusside (SNP) in healthy
volunteers. We hypothesized a blunted MCA response to SNP in POTS.
Using combined transcranial-Doppler-ultrasound to measure CBF velocity
(CBFv), and near-infrared spectroscopy (NIRS) to measure cerebral
hemoglobin oxygenation while supine. The responses of 17 POTS patients
were compared with 12 healthy controls (ages 14-28). CBFv in POTS and
control were not different at baseline (75 ± 3 vs. 71 ±2 cm • s-1 P =
0.31) and decreased to a lesser degree with SNP in POTS (to 71 ± 3 vs
62 ± 2 cm • s-1; P = 0.02). The changes in total and oxygenated
hemoglobin (8.83 ± 0.45 and 8.13 ± 0.48 µmol/kg tissue) were markedly
reduced in POTS compared to control (14.2 ± 1.4 and 13.6 ± 1.6 µmol/kg
tissue), primarily due to increased venous efflux. The data indicate
reduced cerebral oxygenation, blunting of cerebral arterial
vasodilation and heightened cerebral venodilation. We conclude based
on the current study outcomes decreased bioavailability of NO is
apparent in the vascular beds resulting in a down regulation of NO
receptor sites, ultimately leading to blunted responses to exogenous
NO.