Fersiynau electronig

Dangosydd eitem ddigidol (DOI)

  • Ryan L Hoiland
    University of British Columbia
  • Joshua C Tremblay
    University of British Columbia, Okanagan
  • Benjamin S Stacey
    University of South Wales
  • Geoff B Coombs
    University of British Columbia, Okanagan
  • Daniela Nowak-Flück
    University of British Columbia, Okanagan
  • Michael M Tymko
    University of British Columbia, Okanagan
  • Alexander Patrician
    University of British Columbia, Okanagan
  • Mike Stembridge
    Cardiff Metropolitan University
  • Connor A Howe
    University of British Columbia, Okanagan
  • Damian M Bailey
    University of South Wales
  • Daniel J Green
    University of Western Australia
  • David B MacLeod
    Duke University Medical Center
  • Philip N Ainslie
    University of British Columbia, Okanagan

Changes in haematocrit influence nitric oxide signalling through alterations in shear stress stimuli and haemoglobin scavenging of nitric oxide; these two regulatory factors have not been assessed simultaneously Isovolumic haemodilution led to a marked increase in brachial artery flow-mediated dilatation in humans The increase in flow-mediated dilatation occurred in the face of an unaltered shear stress stimulus for vasodilatation and reduced resting steady-state nitric oxide levels in the blood Collectively, our data point towards haemoglobin scavenging of nitric oxide as a key regulatory factor of brachial flow-mediated dilatation and highlight the importance of the simultaneous consideration of nitric oxide production and inactivation when investigating vascular function in humans ABSTRACT: Haemoglobin (Hb) may impact the transduction of endothelium-dependent and nitric oxide (NO)-mediated vasodilator activity, given its contribution to shear stress stimuli and diverse biochemical reactions with NO. We hypothesized that an acute reduction in [Hb] and haematocrit (Hct) would increase brachial artery flow-mediated dilatation (FMD). In 11 healthy males (28 ± 7 years; 23 ± 2 kg m-2 ), FMD (Duplex ultrasound), arterial blood gases, Hct and [Hb], blood viscosity, and NO metabolites (ozone-based chemiluminescence) were measured before and after isovolumic haemodilution, where ∼20% of whole blood was removed and replaced with 5% human serum albumin. Haemodilution reduced Hct by 18 ± 2% (P < 0.001) and whole blood viscosity by 22 ± 5% (P < 0.001). Plasma nitrite (P = 0.01), S-nitrosothiols (P = 0.03) and total red blood cell NO (P = 0.001) were collectively reduced by ∼15-40%. Brachial artery FMD increased by ∼160% from 3.8 ± 2.1 to 9.7 ± 4.5% (P = 0.004). Statistical covariation for the shear stress stimulus did not alter FMD, indicating that the increase in FMD was not directly related to alterations in whole blood viscosity and the shear stimulus. Collectively, these findings indicate that haemoglobin scavenging of NO appears to be an important factor in the regulation of FMD under normal conditions through constraint of endothelium-dependent NO-mediated vasodilatation in healthy humans.

Allweddeiriau

Iaith wreiddiolSaesneg
Tudalennau (o-i)4225-4236
Nifer y tudalennau12
CyfnodolynJournal of Physiology
Cyfrol598
Rhif y cyfnodolyn19
Dynodwyr Gwrthrych Digidol (DOIs)
StatwsCyhoeddwyd - Hyd 2020
Cyhoeddwyd yn allanolIe
Gweld graff cysylltiadau