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Ensayo controlado aleatorizado2014

Dietary nitrate facilitates an acetazolamide-induced increase in cerebral blood flow during visual stimulation

Aamand R, Ho YC, Dalsgaard T, Roepstorff A, Lund TE

Journal of applied physiology (Bethesda, Md. : 1985) · 9 citas

Cómo se estudió

Diseño
Ensayo controlado aleatorizado (indexado por PubMed)
Estudiado en
Personas
Resultado principal
Marcadores de salud y funcionamiento
Consumo medido con
No se indica

Quién lo pagó

Financiación
Financiación independiente
Gobierno
Ministério da Ciência, Tecnologia e Inovação
Organización sin fines de lucro
Augustinus Fonden
Organización sin fines de lucro
Frimodt-Heineke Fonden

Según 3 financiadores declarados.

Publicación

Publicado
2013-12-13 · J Appl Physiol (1985) · vol. 116 · número 3 · págs. 267–273
Editorial
American Physiological Society
Citado
14 citas · más que el 78% de estudios similares · 1.1× el promedio de su campo
Referencias
35 trabajos
Acceso
De pago
Áreas de investigación
Eicosanoids and Hypertension Pharmacology · Nitric Oxide and Endothelin Effects · Traumatic Brain Injury and Neurovascular Disturbances
Palabras clave
Acetazolamide, Stimulation, Cerebral blood flow, Blood flow, Nitrate, Medicine, Anesthesia, Internal medicine, Chemistry, Endocrinology
MeSH
humans, nitrates, nitrites, nitric oxide, acetazolamide, blood flow velocity, cross-over studies, double-blind method, photic stimulation, cerebrovascular circulation, drug synergism, adult, male, young adult

5 autores

  • Rasmus Aamand🇩🇰 · autor de correspondenciaAarhus University
  • Yi-Ching Lynn Ho🇩🇰Aarhus University
  • Thomas Dalsgaard🇩🇰Aarhus University
  • Andreas Roepstorff🇩🇰Aarhus University
  • Torben E. Lund🇩🇰Aarhus University

Resumen

El texto original del estudio, en el idioma en que se publicó.

The carbonic anhydrase (CA) inhibitor acetazolamide (AZ) is used routinely to estimate cerebrovascular reserve capacity in patients, as it reliably increases cerebral blood flow (CBF). However, the mechanism by which AZ accomplishes this CBF increase is not entirely understood. We recently discovered that CA can produce nitric oxide (NO) from nitrite, and that AZ enhances this NO production in vitro. In fact, this interaction between AZ and CA accounted for a large part of AZ's vasodilatory action, which fits well with the known vasodilatory potency of NO. The present study aimed to assess whether AZ acts similarly in vivo in the human cerebrovascular system. Hence, we increased or minimized the dietary intake of nitrate in 20 healthy male participants, showed them a full-field flickering dartboard, and measured their CBF response to this visual stimulus with arterial spin labeling. Doing so, we found a significant positive interaction between the dietary intake of nitrate and the CBF modulation afforded by AZ during visual stimulation. In addition, but contrary to studies conducted in elderly participants, we report no effect of nitrate intake on resting CBF in healthy human participants. The present study provides in vivo support for an enhancing effect of AZ on the NO production from nitrite catalyzed by CA in the cerebrovascular system. Furthermore, our results, in combination with the results of other groups, indicate that nitrate may have significant importance to vascular function when the cerebrovascular system is challenged by age or disease.

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