scholarly journals Molecular Magnetic Resonance Imaging of Nitric Oxide in Biological Systems

ACS Sensors ◽  
2020 ◽  
Vol 5 (6) ◽  
pp. 1674-1682
Author(s):  
Ali Barandov ◽  
Souparno Ghosh ◽  
Nan Li ◽  
Benjamin B. Bartelle ◽  
Jade I. Daher ◽  
...  
Keyword(s):  
Magnetic Resonance Imaging ◽  
Nitric Oxide ◽  
Magnetic Resonance ◽  
Biological Systems ◽  
Resonance Imaging

The measurement of diffusion and perfusion in biological systems using magnetic resonance imaging

2000 ◽  
Vol 45 (8) ◽  
pp. R97-R138 ◽  
Author(s):  
David L Thomas ◽  
Mark F Lythgoe ◽  
Gaby S Pell ◽  
Fernando Calamante ◽  
Roger J Ordidge
Keyword(s):  
Magnetic Resonance Imaging ◽  
Magnetic Resonance ◽  
Biological Systems ◽  
Resonance Imaging

Nitric oxide mediates hypoxia-induced cerebral vasodilation in humans

2002 ◽  
Vol 92 (3) ◽  
pp. 962-966 ◽  
Author(s):  
Annette H. M. Van Mil ◽  
Aart Spilt ◽  
Mark A. Van Buchem ◽  
Edward L. E. M. Bollen ◽  
Luc Teppema ◽  
...  
Keyword(s):  
Magnetic Resonance Imaging ◽  
Nitric Oxide ◽  
Magnetic Resonance ◽  
Phase Contrast ◽  
Vascular Tone ◽  
Resonance Imaging ◽  
Contrast Magnetic Resonance Imaging ◽  
Phase Contrast Magnetic Resonance ◽  
Contrast Magnetic Resonance ◽  
Cerebral Vasodilatation

Nitric oxide (NO) plays a pivotal role in the regulation of peripheral vascular tone. Its role in the regulation of cerebral vascular tone in humans remains to be elucidated. This study investigates the role of NO in hypoxia-induced cerebral vasodilatation in young healthy volunteers. The effect of the NO synthase inhibitor N G-monomethyl-l-arginine (l-NMMA) on the cerebral blood flow (CBF) was assessed during normoxia and during hypoxia (peripheral O2saturation 97 and 80%, respectively). Subjects were positioned in a magnetic resonance scanner, breathing normal air (normoxia) or a N2-O2 mixture (hypoxia). The CBF was measured before and after administration of l-NMMA (3 mg/kg) by use of phase-contrast magnetic resonance imaging techniques. Administration of l-NMMA during normoxia did not affect CBF. Hypoxia increased CBF from 1,049 ± 113 to 1,209 ± 143 ml/min ( P < 0.05). After l-NMMA administration, the augmented CBF returned to baseline (1,050 ± 161 ml/min; P < 0.05). Similarly, cerebral vascular resistance declined during hypoxia and returned to baseline after administration of l-NMMA ( P < 0.05 for both). Use of phase-contrast magnetic resonance imaging shows that hypoxia-induced cerebral vasodilatation in humans is mediated by NO.

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