Dataset Information

Quantum rotor induced hyperpolarization.

ABSTRACT: Despite its broad applicability NMR has always been limited by its inherently low sensitivity. Hyperpolarization methods have the potential to overcome this limitation and, in the case of ex situ dynamic nuclear polarization (DNP), large enhancement factors have been achieved. Although many other polarization methods have been described in the past, including chemically and parahydrogen-induced polarization and optical pumping, DNP has recently been the most popular. Here we present an additional polarization mechanism arising from quantum rotor effects in methyl groups, which generates polarizations at temperatures < 1.5 K and interferes with DNP at such temperatures. The polarization generated by this mechanism is efficiently transferred via carbon bound protons. Although quantum rotor polarizations have been studied for a small range of molecules in great detail, we observe such effects for a much broader range of substances with very different polarization rates at temperatures < 1.5 K. Moreover, we report transfer of quantum rotor polarization across a chain of protons. The observed effect not only influences the polarization in low-temperature DNP experiments but also opens a new independent avenue to generate enhanced sensitivity for NMR.

SUBMITTER: Ludwig C

PROVIDER: S-EPMC2890774 | biostudies-literature | 2010 Jun

REPOSITORIES: biostudies-literature

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Quantum rotor induced hyperpolarization.

Ludwig Christian C Saunders Martin M Marin-Montesinos Ildefonso I Günther Ulrich L UL

Proceedings of the National Academy of Sciences of the United States of America 20100526 24

Despite its broad applicability NMR has always been limited by its inherently low sensitivity. Hyperpolarization methods have the potential to overcome this limitation and, in the case of ex situ dynamic nuclear polarization (DNP), large enhancement factors have been achieved. Although many other polarization methods have been described in the past, including chemically and parahydrogen-induced polarization and optical pumping, DNP has recently been the most popular. Here we present an additiona ...[more]

PMID: 20505118

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Project description:BackgroundThe vascular endothelium plays a critical role in the control of blood flow. Altered endothelium-mediated vasodilator and vasoconstrictor mechanisms underlie key aspects of cardiovascular disease, including those in obesity. Whilst the mechanism of nitric oxide (NO)-mediated vasodilation has been extensively studied in obesity, little is known about the impact of obesity on vasodilation to the endothelium-derived hyperpolarization (EDH) mechanism; which predominates in smaller resistance vessels and is characterized in this study.Methodology/principal findingsMembrane potential, vessel diameter and luminal pressure were recorded in 4(th) order mesenteric arteries with pressure-induced myogenic tone, in control and diet-induced obese rats. Obesity, reflecting that of human dietary etiology, was induced with a cafeteria-style diet (?30 kJ, fat) over 16-20 weeks. Age and sexed matched controls received standard chow (?12 kJ, fat). Channel protein distribution, expression and vessel morphology were determined using immunohistochemistry, Western blotting and ultrastructural techniques. In control and obese rat vessels, acetylcholine-mediated EDH was abolished by small and intermediate conductance calcium-activated potassium channel (SK(Ca)/IK(Ca)) inhibition; with such activity being impaired in obesity. SK(Ca)-IK(Ca) activation with cyclohexyl-[2-(3,5-dimethyl-pyrazol-1-yl)-6-methyl-pyrimidin-4-yl]-amine (CyPPA) and 1-ethyl-2-benzimidazolinone (1-EBIO), respectively, hyperpolarized and relaxed vessels from control and obese rats. IK(Ca)-mediated EDH contribution was increased in obesity, and associated with altered IK(Ca) distribution and elevated expression. In contrast, the SK(Ca)-dependent-EDH component was reduced in obesity. Inward-rectifying potassium channel (K(ir)) and Na(+)/K(+)-ATPase inhibition by barium/ouabain, respectively, attenuated and abolished EDH in arteries from control and obese rats, respectively; reflecting differential K(ir) expression and distribution. Although changes in medial properties occurred, obesity had no effect on myoendothelial gap junction density.Conclusion/significanceIn obese rats, vasodilation to EDH is impaired due to changes in the underlying potassium channel signaling mechanisms. Whilst myoendothelial gap junction density is unchanged in arteries of obese compared to control, increased IK(Ca) and Na(+)/K(+)-ATPase, and decreased K(ir) underlie changes in the EDH mechanism.

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Quantum rotor induced hyperpolarization.

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Quantum rotor induced hyperpolarization.

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