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人体胃部由膳食硝酸盐进行一氧化氮的化学合成。

Chemical synthesis of nitric oxide in the stomach from dietary nitrate in humans.

作者信息

McKnight G M, Smith L M, Drummond R S, Duncan C W, Golden M, Benjamin N

机构信息

Department of Medicine and Therapeutics, Medical School, University of Aberdeen.

出版信息

Gut. 1997 Feb;40(2):211-4. doi: 10.1136/gut.40.2.211.

Abstract

BACKGROUND/AIMS: It has been suggested that dietary nitrate, after concentration in the saliva and reduction to nitrite by tongue surface bacteria, is chemically reduced to nitric oxide (NO) in the acidic conditions of the stomach. This study aimed to quantify this in humans.

METHODS

Ten healthy fasting volunteers were studied twice, after oral administration of 2 mmol of potassium nitrate or potassium chloride. Plasma, salivary and gastric nitrate, salivary and gastric nitrite, and gastric headspace NO concentrations were measured over six hours.

RESULTS

On the control day the parameters measured varied little from basal values. Gastric nitrate concentration was 105.3 (13) mumol/l (mean (SEM), plasma nitrate concentration was 17.9 (2.4) mumol/l, salivary nitrate concentration 92.6 (31.6) mumol/l, and nitrite concentration 53.9 (22.8) mumol/l. Gastric nitrite concentrations were minimal (< 1 mumol/l). Gastric headspace gas NO concentration was 16.4 (5.8) parts per million (ppm). After nitrate ingestion, gastric nitrate peaked at 20 minutes at 3430 (832) mumol/l, plasma nitrate at 134 (7.2) mumol/l, salivary nitrate at 1516.7 (280.5) mumol/l, and salivary nitrite at 761.5 (187.7) mumol/l after 20-40 minutes. Gastric nitrite concentrations tended to be low, variable, and any rise was non-sustained. Gastric NO concentrations rose considerably from 14.8 (3.1) ppm to 89.4 (28.6) ppm (p < 0.0001) after 60 minutes. All parameters remained increased significantly for the duration of the study.

CONCLUSIONS

A very large and sustained increase in chemically derived gastric NO concentrations after an oral nitrate load was shown, which may be important both in host defence against swallowed pathogens and in gastric physiology.

摘要

背景/目的:有人提出,膳食硝酸盐在唾液中浓缩并被舌面细菌还原为亚硝酸盐后,在胃的酸性环境中会被化学还原为一氧化氮(NO)。本研究旨在对人体中的这一过程进行量化。

方法

对10名健康的空腹志愿者进行了两次研究,分别在口服2 mmol硝酸钾或氯化钾后进行。在6小时内测量血浆、唾液和胃中的硝酸盐、唾液和胃中的亚硝酸盐以及胃内气相中的NO浓度。

结果

在对照日,所测参数与基础值相比变化不大。胃中硝酸盐浓度为105.3(13)μmol/L(均值(标准误)),血浆硝酸盐浓度为17.9(2.4)μmol/L,唾液硝酸盐浓度为92.6(31.6)μmol/L,亚硝酸盐浓度为53.9(22.8)μmol/L。胃中亚硝酸盐浓度极低(<1μmol/L)。胃内气相中NO浓度为16.4(5.8)ppm(百万分之一)。摄入硝酸盐后,胃中硝酸盐在20分钟时达到峰值,为3430(832)μmol/L,血浆硝酸盐在20 - 40分钟后达到134(7.2)μmol/L,唾液硝酸盐在20 - 40分钟后达到1516.7(280.5)μmol/L,唾液亚硝酸盐在20 - 40分钟后达到761.5(187.7)μmol/L。胃中亚硝酸盐浓度往往较低且变化不定,任何升高都不持久。60分钟后,胃中NO浓度从14.8(3.1)ppm大幅升至89.4(28.6)ppm(p < 0.0001)。在研究期间,所有参数均持续显著升高。

结论

口服硝酸盐负荷后,化学衍生的胃中NO浓度出现非常大且持续的升高,这在宿主抵御吞咽病原体以及胃生理学方面可能都很重要。

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本文引用的文献

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Stomach NO synthesis.胃一氧化氮合成。
Nature. 1994 Apr 7;368(6471):502. doi: 10.1038/368502a0.
2
Intrinsic source of stomach NO.胃一氧化氮的内源性来源。
Nature. 1994 Jul 7;370(6484):25-6. doi: 10.1038/370025a0.
3
Nitric oxide: mediator, murderer, and medicine.一氧化氮:介质、杀手与药物。
Lancet. 1994 May 14;343(8907):1199-206. doi: 10.1016/s0140-6736(94)92405-8.
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The L-arginine-nitric oxide pathway.L-精氨酸-一氧化氮途径
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