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Monitoring of L-Arginine and Endogenous Dimethylarginines in Survivor Septic Patients - A Pilot Study.脓毒症存活患者中L-精氨酸和内源性二甲基精氨酸的监测——一项初步研究
In Vivo. 2016;30(5):663-9.
2
[Asymmetric dimethylarginine: predictor of cardiovascular diseases?].[不对称二甲基精氨酸:心血管疾病的预测指标?]
Orv Hetil. 2016 Mar 27;157(13):483-7. doi: 10.1556/650.2016.30396.
3
Protective role of carbon dioxide (CO2) in generation of reactive oxygen species.二氧化碳(CO₂)在活性氧生成中的保护作用。
Mol Cell Biochem. 2016 Jan;411(1-2):317-30. doi: 10.1007/s11010-015-2594-9. Epub 2015 Nov 5.
4
Asymmetric dimethylarginine and cardiovascular risk: systematic review and meta-analysis of 22 prospective studies.不对称二甲基精氨酸与心血管风险:22项前瞻性研究的系统评价和荟萃分析
J Am Heart Assoc. 2015 May 28;4(6):e001833. doi: 10.1161/JAHA.115.001833.
5
Asymmetric dimethylarginine and augmentation index in newly diagnosed patients with hypertension.新诊断高血压患者的不对称二甲基精氨酸与增强指数
Angiology. 2015 Jan;66(1):43-8. doi: 10.1177/0003319713513145. Epub 2013 Dec 3.
6
Asymmetric dimethylarginine reduces nitric oxide donor-mediated dilation of arterioles by activating the vascular renin-angiotensin system and reactive oxygen species.不对称二甲基精氨酸通过激活血管肾素-血管紧张素系统和活性氧来降低一氧化氮供体介导的小动脉扩张。
J Vasc Res. 2012;49(4):363-72. doi: 10.1159/000337485. Epub 2012 May 30.
7
A novel system for transcutaneous application of carbon dioxide causing an "artificial Bohr effect" in the human body.一种新型的二氧化碳经皮应用系统,可在人体中产生“人工波尔效应”。
PLoS One. 2011;6(9):e24137. doi: 10.1371/journal.pone.0024137. Epub 2011 Sep 8.
8
The Role of Asymmetric Dimethylarginine (ADMA) in Endothelial Dysfunction and Cardiovascular Disease.不对称二甲基精氨酸(ADMA)在内皮功能障碍和心血管疾病中的作用
Curr Cardiol Rev. 2010 May;6(2):82-90. doi: 10.2174/157340310791162659.
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Effects of coronary revascularization with or without cardiopulmonary bypass on plasma levels of asymmetric dimethylarginine.冠状动脉血运重建术(无论是否使用体外循环)对血浆不对称二甲基精氨酸水平的影响。
Coron Artery Dis. 2011 Jun;22(4):245-52. doi: 10.1097/MCA.0b013e3283441d5c.
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Clinical and microcirculatory effects of transcutaneous CO2 therapy in intermittent claudication. Randomized double-blind clinical trial with a parallel design.经皮二氧化碳疗法治疗间歇性跛行的临床及微循环效应。平行设计的随机双盲临床试验。
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血管紧张素转换酶抑制可提高经皮二氧化碳治疗的有效性。

Angiotensin-converting Enzyme Inhibition Improves the Effectiveness of Transcutaneous Carbon Dioxide Treatment.

作者信息

Nemeth Balazs, Kiss Istvan, Jencsik Timea, Peter Ivan, Kreska Zita, Koszegi Tamas, Miseta Attila, Kustan Peter, Boncz Imre, Laczo Andrea, Ajtay Zeno

机构信息

Department of Public Health Medicine, Medical School, University of Pecs, Pecs, Hungary

Zsigmondy Vilmos SPA Hospital, Harkany, Hungary.

出版信息

In Vivo. 2017 May-Jun;31(3):425-428. doi: 10.21873/invivo.11077.

DOI:10.21873/invivo.11077
PMID:28438873
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5461455/
Abstract

AIM

To study the effect of carbon dioxide (CO) therapy on the nitric oxide (NO) pathway by monitoring plasma asymmetric dimethylarginine (ADMA) concentrations.

PATIENTS AND METHODS

Forty-seven hypertensive patients who underwent transcutaneous CO therapy were enrolled. Thirty healthy individuals were recruited for the control group. Blood samples were taken one hour before, as well as one hour, 24 hours and 3 weeks after the first CO treatment. Controls did not undergo CO treatment. Plasma ADMA levels were measured by ELISA.

RESULTS

ADMA levels decreased significantly one hour after the first CO2 treatment compared to the baseline concentrations (p=0.003). Significantly greater reduction was found among patients in whom angiotensin converting enzyme inhibitors (ACEIs) were administered (p=0.019).

CONCLUSION

The short- and long-term decrease of ADMA levels suggests that CO is not only a vasodilator, but also has a beneficial effect on the NO pathway. ACE inhibition seems to enhance the effect of CO treatment.

摘要

目的

通过监测血浆不对称二甲基精氨酸(ADMA)浓度,研究二氧化碳(CO)疗法对一氧化氮(NO)途径的影响。

患者与方法

纳入47例接受经皮CO疗法的高血压患者。招募30名健康个体作为对照组。在首次CO治疗前1小时以及治疗后1小时、24小时和3周采集血样。对照组未接受CO治疗。采用酶联免疫吸附测定法(ELISA)测量血浆ADMA水平。

结果

与基线浓度相比,首次CO₂治疗后1小时ADMA水平显著降低(p = 0.003)。在服用血管紧张素转换酶抑制剂(ACEIs)的患者中发现下降幅度明显更大(p = 0.019)。

结论

ADMA水平的短期和长期下降表明,CO不仅是一种血管扩张剂,而且对NO途径有有益作用。ACE抑制似乎增强了CO治疗的效果。