First evaluation of real-time nitric oxide changes in the coronary circulation in patients with non-ischaemic dilated cardiomyopathy using a catheter-type sensor

Aims No direct method has yet been developed to measure real-time plasma nitric oxide (NO) concentration in humans. In this study, we evaluated a new method for measuring plasma NO concentration in patients with dilated cardiomyopathy (DCM) and in normal controls using a catheter-type sensor. Method...

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Published inEuropean heart journal Vol. 31; no. 23; pp. 2862 - 2870
Main Authors Takarada, Shigeho, Imanishi, Toshio, Goto, Masami, Mochizuki, Seiichi, Ikejima, Hideyuki, Tsujioka, Hiroto, Kuroi, Akio, Takeshita, Tatsuya, Akasaka, Takashi
Format Journal Article
LanguageEnglish
Published Oxford Oxford University Press 01.12.2010
SeriesEditor's Choice
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Summary:Aims No direct method has yet been developed to measure real-time plasma nitric oxide (NO) concentration in humans. In this study, we evaluated a new method for measuring plasma NO concentration in patients with dilated cardiomyopathy (DCM) and in normal controls using a catheter-type sensor. Methods and results We simultaneously measured average peak velocity (APV) of the coronary artery flow and change in plasma NO concentration using the NO sensor placed in the great cardiac vein of 10 DCM patients and 10 control subjects. These evaluations were performed in response to sequential intracoronary infusions of acetylcholine (ACh, 10−8–10−6 M), NG-monomethyl-l-arginine (l-NMMA, 200 µmol) and co-infusion of ACh and l-NMMA. The change in plasma NO concentration in DCM patients was significantly impaired compared with the control group (P < 0.01). Pretreatment with l-NMMA completely suppressed the ACh-induced NO concentration, whereas APV in the left anterior descending coronary artery was partially suppressed in both groups. Plasma NO concentration reached its peak value later than the maximum APV following the injection of ACh (10−6 M) in both groups. Conclusion The catheter-type NO sensor could be applied to clinically evaluate the endothelial function (i.e. reduced endothelium-derived NO bioavailability) in patients with cardiovascular diseases.
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ISSN:0195-668X
1522-9645
DOI:10.1093/eurheartj/ehq156