dimethylarginine has been researched along with Dilatation--Pathologic* in 2 studies
1 trial(s) available for dimethylarginine and Dilatation--Pathologic
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Reduction of postchallenge hyperglycaemia prevents acute endothelial dysfunction in subjects with impaired glucose tolerance.
To investigate whether selective reduction of postchallenge hyperglycaemia influences acute endothelial dysfunction, a very early manifestation of vascular disease, in patients with impaired glucose tolerance.. In a randomized, double-blind, placebo-controlled, cross-over study the acute effect of 200-mg acarbose was investigated in 28 subjects with diagnosed impaired glucose tolerance. Flow-mediated dilation (FMD) of the brachial artery was determined as a measure of endothelial function before and 2 and 3 h after ingestion of 100-g saccharose. Asymmetrical dimethylarginine (ADMA) was measured by high-performance liquid chromatography.. A negative correlation was observed between the changes of glucose and FMD (r = 0.416, P = 0.0018) 2 h after ingestion of saccharose. At 3 h, neither blood glucose nor FMD were different from baseline. Changes of both blood glucose (P = 0.0007) and FMD (P = 0.046) were significantly lower after administration of acarbose. Subgroup analysis revealed that the effect of acarbose was restricted to those subjects with an increase of blood glucose above the median increase of glycaemia. No changes of plasma ADMA were observed.. Our data clearly demonstrate that the postchallenge alteration of vascular function in patients with impaired glucose tolerance is caused by the acute elevation of glycaemia but not mediated by ADMA. Topics: Acarbose; Administration, Oral; Arginine; Blood Glucose; Brachial Artery; Cross-Over Studies; Dilatation, Pathologic; Double-Blind Method; Endothelium, Vascular; Female; Glucose Intolerance; Humans; Hyperglycemia; Insulin; Male; Middle Aged; Prospective Studies; Sucrose | 2005 |
1 other study(ies) available for dimethylarginine and Dilatation--Pathologic
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Asymmetric dimethylarginine levels in patients with coronary artery ectasia.
Endothelial dysfunction might be one of the pathophysiological mechanisms in the development of coronary artery ectasia (CAE) although the exact mechanisms have not yet been demonstrated. Asymmetric dimethylarginine (ADMA), an endogenous competitive inhibitor of nitric oxide synthase, is also related to endothelial and structural dysfunction.. To asses the relationship between CAE and ADMA plasma concentrations.. Thirty patients with CAE in a mean age of 55.5 +/- 3.6 years and 40 patients with normal coronary arteries in a mean age of 53.3 +/- 11.6 years were studied. The ADMA levels of all patients were analysed by ELISA method.. The mean ADMA level in the CAE group was found to be significantly higher than the mean ADMA level in the normal coronary artery group (2.26 +/- 0.47 vs. 1.43 +/- 0.40 micromol/l, p < 0.001). The elevated ADMA level (> 1.80 micromol/l) was present in 83.0% of patients from the CAE group and 25.0% of patients from the normal coronary artery group (p < 0.001). Having an increased ADMA level enhanced the risk of CAE 15-fold. The multiple-adjusted OR of the risk of CAE was 18.71 (95% CI 4.95-70.68) for the higher ADMA level compared to the lower level.. Asymmetric dimethylarginine level is significantly associated with the presence of coronary artery ectasia. These findings suggest that increased ADMA level may be associated with endothelial dysfunction leading to the development of coronary artery ectasia. Topics: Adult; Aged; Arginine; Biomarkers; Coronary Angiography; Coronary Vessel Anomalies; Cross-Sectional Studies; Dilatation, Pathologic; Female; Humans; Male; Middle Aged; Reference Values; Serum | 2009 |