ArticleAnnals of vascular diseases2011
Platelet nitric oxide signaling system in patients with coronary artery disease.
Article in Annals of vascular diseases, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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4 authors at 2 institutions in 2 countries.
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Abstract
backgroundCoronary artery disease (CAD) is the leading cause of death worldwide, and the major cause of hospital admissions in the Western countries. The pathogenesis of CAD is closely related to nitric oxide release and formation. The purpose of this study was to investigate the status of platelets nitric oxide in patients with coronary artery disease.
methodsWe measured platelets aggregation, cGMP, NO (nitrite/nitrate level), NO synthase activity, plasma NO, and ionized Ca(2+) in 40 healthy volunteers and 120 patients with myocardial infarction, unstable and stable angina, with 40 subjects in each group. The subjects' age mean range was from 40-51 years.
resultsPlatelets aggregation, NO, cGMP, NO synthase activity, plasma NO and ionized Ca(2+) have increased significantly (P <0.001) across the patients groups compared to controls. Platelets NO synthase activity (mean ± SD / U / 10(9) platelets) in healthy controls, MI, unstable angina and stable angina patients were 1.19 ± 0.56, 1.21 ± 0.64, 1.64 ± 0.98 and 1.57 ± 0.81 respectively. The cGMP (mean ± SD / pmole / 10(9) platelets) levels were 0.95 ± 0.41, 1.53 ± 0.64, 3.18 ± 0.77, and 5.12 ± 1.5 respectively.
conclusionsThe present study demonstrated that platelets aggregation, NO, cGMP, NO synthase activity, plasma NO, and ionized Ca(2+) profoundly increased in CAD. The increases in NO-cGMP components may have resulted as a compensatory response to ameliorate platelet activity and Ca(2+) levels in CAD patients.
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