This study was designed to determine the effect of pteridines, R-and S-tetrahydrobiopterin, sepiapterin, and dihydrobiopterin on endothelium-dependent contractions to acetylcholine in isolated aortas from spontaneously hypertensive rat and normotensive Wistar-Kyoto rat. The noncumulative addition of redox-active pteridines R- and S-tetrahydrobiopterin (but not the oxidized analogues sepiapterin and dihydrobiopterin) produced a concentrationdependent transient contraction in isolated aortic rings from both normotensive and hypertensive rats. R-and S-tetrahydrobiopterin (but not sepiapterin or dihydrobiopterin) potentiated the endothelium-dependent contractions to acetylcholine but only in aortas from hypertensive rats and in the presence of NG-nitro-L-arginine. In these aortas, the generation of oxygen-derived free radicals by the combination of xanthine plus xanthine oxidase also potentiated the endothelium-dependent contractions to acetylcholine. The presence of R-tetrahydrobiopterin did not alter the characteristics of the endothelium-dependent contractions because they were inhibited by valeryl salicylate, an inhibitor of cyclooxygenase-1, by S18886, a TP-receptor antagonist or by Tiron, a cell permeable superoxide anion scavenger. However, the contractions to acetylcholine, which are unaffected by the combination of superoxide dismutase and catalase, become significantly inhibited by these two scavengers in the presence of R-tetrahydrobiopterin. In the presence of NG-nitro-L-arginine, R-tetrahydrobiopterin did not affect the contractions to phenylephrine, U 46619, or to oxygen-derived free radicals generated by xanthine plus xanthine oxidase. These results indicate that the production of superoxide by the autoxidation of tetrahydrobiopterin selectively enhances endothelium-dependent contractions in the spontaneously hypertensive rat when nitric oxide synthase is inhibited.

An anodic stripping voltammetric method for the determination of cardiac troponin I (cTnI) at a MCM-41 mesoporous material modified carbon paste electrode (MCM-MCPE) was investigated. The test was based on the dual monoclonal antibody “sandwich” principle using colloidal gold as a labeled substrate. Four main steps were carried out to obtain the analytical signal, i.e. electrode preparation, immunoreaction, silver enhancement, and anodic stripping voltammetric detection. The anodic stripping peak current increased linearly with the concentration of cTnI over the range of 0.8–5.0 ng/ml. A detection limit of 0.5 ng/ml was obtained. The established method was applied to detect cTnI in acute myocardial infarction (AMI) samples using routine enzyme-linked immunoadsorbent assay (ELISA) for comparison analysis, and good results were obtained.

Aims: To investigate whether patients with acute coronary syndrome (ACS) possessed high levels of platelet-monocyte aggregates (PMAs) and related circulating biomarkers.Methods: 74 ACS patients, 58 stable angina pectoris (SAP) patients and 46 control patients without coronary artery disease were selected and their PMAs were measured by flow cytometry. Their plasma IL-6, IL-8, MCP-1, soluble CD40L and soluble P-selectin were also measured simultaneously by flow cytometry. Results: Patients with ACS exhibited higher level of PMAs compared with SAP patients and the control. Furthermore, the levels of IL-6, IL-8, MCP-1, soluble CD40L, soluble P-selectin and CRP were also significantly higher in ACS patients than in SAP patients and the control group. However, there were no significant difference in the levels of IL-8, sCD40L, sP-selectin and CRP between SAP patients and the control group. Correlation analysis showed that high levels of IL-6 and sP-selectin were significantly correlated with PMAs. Logistic analysis further demonstrated that the presence of elevated CRP, IL-6 and PMAs level each confers an increased risk of ACS. Conclusion: Elevated levels of PMAs and related circulating biomarkers might indicate the unstable coronary syndrome in ACS patients, and the levels of PMAs, CRP and IL-6 could be used for monitoring and guiding the early intervention of ACS patients.