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Background: Inflammatory processes are involved in the pathogenesis of coronary artery disease and acute myocardial infarction (AMI). Yet there is little known about concentrations of pro-inflammatory mediators in the cardiac milieu of patients suffering from AMI. The aim of this study was to evaluate blood samples directly obtained from the culprit coronary artery during AMI. Materials and Methods: Serum samples were obtained from the culprit coronary artery of AMI patients (n=39) using a X-sizer thrombectomy system. Sera from patients with stable angina (SA, n=34) and unstable angina (UA, n=37) served as controls. Levels of sCD40, sCD40L, TNFalpha, and sTNF-RI were determined by enzyme-linked immunosorbent assays. Results: Levels of sCD40L and sCD40 were increased in the AMI group when compared to patients suffering from SA and UA. Levels of both inflammatory markers were highest in the culprit coronary artery. Increased concentrations of TNFalpha and sTNF-RI evidenced a further inflammatory response at the site of infarction. Conclusions: We conclude that mediators of inflammation are heightened in the coronary blood flow during myocardial infarction. Our observations extend the current knowledge of the inflammatory cascade during myocardial infarction. [ABSTRACT FROM AUTHOR]

Objective: phosphate buffered saline (PBS) solutions are commonly used in laboratories for dilutions, washing cell suspensions, and rinsing, as well as additives to cell culture media. In the present study, we evaluated pro- and anti-inflammatory cytokine secretion of peripheral blood mononuclear cells (PBMCs) incubated in medium containing different PBS solutions. Methods: Human PBMCs were incubated in cell culture medium with different concentrations of PBS containing calcium (Ca++) and magnesium (Mg++)(+/+ PBS). Cells in medium alone or in suspensions containing PBS without Ca++ and Mg++ (-/- PBS) served as controls. Results: A dose-dependent increase of interleukin-1 receptor antagonist was found when PBMCs were cultured in medium supplemented with increasing concentrations of +/+ PBS. No significant differences were observed for interleukin-1ß, interleukin-4, interleukin-10, or transofrming growth factor ß. Conclusions: The release of the anti-inflammatory cytokine interleukin-1 receptor antagonist in addition to unchanged levels of pro-inflammatory mediators suggests an important modulatory mechanism of heightened extracellular calcium levels. [ABSTRACT FROM AUTHOR]