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Purpose. Staphylococcus aureus is responsible for the majority of wound infections in clean surgical procedures that involve implantation of foreign material, grafts or prosthetic devices. The aim of the study was to assess the effect of low molecular weight heparin on the development and progression of S. aureus arthritis.Materials and methods. The murine model of hematogenously acquired septic arthritis was used injecting intravenously toxic shock syndrome toxin-1 (TSST-1) producing S. aureus of LS-1 strain. Mice lacking prosthetic implants were treated with intraperitoneal injections of low molecular weight heparin, used routinely as anti-thrombotic prophylaxis following joint prosthetic surgery. Evaluation of arthritis was performed clinically and histopathologically. In addition, the effect of low molecular weight heparin on T cell dependent and independent inflammation was assessed.Results. Seven days after inoculation with bacteria 18 out of 19 low molecular weight heparin treated mice displayed clinical symptoms of arthritis as compared to 9 out of 23 control animals (p<0.05), and the severity of arthritis, expressed as arthritic index, was 2.6±0.5 versus 1.6±0.5 (p=0.05). The histopathological examination confirmed the clinical findings showing that both inflammation and joint destruction were more substantial in heparin treated animals.Conclusion. Our findings indicate that the routine anti-coagulation treatment with heparin contributes to more severe course of joint infection. [Copyright &y& Elsevier]

The aim of the study was to assess the role of the complement system in Staphylococcus aureus arthritis and septicaemia. The murine model of haematogenously acquired septic arthritis was used, injecting intravenously toxic shock syndrome toxin-1 (TSST-1), producing S. aureus LS-1. Complement was depleted using cobra venom factor (CVF). Evaluation of arthritis was performed clinically and histopathologically. In addition, the effect of complement depletion on the phagocytic activity of leucocytes was assessed in vivo and in vitro. Six days after inoculation of S. aureus the prevalence of arthritis in decomplemented mice was three-fold higher than that in controls (91% versus 25%). The clinical severity of arthritis at the end of the experiment, expressed as arthritic index, was 7.3 and 1.9, respectively. These findings were confirmed by histological index of synovitis as well as of cartilage and/or bone destruction being significantly higher in decomplemented mice than in controls (9.8 ± 1.7 versus 4.9 ± 1.2, P < 0.05; and 7.9 ± 1.7 versus 3.0 ± 0.9, P < 0.05, respectively). Also, the septicaemia-induced mortality was clearly higher in decomplemented mice compared with the controls. CVF treatment significantly reduced in vivo polymorphonuclear cell-dependent inflammation induced by subcutaneous injection of olive oil and mirroring the capacity of polymorphonuclear cells (PMNC) to migrate and/or extravasate. Besides, the decomplementation procedure significantly impaired phagocytic activity of peripheral blood leucocytes in vitro, since the number of phagocytes being able to ingest bacteria decreased by 50% when the cells were maintained in decomplemented serum compared with those in intact serum. The conclusion is that complement depletion aggravates the clinical course of S. aureus arthritis and septicaemia, possibly by a combination of decreased migration/extravasation of PMNC and an impairment of phagocytosis. [ABSTRACT FROM AUTHOR]

Background: The endothelin-1 (ET-1) system plays a pathophysiologic role in patients with pulmonary arterial hypertension (PAH). Results from previous studies assessing the transpulmonary gradient of ET-1 have been inconsistent. The influence of an intravenous epoprostenol infusion on the transpulmonary ET-1 gradient is unknown. Methods: In a prospective investigation, serum concentrations of ET-1 were measured in 39 consecutive patients (31 women; mean age, 20–77 years) with pulmonary hypertension (33 with PAH) and compared with 20 controls. The effect of intravenous epoprostenol administration on the transpulmonary gradient of ET-1 was analyzed in 13 patients with pulmonary hypertension. Blood samples were taken simultaneously from the pulmonary artery and radial artery. Results: The serum levels of ET-1 were significantly higher in the arterial (3.9 ± 1.28 vs 2.53 ± 0.24 pg/ml, p < 0.001) and mixed venous blood samples (3.9 ± 1.21 vs 2.52 ± 0.29 pg/ml, p < 0.001) in patients with pulmonary hypertension than in controls. The arterial/venous ratio of ET-1 in patients (1.0 ± 0.1) and in the control group (1.0 ± 0.05) was similar (p = 0.79). During intravenous epoprostenol infusion, there were no changes in the mean transpulmonary ET-1 gradient (0.98 ± 0.07 vs 0.96 ± 0.09, p = 0.52), despite significant hemodynamic changes. Conclusion: The ET-1 radial artery/pulmonary artery ratio of unity indicates a balanced release and clearance of ET-1 across the lung circulation in controls and in patients with different forms of pulmonary hypertension. ET-1 levels across the pulmonary circulation did not change during epoprostenol infusion. [Copyright &y& Elsevier]

Purpose: Staphylococcus aureus is responsible for the majority of wound infections in clean surgical procedures that involve implantation of foreign material, grafts or prosthetic devices. The aim of the study was to assess the effect of low molecular weight heparin on the development and progression of S. aureus arthritis., Materials and Methods: The murine model of hematogenously acquired septic arthritis was used injecting intravenously toxic shock syndrome toxin-1 (TSST-1) producing S. aureus of LS-1 strain. Mice lacking prosthetic implants were treated with intraperitoneal injections of low molecular weight heparin, used routinely as anti-thrombotic prophylaxis following joint prosthetic surgery. Evaluation of arthritis was performed clinically and histopathologically. In addition, the effect of low molecular weight heparin on T cell dependent and independent inflammation was assessed., Results: Seven days after inoculation with bacteria 18 out of 19 low molecular weight heparin treated mice displayed clinical symptoms of arthritis as compared to 9 out of 23 control animals (p < 0.05), and the severity of arthritis, expressed as arthritic index, was 2.6+/-0.5 versus 1.6+/-0.5 (p = 0.05). The histopathological examination confirmed the clinical findings showing that both inflammation and joint destruction were more substantial in heparin treated animals., Conclusion: Our findings indicate that the routine anti-coagulation treatment with heparin contributes to more severe course of joint infection.