Background. Disorder of hemostasis in hemodialysis patients is focused in two directions, towards the development of thrombosis and bleeding. Both complications make it difficult to treat and are life-threatening for the patient.  Monitoring of hemostatic parameters, it is possible to detect the first changes in the coagulation system and correct the factors that lead to changes and thus prevent or stop the further development of complications. Aim. To determine the hemostatic and dialysis parameters and their influence on the occurrence and development of complications. Patients and methods. From a total of 175 patients, 46 had signs of hemorrhagic syndrome and 16 of them had thrombosis. Parameters of primary and secondary hemostasis were determined and vascular access of ultrasound was examined. Results. In the patients with thrombosis D-dimer level was significantly higher and amounted to 4.18 mg / l, while AT III levels were decreased for 54%. Elevated level of APTT was significant for the patients who had bleeding. In 86% of patients with thrombosis, ultrasound findings correlated with findings of D-dimer. Both complications were more pronounced in the older age group above 46 years. Conclusion. Hemorrhagic syndrome is a frequent complication of thrombosis. The level of D-dimer is directly correlated with ultrasound detection of thrombotic formation. Elevated levels of APTT was in direct correlation with bleeding. The development of complica-tions are affected by other factors, such as: age, access type, type of dialysis membrane, the blood flow. Frequent control of hemostatic parameters is essential for early detection of complications. In the event of changes in coagulation system, type and dose of anticoagulant should be corrected and introducing additional oral anticoagulants should be considered.

Endothelin 1 (ET-1) is vasoactive peptide that acts via ET-A receptors coupling inducing vascular smooth muscle cell proliferation and contraction. ET-1 is involved in the development and maintenance of hypertension. Aim of this study was to determine the contribution of Ras farnesyl transferase, mitogen activated protein kinase (MAP kinase) and cytochrome P¬450 (CYP450) metabolites to ET-1 induced hypertension. ET-1 (5 pmol/kg per minute) was chronically infused into to the jugular vein by use of mini-osmotic pump for 9 days in male Sprague-Dawley rats. Mean arterial blood pressure (MABP) in ET-1-treated rats was 154±2 mm Hg (hypertensive rats) compared with 98±3 mm Hg in control (normotensive) rats. Infusion of Ras farnesyl transferase inhibitor FPTIII (138 ng/min), MAP kinase inhibitor PD-98059 (694 ng/min) and CYP450 inhibitor 17-ODYA (189 ng/min) significantly attenuated MABP to 115±2.5 mm Hg, 109±3 mm Hg and 118±1.5 mm Hg, respectively. These results suggest that CYP-450 metabolites and Ras/MAP kinase pathway contribute to the development of ET-1 induced hypertension. Further investigation has to be done to confirm whether activation of RAS/MAP kinase pathway by arachidonic acid metabolites plays an important role in the development of ET-1 induced hypertension.

BACKGROUND: Heart failure is a common disease that requires frequent and long hospitalizations, the active participation of health workers and family members in the care of such patients, and it leads to reduction of physical activity and lifestyle changes with the patient, which significantly affects the quality of life of patients with heart failure. OBJECTIVE: To determine the quality of life of patients with heart failure in relation to severity of the clinical features. RESPONDENTS AND METHODOLOGY: Analysis of life quality was performed for 120 patients suffering from heart failure, both genders, all age groups in relation to severity of the clinical features. Patients were divided into 4 groups according to NYHA classification of heart failure. The control group consisted of 10 subjects who do not suffer from heart failure. Assessment of quality of life was performed using the SF-36 questionnaire which consists of 8 segments classified in the dimension of physical and mental health. RESULTS: Study group consisted of 130 participants with heart failure had 66 (51%) of male, and other were females, divided into 4 NYHA groups, where every group had 30 subjects (23.1%), and one control group of 10 subjects (7.7%). The analysis of gender and age distribution within the groups found no statistically significant difference (X2=1.70; df=4; p=0.79), (ANOVA; F=0.74; p=0.57). The values of SF-36 score expressed as the median in the control and 4 NYHA groups were decreasing as the functional class progressed. The Spearman Correlation Coefficient showed that there is a strong negative correlation between the scores of SF 36 (total, segments and dimensions) and heart failure expressed through the NYHA classes. CONCLUSION: Quality of life in patients with heart failure was exacerbated and associated with severity of the clinical features.

Endothelins (ETs) are a family of three peptides (ET-1, ET-2, ET-3) that are implicated in the physiological control of vascular smooth muscle cell (VSMC) and myocardial contractility and growth. ET-1 is vasoactive peptide that acts via ET-A receptors coupling inducing vascular smooth muscle cell contraction. ET-1 is involved in the development and maintenance of hypertension. Aim of this study was to investigate whether ET-1 can induce vascular smooth muscle cell proliferation through arachidonic acid (AA) metabolites formed via cytochrome P¬450 (CYP-450). VSMC proliferation was measured by [3H]thymidine incorporation in cultured cells treated by ET-1 (10 to l00 nmol/L) in presence of different inhibitors of CYP-450 (17-ODYA 5 μmol/L), lipoxygenase (LO) (baicalein 20 μmol/L) and cyclooxygenase (COX) (indomethacin 5 μmol/L). ET-1 (10 to 100 nmol/L) induced VSMC proliferation and this effect was attenuated by CYP-450 inhibitor (17-ODYA) and lipoxygenase (LO) inhibitor (baicalein) but not by cyclooxygenase (COX) inhibitor (indomethacin). CYP-450 and LO metabolites of AA, 20-hydroxyeicosatetraenoic acid (HETE) and 12-HETE increased [3H]thymidine incorporation in VSMC. Inhibitors of MAP kinase (PD-98059 50 μmol/L) and cPLA2 (MAFP 50 μmol/L) attenuated ET-1 as well as 20-HETE induced VSMC proliferation. These results suggest AA metabolites via CYP-450 mediates ET-1 induce VSMC proliferation.

Aim: The prognostic value of circulating antibodies to oxidized low-density lipoprotein (anti-oxLDL) in patients with coronary heart disease is not completely clear. We aimed to investigate the association between levels of anti-oxLDL in three groups of patients with different grades of severity of coronary heart disease. Patients and methods: The study included 101 patients classified into three groups: one (N=35) with acute myocardial infarction (AMI), a group (N=35) with angiographicallly proven coronary artery disease (APCAD), and a group without angiographicallly proven coronary artery disease (N=31) designated as a control group. Levels of IgG anti-oxLDL antibodies were meausured by enzyme-linked immunosorbent assay. Results: Mean anti-oxLDL value was significantly higher in patients with AMI than in patients with APCAS (1342.1±581.5 mIU/ml vs. 553.0±183.3 mIU/ml, p<0.001), as well as compared with control group (1342.1±581.5 mIU/ml vs. 246.5±114.3, p<0.001). Similarly, significant difference in anti-oxLDL levels was found between the patients with APCAS and control group (p<0.001). Conclusions: The present study showed that elevated levels of anti-oxLDL are positively related with a severity of coronary artery disease. Hence, elevated levels of anti-oxLDL may identify patients with unstable coronary heart disease. Oxidized LDL in circulating plasma could serve as a marker of cardiovascular events.