Replacement of infected aortoiliac vascular grafts with bifurcated BioIntegral Surgical No-React bovine pericardial xenografts.

The infection of a vascular prosthesis is potentially fatal, and its effective treatment still remains the greatest challenge for vascular surgeons. We present our initial experience using bovine pericardial vascular prostheses to replace infected aortoiliac vascular grafts. Six consecutive patients with infection of the graft were prospectively included in this study.

Metabolic Effects of Metformin in the Failing Heart.

Accumulating evidence shows that metformin is an insulin-sensitizing antidiabetic drug widely used in the treatment of type 2 diabetes mellitus (T2DM), which can exert favorable effects on cardiovascular risk and may be safely used in patients with heart failure (HF), and even able to reduce the incidence of HF and to reduce HF mortality. In failing hearts, metformin improves myocardial energy metabolic status through the activation of AMP (adenosine monophosphate)-activated protein kinase (AMPK) and the regulation of lipid and glucose metabolism. By increasing nitric oxide (NO) bioavailability, limiting interstitial fibrosis, reducing the deposition of advanced glycation end-products (AGEs), and inhibiting myocardial cell apoptosis metformin reduces cardiac remodeling and hypertrophy, and thereby preserves left ventricular systolic and diastolic functions.

Tempol, a Membrane-Permeable Radical Scavenger, Exhibits Anti-Inflammatory and Cardioprotective Effects in the Cerulein-Induced Pancreatitis Rat Model.

To date, it remains unclear whether mild form of acute pancreatitis (AP) may cause myocardial damage which may be asymptomatic for a long time. Pathogenesis of AP-related cardiac injury may be attributed in part to ROS/RNS overproduction. The aim of the present study was to evaluate the oxidative stress changes in both the pancreas and the heart and to estimate the protective effects of 1-oxyl-2,2,6,6-tetramethyl-4-hydroxypiperidine (tempol) at the early phase of AP.

Patients' satisfaction with therapy methods of advanced chronic venous disease.

Background: To assess patients' satisfaction from the therapy of advanced chronic venous disorders (CVD) in everyday clinical practice in Poland, and to compare the efficacy of various venoactive drugs (VADs) in venous ulcers healing process.

Methods: Seven hundred and eighty unselected adult patients with active (N.=441) or healed (N.

Efficacy evaluation of bio trombina ® 400 in mini mall y invasive treatment of complications (pseudoaneurysms), after venipuncture for diagnostic purposes. Authors' own experience - case study of 38 patients.

Unlabelled: Common use of venipuncture on upper and lower limbs for diagnostic purposes (such as coronarography or arteriography), and also during the course of treatment (angioplasty), very often bares a complication in the form of pseudoaneurysms. According to various reports, the incidence of pseudoaneurysms ranges from 0.005% to 0.

Nucleoside monophosphorothioates as the new hydrogen sulfide precursors with unique properties.

Hydrogen sulfide (H2S) is the gasotransmitter enzymatically synthesized in mammalian tissues from l-cysteine. H2S donors are considered as the potential drugs for the treatment of cardiovascular, neurological and inflammatory diseases. Recently, it has been demonstrated that synthetic nucleotide analogs, adenosine- and guanosine 5'-monophosphorothioates (AMPS and GMPS) can be converted to H2S and AMP or GMP, respectively, by purified histidine triad nucleotide-binding (Hint) proteins.

Chronic hyperleptinemia induces resistance to acute natriuretic and NO-mimetic effects of leptin.

Apart from controlling energy balance, leptin, secreted by adipose tissue, is also involved in the regulation of cardiovascular function. Previous studies have demonstrated that acutely administered leptin stimulates natriuresis and vascular nitric oxide (NO) production and that these effects are impaired in obese animals. However, the mechanism of resistance to leptin is not clear.

Renal antioxidant enzymes and glutathione redox status in leptin-induced hypertension.

Previously, we have demonstrated that leptin increases blood pressure (BP) in the rats through two oxidative stress-dependent mechanisms: stimulation of extracellular signal-regulated kinases (ERK) by H(2)O(2) and scavenging of nitric oxide (NO) by superoxide (O(2-.)). Herein, we examined if renal glutathione system and antioxidant enzymes determine the mechanism of prohypertensive effect of leptin.