The new tools to carry out researches into the vascular diseases modified the approach to define precise diagnosis and consequently, the therapy [1-5]. The duplex scanning is useful for the decisions of medical, endovascular or surgical treatment on young and old patients, easy to repeat non-invasive, if performed by an expert operator and a good instrument [5]. We will consider some of the most frequent pathologies: 1. Carotid stenosis 2. Abdominal aortic aneurysm 3. Venous thrombosis 4. Chronic venous insufficiency

Objective To investigate the effect of cytoflavin on cerebral hemodynamics at various stages of arterial hypertension. Materials and methods One hundred forty patients with hypertension of I-III stages were divided into two groups taking into account their stratification: I. The patients of treatment group 1 received a comprehensive therapy consisting of antihypertensive therapy and a metabolic drug, cytoflavin, 10 mg from the first to the tenth day by an intravenous drop infusion, then for 60 days - they received 2 tablets in a dose of 320 mg twice a day; II. The patients of treatment group 2 - received antihypertensive therapy only; III. The control group was composed of 30 apparently healthy people. All the patients were examined clinically and instrumentally before the therapy administration and in 70 days after the beginning of treatment. The state of cerebral hemodynamics was assessed with the use of a comprehensive ultrasonic examination algorithm of the cerebral vascular system based on the concept that it is composed of five functional and morphological levels. Results The signs of cerebral vascular remodeling are observed in patients with hypertension which are characterized by a change of PI, RI values, intimа mediа complex, the decrease of blood flow in the common carotid arteries, internal arteries, vertebral and medial cerebral arteries, by the decrease of Rosenthal veins reactivity, blood flow decrease in Rosenthal veins, the internal jugular veins and increase of blood flow in the vertebral veins in stages I-III of the disease. A complex therapy with application of cytoflavin is accompanied by blood flow increase in the common carotid arteries, internal carotid arteries, medial cerebral arteries in the first stage of the disease; in vertebral arteries in stages I-II of the disease it is accompanied by the improvement of Rosenthal vein reactivity, the restoration of the blood flow values to control ones in Rosenthal veins, internal jugular veins and also by the blood flow decrease in vertebral veins while examining a patient in recumbent position. Conclusion Changes of cerebral hemodynamics have been found in all structural and functional levels of the vascular system in the brain beginning with hypertension stage I. A complex therapy with application of cytoflavin was administered in the following regimen: an intravenous drop infusion of 10 mg from day 1 to day 10, then for 60 days the patients received 2 tablets twice a day that lead to the abatement of marked manifestations of cerebral arterial insufficiency at the incipient stages of the disease, microcirculatory disorders and venous insufficiency in stages I-III of the disease. The obtained results have shown the need of investigating cerebral haemodynamics at five structurally functional levels of the cerebrovascular system and allow us to recommend cytoflavin for use in a complex therapy of patients with arterial hypertensive from the first stage.

Abnormal arterial smooth muscle (ASM) growth is a major contributor to the etiology of many occlusive vascular disorders, yet to date no target or process capable of completely controlling pathologic ASM growth has been identified. In turn, lack of precision in identifying full causation of abnormal ASM growth has limited utility of feasible biomarkers for early identification and perhaps prophylaxis for ensuing cardiovascular events. In this light we recently reported capacity of the metabolic sensor AMP-activated protein kinase (AMPK) to inhibit ASM cell proliferation and migration under in vitro and in vivo conditions. Microfilament-associated vasodilator-stimulated phosphoprotein (VASP) has also been implicated in the control of pathologic ASM cell growth via dynamic interaction with the actin cytoskeleton and focal adhesion complexes, and new findings published by our lab suggest interdependence between AMPK and VASP in ASM. In the current study we hypothesized that AMPK reduces ASM cell growth through mechanisms dependent upon VASP and theorized that VASP phosphorylation status may represent a useful biological marker for AMPK-related metabolic and cardiovascular disorders. In rat A7r5 ASM cells, activation of AMPK by the AMP-mimetic AICAR significantly increased phosphorylation of VASPThr278 and the protein kinase A target VASPSer157, proposed VASP inhibitory sites [1,2], with little effect on the protein kinase G marker VASPSer239 after 60 minutes. At this time point AICAR-stimulated AMPK doubled G-actin to F-actin ratio (G:F), significantly reduced (~40%) catalytic Tyr397 phosphorylation of focal adhesion kinase (FAK) and significantly increased (~100%) cytostatic paxillin compared to vehicle controls. Functionally, AMPK significantly inhibited PDGF-stimulated transwell migration of ASM cells after 18 hours and serum-stimulated cell cycle progression after 24 hours compared to vehicle controls. To determine VASP-dependency of these events we performed studies using Lentiviral non-targeting control (Lv-NTC) and short hairpin RNA (Lv-shRNA)-mediated VASP-deficient ((-)VASP) ASM cells. Results showed that (-)VASP cells displayed significantly reduced (~75%) VASP expression (normalized to DNA content) 48 hours post-infection compared to Lv-NTC cells and significantly diminished AMPK-stimulated VASPSer157 and VASPThr278 compared to controls. (-)VASP cells demonstrated significantly increased G:F actin ratios yet had similar levels on FAKTyr397 and paxillin compared to AMPK-stimulated cells. Interestingly, VASP deficiency failed to markedly alter the inhibitory effects of AMPK on ASM cell migration yet fully reversed AMPK-mediated cell cycle inhibition compared to controls. These findings suggest that AMPK has ability to reduce ASM cell growth by inhibiting VASP-directed actin cytoskeletal dynamics and provide rationale for continued exploration of AMPK and VASP as targets for vascular growth control. Lastly, these new observations lend credence for VASP as a potential biological marker for AMPK-driven metabolic and associated cardiovascular disorders.

Purpose: To define clinical and neuroimaging characteristics of venous stroke. Materials and methods: 84 patients with clinical signs of acute stroke and constitutional venous insufficiency were examined. Clinical criteria constitutional venous insufficiency was the presence of complaints caused by venous cerebral blood circulation, the presence of several typical localizations of venous pathology (varicose and thrombosis of the veins of the lower extremities, hemorrhoids, varicocele and varicose veins of the esophagus), family “venous” history. It was revealed that 20 of them are suffering from venous stroke and 64 - from arterial stroke. Verification of diagnosis was made out by the methods of neuroimaging. Results: The age in the studied groups was statistically significant and different in the group of patients with venous stroke [52, 7 (41; 64) years] in comparison with arterial stroke [65, 3 (45; 80) years] in distribution of patients on sex the prevalence of women has been revealed in comparison with men in the venous stroke group. The onset of clinical manifestations occurred in the compared groups unequally: sub acute, slow progression of the disease within more than 48 hours was noted in the group of patients with venous stroke in 80% and in the group of patients with arterial stroke in 25% cases. The main symptom, along with focal symptoms, was a headache. During venous stroke it had diffuse character and progressed within a few days or even weeks. Patients with arterial stroke showed complaints to headaches “as a hoop”, pressing or the gripping character more often. However, the severity of headaches in patient with venous stroke was statistically significantly higher than in patients with arterial stroke (р< 0.05). During venous stroke there is a trend of relatively rapid regression of general cerebral symptoms. In the clinical picture of the disease of patients with venous stroke a significant place is occupied by the symptoms that indicate cerebral venous circulatory distress. According to magnetic resonance imaging findings, parietal-occipital region are most commonly tends to affect in the group of patients with venous stroke (in 70% cases). Magnetic resonance signal lesion venous stroke is in most cases heterogeneous. A distinctive feature of venous stroke is the presence of signs of vasogenic cerebral edema by magnetic resonance modes DWI and ADC-mapping in the first days of the disease (in 80% cases in patients with venous stroke and in patients with arterial stroke - in 39.4%). Conclusion: Venous stroke developed in patients at rather young age and more often in women. The clinical picture of a venous stroke is characterized by: a sub acute, slow development of clinical manifestations; the prevalence of cerebral symptoms and signs over focal; the presence of symptoms testifying to venous cerebral discirculation; a tendency to relatively fast regress of cerebral symptoms and signs. According to magnetic resonance imaging findings, in case of a venous stroke the localization of venous stroke does not coincide with blood supply “districts” of the main intracranial arteries; the shape of foci is irregular and boundaries are uneven and indistinct. The signs of cerebral venous discirculation are visualized as well as intracranial venous stasis and vasogenic edema.

The study aimed to describe microcirculation at different parts of the foot with two different methods in healthy controls. Furthermore, the effect of oxygen inhalation and the relationship between results with these two methods were evaluated. Methods: Microcirculation of the foot was evaluated on 15 healthy subjects (aged 22-37 years) by two methods: Transcutaneous Oxygen Pressure (TcPO2) with and without oxygen provocation and Laser Doppler Flux (LDF) with heat provocation. Four different measuring sites were used: one distal and one proximal point at the dorsal foot (the distal is the standard position), one point at the medial plantar part and one at the anterolateral part of the foot. The measuring points were distributed on parts of the foot supplied by three different end-arteries (so called angiosome). Results: TcPO2 levels were significantly higher at all three measuring points than at the standard position at the distal dorsal foot. Median TcPO2 was 68 mm Hg at the standard position compared with 76 mm Hg at the dorsal proximal, 73 mm Hg at the medial and 83 mm Hg at the anterolateral electrode position. After oxygen provocation only the proximal dorsal point remained significantly higher than the standard position. Heat-provoked LDF did not differ between different parts of the foot with an increase of more than 400% seen at all probe positions in all subjects. Oxygen inhalation increased TcPO2 to median levels around 200 mm Hg, without affecting LDF. Both TcPO2 and LDF results were unrelated to different angiosome. Conclusion: In healthy subjects TcPO2 levels are slightly higher at proximal than at distal parts of the foot, but LDF did not differ between different parts of the foot. Although both methods are used to study the microcirculation there are no correlations between TcPO2 and LDF, which reflect that these methods use different mechanisms and different measurement principles.