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Biomedical subjects

Z Marecková

Publications and source records attributed to Z Marecková.

4 recordsLinked to original sources

[Portal hypertension and the endothelium].

Portal hypertension is defined as a rise in the pressure gradient between the portal vein and the inferior vena cava by more than 10 mmHg. The basic factors in the development of portal hypertension include increased resistance in intrahepatic circulation, increased portal blood flow, and development of the hyperdynamic syndrome. Apart from structural changes in the hepatic tissue, the major role in the pathogenesis of portal hypertension is played by endothelial dysfunction. In patients with portal hypertension, endothelial dysfunction reduced the activity of vasodilator, anti-aggregation, and anti-adhesion substances (NO/EDRF, prostacyclin, CO) and to increased production of vasoconstrictor and proliferative substances (endothelins in particular) in intrahepatic the circulation. On the other hand, vasodilator agents become predominant in splanchnic and systemic circulation. As a result, the intrahepatic vascular resistance and portal blood flow rise. It was followed by a subsequent increase in portal pressure and the development of hyperdynamic circulation. Identification of the pathophysiological mechanisms of portal hypertension has paved the way to new trends in pharmacological therapy. The aim of effective treatment of portal hypertension is the permanent reduction of the portal pressure, which markedly decreases the risk for complications, and the risk for esophageal variceal bleeding in particular. The currently most preferred agents are those with vasodilator and vasoconstrictor effects.

Endothelium, Vascular↗

[Humoral profile of patients with severe aortic stenosis].

BACKGROUND: While the effect of neurohormones is often studied in congestive heart failure, their role in aortic stenosis needs to be elucidated. METHODS: 54 consecutive patients with symptomatic aortic stenosis without overt heart failure were studied at the age of 64.4 +/- 9.3 yrs with echocardiography, x-ray and catheterization. Levels of circulating atrial natriuretic factor endothelin-1, catecholamines, plasma renin activity, immunoreactive insulin and C-peptide were assessed, related to hemodynamic data and compared to those in 23 healthy controls, aged 59.2 +/- 12.8 yrs. RESULTS: Patients had significantly higher plasma levels of endothelin-1 (z-value 0.64 +/- 1.19, p = 0.019), atrial natriuretic factor (z-value 2.46 +/- 2.46, p < 0.001) and dopamine (z-value 0.91 +/- 2.33, p = 0.02). Levels of endothelin-1 and ANF positively correlated with mean (r = 0.631, p < 0.001) and wedged pulmonary artery pressures and with left atrial diameter index (r = 0.602, p < 0.001). Endothelin-1 levels correlated negatively with aortic valve area (r = -0.306, p = 0.041). No correlation was found between neurohumoral plasma concentrations and left ventricular mass index. CONCLUSIONS: In patients with symptomatic aortic stenosis without overt heart failure, elevated plasmatic levels of endothelin-1, atrial natriuretic factor and dopamine were documented. The increase of ET-1 levels is related to pulmonary hypertension and severity of the disease. Left ventricular hypertrophy is not related to neurohormonal levels. Neither circulating system renin-angiotensin nor noradrenaline are activated in these patients.

Adult↗

[Cell adhesion molecules and their role in pathophysiologic processes].

Cell adhesion molecules are substances with a protein character expressed on the cell surface of all tissues. They participate in the control of basic vital processes, in processes of embryogenesis, cellular growth and differentiation, they ensure the interaction of cells with the environment. At present four main classes of cytoadhesion molecules are known: integrins, the immunoglobulin group of adhesion molecules, cadherins and selectins. Cytoadhesion molecules play an important role in the pathophysiology of cardiovascular, neoplastic, infectious and skin diseases. Some cardiovascular diseases are associated with pathological impairment of the structure and function of endothelial cells-with endothelial dysfunction. In case of damage or inflammatory processes of the blood vessels due to the action of released cytokines increased expression of adhesion molecules of the integrin, selectin and immunoglobulin groups occurs and subsequently increased adhesion and migration of inflammatory cells across the vascular wall. Impaired function of the vascular endothelium is also the first step in the genesis and development of chronic vascular disease--atherosclerosis. In the initial stage of development of atherosclerosis--during rolling, adhesion and migration of leucocytes across the endothelium the cytoadhesion molecules play a crucial role.

Cardiovascular Diseases↗

[Endothelial dysfunction and arterial hypertension].

The endothelium lines all blood vessels in the human body, it is the basic structure which ensures the action of substances circulating in the blood stream on the vascular wall. It is an organ the sound state of which is essential for the physiological function of the vascular system. Its impaired function is a basic factor in the genesis and development of vascular disease. Under physiological conditions the endothelium has antiadhesive and antithrombotic properties, it produces vasoactive substances, prevents the penetration of circulating substances and formed elements across the vascular wall, and via adhesion molecules it participates in the interaction with cells in the circulation. Risk factors of cardiovascular diseases such as hypertension, hyperlipidaemia, hyperglycaemia, smoking damage the function of endothelial cells and cause the development of endothelial dysfunction. In patients with arterial hypertension endothelial dysfunction is characterized by an impaired endothelium dependent relaxation, increased adhesion and permeability of endothelial cells, structural changes of the vascular wall. When the endothelium is damaged by released cytokines an increased expression of adhesion molecules occurs, adhesion and migration of inflammatory cells across the vascular wall. Cytoadhesion molecules are released from the surface of the endothelium into the circulation where the rise of their plasma levels can serve as a marker of endothelial damage. Endothelial dysfunction in hypertonic subjects contributes in a significant way to the development and progression of chronic vascular disease--atherosclerosis. Improvement of the damaged endothelial function is therefore at present a desirable therapeutic objective in the treatment of hypertension.

Arteriosclerosis↗