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Biomedical subjects

A I Ershov

Publications and source records attributed to A I Ershov.

At least 19 recordsLinked to original sources
PubMed1996

[The significance of exacerbations of lung diseases in the development of chronic cor pulmonale and their treatment].

In 61 patients, pulmonary tuberculosis was complicated by thrombosis of the pulmonary artery or its embolism and by bronchial asthma. In various lung diseases, there was a combination of some factors predisposing to chronic cor pulmonale. These included specific infection, sympathoadrenal activation, reduced capillaries, and hypoxia in pulmonary tuberculosis, alveolar hypoventilation with arteriolar spasms, and elevated intrathoracic pressure in bronchial asthma; higher pulmonary arterial systolic pressure due to spasms of the pulmonary branches and drastically reduced arterial bed in pulmonary thromboembolism.

Asthma↗
PubMed1995

[Hemosorption in the treatment of chronic pulmonary heart in patients with tuberculosis].

Hemosorption was tried in 32 patients with pulmonary tuberculosis complicated with chronic cor pulmonale. Hemosorption is shown to regulate hemodynamics and immunological condition of the above patients. Thus, CIC levels lowered to normal, while IgM tended to elevation, systolic pressure in the pulmonary artery decreased, hemodynamic shifts got corrected.

Adult↗
PubMed1994

[Significance of cyclic nucleotides in pathogenesis of cor pulmonale in tuberculosis of respiratory organs and the use of beta adrenoblockers].

Blood levels of cyclic nucleotides and their actions on central hemodynamics were studied in 129 patients with pulmonary tuberculosis. A direct correlation was established between heart rate, pulmonary artery systolic pressure and concentrations of cyclic adenosine monophosphate. Basing on this finding, the authors propose introduction of beta-adrenoblockers in hyperkinetic circulation tuberculous patients to prevent cor pulmonale. Administration of anapriline in tuberculous patients with compensated cor pulmonale and symptoms of sympathoadrenal hyperfunction improves the patients' condition, promotes a decrease in cardiac output, cardiac index, systolic pressure in the pulmonary artery. No side effects of the drug were reported.

Adult↗
PubMed1994

[Development of chronic cor pulmonale in restrictive and obstructive pulmonary dysfunctions].

A total of 2840 patients with pulmonary tuberculosis and bronchial asthma were studied. Antigens are shown to induce a systemic vascular response with elevated systolic pressure in the pulmonary artery, peripheral venous spasms. There is activation of the sympathoadrenal system and desensitization of beta-adrenoreceptors with lower levels of cyclic adenosine monophosphate (CAMP). There is a direct correlation between the CAMP levels and the cardiac output, between those and the pulmonary systolic pressure (PSP). This determines hyperkinetic hemodynamics in tuberculosis with the volume- and pressure-loaded heart. Paresis of pulmonary circulation, as well as hypokinetic hemodynamics occur as a result of an allergic immunological reaction in severe fibrocavernous processes in the area of tuberculosis. There is a direct correlation between the circulating immune complexes and CAMP. In bronchial asthma microcirculation is impaired due to antigenic exposures and elevated intrathoracic pressure. Pulmonary capillary reduction in restrictive processes results in higher levels of CAMP and right-to-left shunt, leading to hypoxemia. In obstructive pulmonary diseases, hypoxemia is caused by hypoventilation and impaired ventilation-perfusion ratios.

Aged↗
PubMed1992

[Ventricular ejection fraction in oxygen therapy of patients with pulmonary tuberculosis].

Radionuclide study of ejection fraction of the right heart ventricle was carried out in lung tuberculosis patients with respiratory insufficiency and cor pulmonale. Oxygen therapy was found to promote reduction of right ventricle heart failure in effective treatment of lung tuberculosis. The greatest reduction of heart failure was recorded in cases where oxygen therapy was combined with cardiac glycosides. As the tuberculosis process progresses, oxygen therapy does not decrease right ventricle heart failure. The treatment by antibacterial agents alone without using oxygen does not lead to the rise of ejection fraction of the right ventricle of the heart.

Antitubercular Agents↗
PubMed1990

[Classification of respiratory insufficiency in pulmonary tuberculosis].

605 patients with different forms of pulmonary tuberculosis were examined. Blood gases and acid-base condition (ABC) were studied. In 22.2 per cent of the patients, hypoxemia was lacking with normal ABC and no respiratory failure (RF); in 36.6 per cent, hypoxemia was not accompanied by ABC changes and hence was caused by circulatory disturbances; in 15.6 per cent, it was combined with respiratory alcoholism; and in 6.8 per cent, with respiratory acidosis. The rest of the cases found to have metabolic disturbances of the ABC. Thus, hypoxemia is observed both with chronic forms of tuberculosis and with infiltrative/focal one, i.e. it follows a subacute course. In case of pulmonary tuberculosis, it is recommended to isolate subacute RF with PaO2 of 68.3 +/- 0.56 mm Hg, chronic RF of the 1-st phase with PaO2 of 71.8 +/- 0.7 mm Hg and chronic RF of the 2-nd phase with PaO2 of 64.2 +/- 0.88 mm Hg and accompanied by chronic cor pulmonale. In this case it seems necessary to find the basic mechanism of RF which is important for the treatment purposes.

Humans↗
PubMed1989

[Chronic cor pulmonale in pulmonary tuberculosis and its treatment].

New data on the pathogenesis of chronic cor pulmonale were obtained. The reduction of pulmonary capillaries at the site of the tuberculosis process beyond this site was found to contribute much to the development of pulmonary artery hypertension. Irreversible injuries to the vessels are due to both the pneumosclerotic changes and the specific circulating immune complexes (CIC) effects. Acting on the peripheral veins (in Koch's test), CICs influence the central hemodynamics, decreasing circulating blood volume by 30-40% and reducing cardiac output, thus resulting in deficit of the blood inflow to the right compartments of the heart. In this case the atrium functions at a higher load, like a suction pump, thus leading to cardiac hypertrophy. Peripheral vasodilators (apressin, nitrong) combined with cardiac glycosides (digoxin), favorably influencing the central hemodynamics, are recommended for the prevention and treatment of chronic cor pulmonale.

Chronic Disease↗