title: [Development of chronic cor pulmonale in restrictive and obstructive pulmonary dysfunctions].
abstract: 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.
authors.forename: A I
authors.initials: AI
authors.lastname: Ershov
authors.forename: V A
authors.initials: VA
authors.lastname: Tikhonov
authors.forename: S I
authors.initials: SI
authors.lastname: Sharunov
authors.forename: M P
authors.initials: MP
authors.lastname: Gracheva
authors.forename: Iu A
authors.initials: IuA
authors.lastname: Evstafév
authors.forename: S P
authors.initials: SP
authors.lastname: Zavrazhnov
authors.forename: Iu G
authors.initials: IuG
authors.lastname: Grigorév
mesh_terms: D000368:Aged; D000936:Antigen-Antibody Complex; D001249:Asthma / Q000097:blood / Q000150:complications* / Q000276:immunology / Q000503:physiopathology; D001794:Blood Pressure; D002302:Cardiac Output; D002306:Cardiac Volume; D002908:Chronic Disease; D000242:Cyclic AMP / Q000097:blood; D005260:Female; D006801:Humans; D000860:Hypoxia / Q000209:etiology / Q000503:physiopathology; D008173:Lung Diseases, Obstructive / Q000097:blood / Q000150:complications* / Q000276:immunology / Q000503:physiopathology; D008297:Male; D011651:Pulmonary Artery / Q000503:physiopathology; D011659:Pulmonary Gas Exchange; D011660:Pulmonary Heart Disease / Q000097:blood / Q000209:etiology* / Q000276:immunology / Q000503:physiopathology; D011943:Receptors, Adrenergic, beta / Q000378:metabolism; D014397:Tuberculosis, Pulmonary / Q000097:blood / Q000150:complications* / Q000276:immunology / Q000503:physiopathology; D014655:Vascular Resistance
chemical_list: D000936:Antigen-Antibody Complex; D011943:Receptors, Adrenergic, beta; D000242:Cyclic AMP
vernacular_title: Razvitie khronicheskogo lëgochnogo serdtsa pri restriktivnom i obstruktivnom tipakh narusheniia funktsii lëgkikh.