[Clinico-pathochemical substantiation of the exacerbation phenomenon in patients with ischemic heart disease during treatment with the helium-neon laser]. / Kliniko-patokhimicheskoe obosnovanie fenomena obostreniia u bol'nykh ishemicheskoi bolezn'iu serdtsa pri lechenii gelii-neonovym lazerom.

Some pathochemical mechanisms of coronary disease aggravation in the course of laser therapy were assessed by means of the measurement of erythrocyte membrane lipids and phospholipids as well as plasma alpha-tocopherol and diene conjugate levels. The aggravation was associated with an activation of metabolic processes aiming to produce regeneration of membrane structures. The regeneration takes place in the presence of chronic deficiency of total phospholipids and inadequate antioxidant protection of biomembranes, therefore complete stabilization and normalization of their composition and activity is impossible.

[Clinico-biochemical parallels against a background of traditional treatment and laser therapy of patients with ischemic heart disease]. / Kliniko-biokhimicheskie paralleli na fone traditsionnogo lecheniia i lazeroterapii bol'nykh ishemicheskoi bolezn'iu serdtsa.

The paper is devoted to analysis of clinico-biochemical indices and a quest for additional pathologico-chemical criteria at the cell membrane level of the efficacy of helium-neon laser therapy in coronary heart disease (CHD). Another task was to decipher a number of metabolic signs of the phenomenon of CHD "exacerbation" in laser therapy (during 4-6 sessions). Positive clinical results were obtained in 98% of the patients. A favorable time course was noted in serum lipoprotein spectrum indices and in lipid and phospholipid structure of erythrocyte membranes. Laser therapy caused mobilization of the cell membrane antioxidant defense. The 4th-6th session of irradiation was marked by temporary clinical deterioration--"exacerbation" of disease accompanied by an increase in the level of erythrocyte total phospholipids (at the expense of PTEA), a decrease in free fatty acid deficiency against a background of advancing alpha-tocopherol deficiency and a rise of the blood level of lipid peroxidation primary products (diene conjugates). A conclusion was that membrane protective drugs and drugs enhancing cell energy and antioxidant defense resources promoting the "deactivation" of influence on the membrane of lipid peroxidation metabolites (tocopherol, Essentiale, retinol, etc.) should be incorporated in therapy of CHD in order to prevent the phenomenon of its "exacerbation".