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Biomedical subjects

M S Surovikina

Publications and source records attributed to M S Surovikina.

At least 19 recordsLinked to original sources
PubMed1991

[Hypokininemia in chronic bronchitis caused by cotton dust].

Examination of 102 patients who developed bronchitis due to exposure to cotton dust running a complicated or noncomplicated course recognized a moderate hyperkininemia in 40% of cases (4.46 +/- 0.43 against the normal 2.90 +/- 0.42) and apparent hypokininemia in 60-63% of cases (0.52 +/- 0.03 against 2.90 +/- 0.42). Hypokininemia appeared in association with pathological shifts in external respiration and central hemodynamics. It is an unfavourable factor contributing to formation of occupation complications of chronic bronchitis: pulmonary emphysema, pulmonary hypertension and cor pulmonale.

Adult↗
PubMed1986

[Diagnostic significance of indices of kininogenesis in infectious-allergic myocarditis].

Three patterns of kininogenetic changes: enhanced (50% of patients), depressed (40%) and qualitatively-different (10%) kininogenesis, were identified through 3 measurements of blood kallikrein-kinin (BKK) activity by kininogenase techniques in patients with infectious allergic myocarditis and myocarditic cardiosclerosis. The intensity of individual phases of kininogenesis is conditioned by the activity of total plasma kallikrein, its conformation and the level of kallikrein inhibitors. During the activated kininogenesis phase, a direct relation can be seen between changes in the activity of the above-mentioned parameters and clinical severity of the disease. The measurement of total kallikrein activity, kaolin adsorption of this enzyme, and kallikrein inhibitors may be useful as an additional diagnostic test. The pattern of changes in BKK activity parameters may be indicative of persisting or progressing myocardial inflammatory allergic process in patients with myocarditic cardiosclerosis. The treatment for myocarditis with conventional anti-inflammatory agents, leaving out the drugs controlling kininogenetic changes, fails to produce complete recovery and the normalization of BKK activity.

Adult↗
PubMed1983

[Clinical evaluation of kininogenesis indices].

The discrepancies between kininogenase, BAEE-esterase and BAPNA-amidase activity in plasma kallikrein were shown in experiments in vitro. The same discrepancies were detected during examination of children aged under 3 years suffering from bronchopulmonary diseases (acute and lingering pneumonia, bronchial asthma). In these children, prekallikrein, kallikrein and kallikrein inhibitor were determined at a time by the 3 methods (esterase, test-tube chromatographic and kininogenase ones). It has been shown that the kininogenesis intensity could be assessed objectively only in the measurement of the kininogenase activity of kallikrein contained by the whole plasma or its fractions. The esterase technique characterizes total factors of contact activation and does not reflect the activity of kallikrein, prekallikrein and kallikrein inhibitor. The test-tube chromatographic method might be regarded as objective only in the measurement of the kininogenase activity of the fractions that contain kallikrein or prekallikrein.

Asthma↗
PubMed1983

[Method of estimating kininogenesis in blood plasma].

It is suggested that the kininogenesis should be assessed from 3 forms of kallikrein which are detected on the basis of their kininogenase activity in whole blood plasma. Heating of blood plasma acidified to pH 3.0 for 15-20 min at 61 degrees C allows for the conditions under which the kallikrein inhibitors (alpha 1-antitrypsin, alpha 2-macroglobulin) are destroyed whereas kallikrein, prekallikrein, low- and high-molecular kininogens (HMK) are preserved, thus constituting a complex of proteins making the kininogenase reaction feasible. Addition of purified preparations of HMK to the neutralized samples of normal and sick individuals' plasma permitted the demonstration that as the kallikrein is raised, the kininogenesis gets actually activated, during which the blood manifests, in the presence of kallikrein hyperactivity, a sufficient amount of HMK. Provided the kallikrein content drops by 50%, the kininogenesis is reduced, which is accounted for by depletion of blood HMK. A 70%- and a greater decrease in the kallikrein content attests to the kininogenesis reduction because of the diminished levels of HMK, prekallikrein and kallikrein. The regularities described have been confirmed by the agreement between the blood plasma kallikrein level and the concentration of blood free kinins revealed during examination of 68 normal individuals and 231 patients suffering from different inflammatory-allergic diseases of the respiratory and hepatobiliary organs, and from diabetes mellitus.

Adult↗
PubMed1981

[Method of determining human and animal plasma kallikrein inhibitors].

A method for determining blood plasma kallikrein inhibitors is suggested. It is based on inhibiting the kininogenase activity of kallikrein. The donors' dry plasma devoid of kininases, of other proteolytic enzymes and their inhibitors was used as source and reference of prekallikrein, kallikrein and high-molecular kininogen. Freshly centrifuged plasma was incubated in the presence of unithiol at 37 degrees C in amounts producing a 30-50% inhibition of the kininogenase activity of kallikrein. The values obtained reflected the activity of kallikrein inhibitors and might be of great importance in the study of the physiological role and biochemical properties of kallikrein inhibitors in different animal species, in the diagnosis and prediction of various diseases, as criterion for laboratory control over administering tissue inhibitors of proteolytic enzymes of animal origin.

Adolescent↗
PubMed1977

[Kallikrein-kinin system of the blood plasma in patients with infectious-allergic myocarditis].

The state of the blood plasma kallikrein-kinin system in infectious-allergic myocarditis was studied for the first time. Biological methods for the determination of kallikrein, kininogen, kininases, and free kinins were used. Changes in the activity of the kinin system were revealed in 92% of 38 individuals examined: activation in the first 2-4 months and exhaustion later (in 6-8 months). It was shown that the generally accepted clinico-laboratory criteria on myocarditis are not always informative. Determination of the components of the plasma kinin system is suggested as an additional diagnostic test. The use of kinin antagonists and inhibitors of the kinin system in the complex of drug therapy in infectious-allergic myocarditis is recommended.

Adult↗
PubMed1976

[Effect of antikinin agents on the course of experimental myocarditis].

The therapeutic action of 5 preparations: specific antikinin substances -- anginin and contrical, and nonspecific -- epsilon-aminocapronic acid, aspirin and indometacine, was tested in 71 rabbits with allergic myocarditis. It has been concluded that in the allergic distruction of the myocardium plasma kinins, which are formed and accumulated in large quantities, take part in the pathogenesis of the disease serving as mediators of the tissue distruction, therefore specific antagonists of kinins and inhibitors of the kinin system should be included as pathogenetic agents into the complex of allergic myocarditis treatment.

Aminocaproates↗
PubMed1976

[Changes in the kinin system components and structure of the myocardium under the influence of antikinin preparations in allergic myocarditis in rabbits].

Experimental allergic myocarditis was induced in rabbits; a study was made of the effect on the kininogen content and on the activity of kininase in the myocardium, and on its morphological structure produced by anginine, contrical, aspirin, indometacine and epsilon-aminocapronic acid. The former two preparations were much more potent (in comparison with the others) in inhibiting the activation of the myocardial kinin system and promoted restoration of the morphological structure of the myocardium. Development of an allergic inflammation in the myocardium could be arrested or decreased by inhibition of the kinin system of the plasma and myocardium by specific agents.

Aminocaproic Acid↗