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Biomedical subjects

V F Kirichuk

Publications and source records attributed to V F Kirichuk.

At least 19 recordsLinked to original sources
PubMed1990

[State of coagulation hemostasis and fibrinolysis processes in dynamics of rapidly progressing forms of botulinal intoxication].

Phase disturbances of coagulation blood potential were revealed in experiments on white rats in dynamics of rapidly progressing form of botulinic intoxication, intoxication being caused by intraperitoneal injection of type C toxin. In preclinical period of intoxication activation of procoagulant and anticoagulant parts of hemostasis system, as well as fibrinolysis system, was noted. Similar shifts were revealed in the developmental period of generalized pareses of skeletal musculature. Only in the terminal stage of intoxication insufficiency of mechanism in formation of prothrombinase activity developed by simultaneous activation of anticoagulant mechanism and fibrinolysis system.

Animals↗
PubMed1989

[Dynamics of the development of disseminated intravascular coagulation syndrome in dystocia].

A comprehensive investigation of the hemostasis system permitted to follow the dynamics of disseminated intravascular hemocoagulation syndrome in patients with dystocia. In patients with spastic contractility and myometrial hypertonicity hypercoagulation stage of the aforementioned syndrome was preserved, in those with uterine inertia a transitory stage persisted, those with hypotonicity demonstrated hypocoagulation stage of the syndrome development. It was concluded that the prevention of acute syndrome stages depended on the rapid recovery of coordinated uterine contractility.

Acute Disease↗
PubMed1981

The role of the heart in the mechanism modifying the functional state of the blood clotting and fibrinolytic systems in thyroxine toxicosis.

In 36 rabbits the role of the heart in the genesis of changes in the tissue components of blood clotting and fibrinolysis in thyroxine toxicosis was studied. It was found that on the 5th and 10th days of toxicosis the thromboplastic (P = 0.002) an anticoagulant (P less than 0.001) myocardial activities decreased, and on the 15th day, increased. On the 20th day the myocardial thromboplastic activity remained increased, whereas the anticoagulant activity was further sinking (P = 0.05). Simultaneously the total fibrinolytic activity in the blood flowing through the heart and in myocardial extract increased (P less than 0.001), and the antiplasmin activity decreased.

Animals↗
PubMed1979

[Changes in platelet aggregation and fibrinolytic activity of blood in healthy persons during the 23-day physical cycle].

The blood of 100 health humans aged 18 to 40 years was analysed. The aggregation of platelets and blood fibrinolytic activity were shown to change within 23-day physical cycle according to Swoboda and Fliess. In the negative phase the platelets count, their aggregation, desaggregation process and blood fibrinolytic activity were higher than in the positive one. No substantial differences in platelets aggregation and blood fibrinolytic activity were found during the positive and negative phases of the emotional or intellectual cycles.

Activities of Daily Living↗
PubMedDate not supplied

[Effect of oxytocin on fibrinolysis and the status of the kallikrein-kinin system].

The effect of the neuropeptide oxytocin, administered i. m., on the state of fibrinolysis and the kallikrein-kinin system was studied throughout an experiment on 88 Wistar albino nonpregnant female rats. Oxytocin was shown to cause fibrinolytic activation as a result of the elevated activity of the plasmin enzyme, plasminogen activators and the suppressed activity of antiplasmins. At the same time oxytocin stimulated the activity of the kallikrein-kinin system as was seen from the reduced level of serum kallikreinogen and the increased level of kallikrein.

Animals↗
PubMedDate not supplied

[Role of thyroxine in releasing tissue plasminogen activators].

Experiments on animals have shown that thyroxin at doses of 10, 50 and 150 micrograms/kg promotes releasing the plasminogen tissue activator from the kidneys, liver and heart. It leads to an increase in the difference in its content in the venous and arterial blood of these organs as compared to control animals. Thyroxin at the above doses simultaneously decreases the level of the plasminogen activator in the pulmonary, renal and liver tissue as well as in the myocardium.

Animals↗