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Biomedical subjects

H Lukjan

Publications and source records attributed to H Lukjan.

At least 37 records · Page 2Linked to original sources

Prophylaxis of recurrent venous thrombosis with long-term enhancement of fibrinolysis.

The effects of 6 months' combined therapy with phenformin and an anabolic steroid were compared in patients with thrombophlebitis migrans (12 patients) and those with superficial thrombophlebitis (15 patients). In both groups of patients an increase in blood fibrinolytic activity, and "capacity" decrease in platelet adhesiveness, plasma fibrinogen, blood lipids, beta lipoproteins as well as serum cholesterol level were found. A statistically significant decrease in frequency of inflammations in patients with thrombophlebitis migrans occurred. In these patients a return of the previously low "fibrinolytic capacity" to normal values was observed. It seems that prolonged activation of fibrinolysis by means of phenformin and an anabolic steriod may be of value in the prophylaxis of venous thrombosis especially thrombophlebitis migrans.

Adult↗

[The 131I-fibrinogen turnover during activation of blood fibrinolysis].

The influence of stanozolol Stromba and phenformin Dibotin (Winthrop) and complamin (Wulfing) on transformation of 131J-fibrinogen administered intravenously was examined in 39 patients with arteriosclerosis obliterans. The patients were divided into 3 groups; one of the groups included untreated patients. Radioactivity of the plasma and of the urine was determined by means of a scintillation counter. The volume of plasma, plasma fibrinogen (g%, g, g/kg), half time of persistance (T 1/2) and degradation of fibrinogen were determined. The patients who received Dibotin and Stromba simultaneously showed statistically significant decrease of the plasma fibrinogen degradation im comparison to the control group. But in patients who received complamin in spite of significant decrease of the plasma fibrinogen (g%), the fibrinogen degradation was not different from the value obtained in the group.

Adult↗

Experimental studies on activation of the kininogenic system after exclusion of the hepatic circulation.

Levels of kininogen and kallikrein activity were studied in the plasma of rabbits with ligated hepatic blood vessels. Ligation of hepatic veins and arteries arrested visceral circulation in the animals and produced symptoms of shock and death of the animals. Ligation of the superior mesenteric artery at the same time prevented these symptoms, creating an experimental model of exclusion of the liver. Fibrinolytic activation of the kininogenic system by intravenous injection of xanthinol nicotinate (Sadamin, Polfa) in rabbits with excluded hepatic blood circulation caused a rise in kallikrein activity and transient drop in levels of kininogen. Return to normal of kininogen levels in the animals with excluded liver indicated that the process of restoration of kininogen deficiency in the blood is a complex one, independent of direct kininogen synthesis in the liver or its release from the liver.

Animals↗

Studies of the plasma kinin-forming system in cirrhosis of the liver.

Kininogen level, that of active kinins and kininase activity in the plasma of patients suffering from cirrhosis of the liver and of healthy people were studied. The kininogen content was determined by different available methods i.e. the trypsin and acetone techniques and by means of the plasma and glandular kallikrein preparation. An increase in kininase activity and a lowered kininogen level as determined by all the methods were found in the sick persons. The maximal decrease in the kininogen level determined by means of the plasma kallikreins is substantiated in connection with the increased fibrinolytic activity of the plasma of the patients with hepatic cirrhosis.

Acetone↗