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Fibrinolysis and interleukin-I. Experimental study
MONDAY JUNE 25 - THURSDAY JUNE 28 1990 109
277 Plasminogen activator in experimental renal
hypertension PODOROLSKAYA LK ANDREENKO Gv; SHELKOVINA DV Moscow State University,Biological Department, Moscow, USSR
It is well known that coagulation and fibrinolytic systems are important contributory factors in progression and stabilization of hypertensive disease. Coagulation process results in high molecularweight aggregates of fibrinogen that increase blood flow resistance, blood viscosity, and arterial blood pressure. The fibrinolytic activity acts as an opposing factor. The role of plasminogen activator in pathogenesis and development of arterial hypertension is unknown. The experimental arterial hypertension was caused in white rats by right nephrectomy and partial occlusion of left renal artery.
278 Fibrinolysis and interleukin-I. Experimental
study ANDREENKO Gv ASHMARIN IP, LYUTOVA Lv KARABASOVA h&4, RYBAKINA EG, KOSINES L4 Moscow State University,Moscow, USSR
After two months arterial blood pressure rose to 180 mm Hg, followed by considerable increase of soluble fibrin monomer complexes, non enzymatic fibrinolysis (fibrinogen and heparin complexes), and increased viscosity. Fibrinolytic activity was depressed. Plasminogen activator activity measured by fibrin plates method was 3 times lower. There was a further great progress of these parameters after 5 months of experiment. The fibrinolysis inhibition in blood was followed by sharp exhaustion of plasminogen activator in renal cortex without any changes in median zone of kidney, when measured by Todd’s histochemical methods. In early stage of hypertension there was a significant rise of activator activity in blood as the reaction to extreme occlusion situation.
hibited enhanced fibrinolysis. A similar action was noted using the model of hyperfibrinolysis caused by dihydroergotoxin. The histochemical investigation of FA in the tissues of the heart, kidney and lung indicated a release of the antiactivator from the endothelial cells.
Interleukin-I (IL-I), a general-purpose mediator, triggers a complex of specific and non-specific defensive reactions of the organism. The standard IL1 preparation was obtained from rabbit peritoneal exudate. The molecular mass of purified preparation is 17 kD, the specific comitogenic activity is 1.0 x 16. The single i.v. administration of IL1 to intact albino rats (5.0 X lo6 u of activity per 1 kg of body weight) resulted in a pronounced decrease of the fibrinolytic activity (FA) of the total plasma and its euglobulin fraction. Multiple administration induced an increase in the levels of fibrinogen and antiplasmins. In the experimentally induced disseminated intravascular coagulation syndrome IL-I in-
279 Does mechanism that prevents hemophiliacs from hemorrhagic phenomena exist? MAKRIS PE, PITFL4R.A E Haemostasis and Thrombosis Unit ofA’Med Prop Clinic, AHEPA Univ Hospital, Salon&e, Greece
Two years ago we observed 6 patients (pts) with von Willebrand disease with a parallel defect in the protein C levels x40%, without having any explanation for it, but this random observation has triggered this study. The defect of coagulation factors exists during the life of pts but these do not have bleeding episodes continuously. Is there a mechanism which when activated, could prevent the hemophiliacs and other similar pts (any time?) from bleeding? i?he aim of this preliminary study was to check this question. Material & Methoak 82 subjects were tested (18 hemophiliacs, I-IA, 11 pts withvon Willebrand disease, WD, 31 pts with established
thrombophilia, T, & 22 normal individuals, NI). All pts with bleeding disease were out of bleeding episodes. Plasminogen activator inhibitor (PAI) was determined using a chromogenic method (Chromotimer System of Behring Co). Resuh: Our findings are presented as mean values & standard deviations. NI=5.0&0.8, I&4=6.4+2.3, WD=7.2+2.0, T=8.0&2.2. u/ml. Using the t-test with common S to compare these mean values of NI & HA pts we observed a statistically significant difference, ~~0.01, but between the NI and WD pts was the difference very significant, pcO.001, similar to that between NI and T pts, p
277 Plasminogen activator in experimental renal
hypertension PODOROLSKAYA LK ANDREENKO Gv; SHELKOVINA DV Moscow State University,Biological Department, Moscow, USSR
It is well known that coagulation and fibrinolytic systems are important contributory factors in progression and stabilization of hypertensive disease. Coagulation process results in high molecularweight aggregates of fibrinogen that increase blood flow resistance, blood viscosity, and arterial blood pressure. The fibrinolytic activity acts as an opposing factor. The role of plasminogen activator in pathogenesis and development of arterial hypertension is unknown. The experimental arterial hypertension was caused in white rats by right nephrectomy and partial occlusion of left renal artery.
278 Fibrinolysis and interleukin-I. Experimental
study ANDREENKO Gv ASHMARIN IP, LYUTOVA Lv KARABASOVA h&4, RYBAKINA EG, KOSINES L4 Moscow State University,Moscow, USSR
After two months arterial blood pressure rose to 180 mm Hg, followed by considerable increase of soluble fibrin monomer complexes, non enzymatic fibrinolysis (fibrinogen and heparin complexes), and increased viscosity. Fibrinolytic activity was depressed. Plasminogen activator activity measured by fibrin plates method was 3 times lower. There was a further great progress of these parameters after 5 months of experiment. The fibrinolysis inhibition in blood was followed by sharp exhaustion of plasminogen activator in renal cortex without any changes in median zone of kidney, when measured by Todd’s histochemical methods. In early stage of hypertension there was a significant rise of activator activity in blood as the reaction to extreme occlusion situation.
hibited enhanced fibrinolysis. A similar action was noted using the model of hyperfibrinolysis caused by dihydroergotoxin. The histochemical investigation of FA in the tissues of the heart, kidney and lung indicated a release of the antiactivator from the endothelial cells.
Interleukin-I (IL-I), a general-purpose mediator, triggers a complex of specific and non-specific defensive reactions of the organism. The standard IL1 preparation was obtained from rabbit peritoneal exudate. The molecular mass of purified preparation is 17 kD, the specific comitogenic activity is 1.0 x 16. The single i.v. administration of IL1 to intact albino rats (5.0 X lo6 u of activity per 1 kg of body weight) resulted in a pronounced decrease of the fibrinolytic activity (FA) of the total plasma and its euglobulin fraction. Multiple administration induced an increase in the levels of fibrinogen and antiplasmins. In the experimentally induced disseminated intravascular coagulation syndrome IL-I in-
279 Does mechanism that prevents hemophiliacs from hemorrhagic phenomena exist? MAKRIS PE, PITFL4R.A E Haemostasis and Thrombosis Unit ofA’Med Prop Clinic, AHEPA Univ Hospital, Salon&e, Greece
Two years ago we observed 6 patients (pts) with von Willebrand disease with a parallel defect in the protein C levels x40%, without having any explanation for it, but this random observation has triggered this study. The defect of coagulation factors exists during the life of pts but these do not have bleeding episodes continuously. Is there a mechanism which when activated, could prevent the hemophiliacs and other similar pts (any time?) from bleeding? i?he aim of this preliminary study was to check this question. Material & Methoak 82 subjects were tested (18 hemophiliacs, I-IA, 11 pts withvon Willebrand disease, WD, 31 pts with established
thrombophilia, T, & 22 normal individuals, NI). All pts with bleeding disease were out of bleeding episodes. Plasminogen activator inhibitor (PAI) was determined using a chromogenic method (Chromotimer System of Behring Co). Resuh: Our findings are presented as mean values & standard deviations. NI=5.0&0.8, I&4=6.4+2.3, WD=7.2+2.0, T=8.0&2.2. u/ml. Using the t-test with common S to compare these mean values of NI & HA pts we observed a statistically significant difference, ~~0.01, but between the NI and WD pts was the difference very significant, pcO.001, similar to that between NI and T pts, p