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1. |
Kinetic Analyses of Potentiation of Plasminogen Activation by Streptokinase in the Presence of Fibrin or Its Degradation Products |
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Pathophysiology of Haemostasis and Thrombosis,
Volume 17,
Issue 1-2,
1987,
Page 1-7
Yumiko Takada,
Akikazu Takada,
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摘要:
When Glu-plasminogen (Glu-plg) was activated by various amounts of streptokinase (SK), Km of the hydrolysis of S-2251 by the mixture of Glu-plg and SK did not change, but Vmax increased with an increase in the amount of SK. Since low concentrations of SK-plg complex do not result in its conversion to the SK-plasmin complex by mutual activation, these results seem to suggest that the SK-plg complex may be a better activator when S-2251 is used as a substrate. When Glu-plg was activated by SK in the presence of fibrin(ogen) or its degradation products (potentiating agents), Km did not change with an increase in the concentration of each potentiating agent, but Vmax increased. The effects of potentiating agents on the kcat E.
ISSN:1424-8832
DOI:10.1159/000215552
出版商:S. Karger AG
年代:1987
数据来源: Karger
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2. |
Structure-Function Relationship of 3-Phosphoglycerate Analogues with Platelet Aggregation and Thromboxane A2Formation |
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Pathophysiology of Haemostasis and Thrombosis,
Volume 17,
Issue 1-2,
1987,
Page 8-13
P.G. Iatridis,
H. Hadd,
M. Kotrotsou,
L. Ling-Indeck,
S.G. Iatridis,
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摘要:
We have studied the effects of 2,3-diphosphoglycerate (2,3-DPG), 3-phospho-glycerate (3-PG), 3-phosphoglyceraldehyde (3-PGA), 2-phosphoglycerate (2-PG) and β-glycerol phosphate (β-GP) on platelet aggregation and on thromboxane B2 (TXB2) formation. The results show that 2,3-DPG, 3-PG, and 3-PGA inhibited platelet aggregation and TXB2 formation induced by norepinephrine, ADP, epinephrine, and collagen; but they also induced platelet aggregation and TXB2 formation in the presence of subthreshold concentrations of Na arachidonate. 2-PG and β-GP were inactive. The results also show that there is a structure-function relationship between 2,3-DPG, 3-PG, and 3-PGA with platelet aggregation phenomena and prostaglandin synthes
ISSN:1424-8832
DOI:10.1159/000215553
出版商:S. Karger AG
年代:1987
数据来源: Karger
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3. |
Spectrophotometric Method for the Assay of Human Blood Coagulation Factor VIII |
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Pathophysiology of Haemostasis and Thrombosis,
Volume 17,
Issue 1-2,
1987,
Page 14-24
G. van Dieijen,
M.P. van Dieijen-Visser,
J. Franssen,
H.C. Hemker,
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摘要:
A spectrophotometric method for the assay of human blood coagulation factor VIII in plasma is presented. The chromogenic assay for factor VIIL·C in plasma is performed in 3 steps: (1) activation of factor VIII by thrombin; (2) activation of factor X in a mixture of factor X, factor IXa, phospholipids/Ca2+ and plasma containing activated factor VIII, and (3) determination of the rate of factor Xa formation with the chromogenic substrate S2337. Within-assay variation was between 5 and 6.9% for factor VIIL·C activities between 20 and 150%. Clotting and chromogenic factor VIIL·C activities were compared in plasma of 50 normal healthy donors (coefficient of correlation r = 0.8
ISSN:1424-8832
DOI:10.1159/000215554
出版商:S. Karger AG
年代:1987
数据来源: Karger
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4. |
The Capillary Thrombometer Revisited |
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Pathophysiology of Haemostasis and Thrombosis,
Volume 17,
Issue 1-2,
1987,
Page 25-31
R.P. Kadota,
E.J.W. Bowie,
H.C. Emslander,
D.N. Fass,
D.M. Ilstrup,
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摘要:
A modified capillary thrombometer was constructed to study the rate of thrombus formation using heparinized whole blood (2 U/ml) obtained from normal adults (n = 22) and children (n = 20) and patients with hemophilia A (n = 10) or von Willebrand’s disease (n = 8). The median thrombosis times were as follows: normal adults =12.8 min (range = 4.5–26.0), normal children = 13.3 min (range = 5.7–29.0), patients with hemophilia A = 37.2 min (range = 20.0–60.0 min), and patients with von Willebrand’s disease = 60.0 min (range = 37.2–60.0). Significant differences were demonstrated between all groups of subjects, except between normal adults and children. The capillary thrombometer appears to measure thrombus formation dependent on adequate Willebrand factor an
ISSN:1424-8832
DOI:10.1159/000215555
出版商:S. Karger AG
年代:1987
数据来源: Karger
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5. |
High-Dose Systemic Streptokinase and Acylated Streptokinase-Plasminogen Complex (BRL 26921) in Acute Myocardial Infarction: Alterations of the Fibrinolytic System and Clearance of Fibrinolytic Activity |
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Pathophysiology of Haemostasis and Thrombosis,
Volume 17,
Issue 1-2,
1987,
Page 32-39
M. Köhler,
P. Hellstern,
P. Doenecke,
H. Schwerdt,
C. Özbek,
C. Miyashita,
R.W. Winter,
G. von Blohn,
L. Bette,
E. Wenzel,
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摘要:
We report the results of two consecutive studies using intravenous bolus injections of streptokinase (SK) or acylated plasminogen-SK complex (BRL 26921) in patients with acute myocardial infarction (AMI). In the first study, 20 patients received either 750,000 units (U) SK (group IA, n = 10) or 1,500,000 U SK (group IB, n = 10) within 5–10 min intravenously. In the second study 10 consecutive patients received 750,000 U SK within 15 min (group IIA) intravenously. The following 10 consecutive patients received 30 mg BRL 26921 within 2 min (group IIB). Early reperfusion was found in 16 patients in the first study (8 in each group) and in 18 patients in the second study (9 in each group). The decrease of fibrinolytic activity was biphasic with a half-disappearance time of 112.5 min for BRL 26921 and 31 (IA) and 18 (IB) min for SK. α2-Antiplasmin depletion and a decrease of fibrinogen was observed with no differences after bolus injections of SK and of BRL 269
ISSN:1424-8832
DOI:10.1159/000215556
出版商:S. Karger AG
年代:1987
数据来源: Karger
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6. |
Effect of Single-Dose Aspirin on TXA2and PGI2Cyclooxygenases in vivo |
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Pathophysiology of Haemostasis and Thrombosis,
Volume 17,
Issue 1-2,
1987,
Page 40-48
Rosemary Zaragoza,
Guy C. Le Breton,
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摘要:
The present study investigated the sensitivities of the thromboxane A2 (TXA2) cyclooxygenase and the prostacyclin (PGI2) cyclooxygenase to aspirin using an in vivo animal model. In this model, arachidonic acid (AA) was administered to mice via cardiac puncture, and plasma levels of thromboxane B2 (TXB2) and 6-keto prostaglandin F1α (6-keto PGF1α) were determined. Infusion of AA (5, 10, 25 and 50 mg/kg) resulted in a dose-dependent increase in both TXB2 and 6-keto PGF1α. Pretreatment with aspirin resulted in a dose-dependent and parallel decrease in TXB2 and 6-keto PGF1α production. This nonselective inhibition occurred at all doses of aspirin (1, 10 and 50 mg/kg) and at all levels of cyclooxygenase activity (5–50 mg/kg AA). These results indicate that the TXA2 and PGI2 cyclooxygenase enzymes are equally sensitive to inhibition by a single dose of as
ISSN:1424-8832
DOI:10.1159/000215557
出版商:S. Karger AG
年代:1987
数据来源: Karger
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7. |
Treatment of Deep Venous Thrombosis with a Very Low Molecular Weight Heparin Fragment (CY 222) |
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Pathophysiology of Haemostasis and Thrombosis,
Volume 17,
Issue 1-2,
1987,
Page 49-58
G. Janvier,
S. Winnock,
G. Dugrais,
A. Vallet,
E. Dardel,
J.M. Serisé,
S. Calen,
C. Vergnes,
F. Toulemonde,
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摘要:
Thirty patients presenting with phlebographically confirmed deep venous thrombosis were treated with a very low molecular weight heparin fragment (CY 222) in an open and prospective phase-2 trial. A uniform dosage of 750 IC anti-factor Xa units/kg/day was administered subcutaneously for 10 days or more to patients whose thromboses were categorized as postsurgical (17 cases) or medical (13 cases). The clinical symptoms of venous thrombosis diminished in 93% of the patients overall. The extent of vascular clearing was assessed by an original scoring system which compared the pre- and posttreatment phlebo-graphies. The effect of treatment was globally rated ‘very good’ (more than 75 % lysis) in 37% of the patients, ‘good’ (about 50% lysis) in 40% and ‘poor’ (0–25% lysis) in 17%; the phle-bographic thrombosis worsened in 6.6%. Little change occurred in laboratory tests exploring thrombolysis, but a strong anti-factor Xa activity
ISSN:1424-8832
DOI:10.1159/000215558
出版商:S. Karger AG
年代:1987
数据来源: Karger
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8. |
Influence of Heparin, Aspirin, Streptokinase and Factor VIII (AHF) on Amorphous Electron-Dense Substance, a Mediator of Platelet and Thrombus Adhesion in vivo |
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Pathophysiology of Haemostasis and Thrombosis,
Volume 17,
Issue 1-2,
1987,
Page 59-65
K.S. Herrmann,
W.-H. Voigt,
H. Kreuzer,
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摘要:
Platelet adherence and aggregation on vessel walls are the first crucial steps in thrombogenesis and atherosclerosis. Whether platelets can be activated on damaged endothelial cells or their activation is achieved only when subendothelial structures are exposed was controversially discussed in the past. Recently, an electron-microscopic study has revealed an amorphous electron-dense substance (AEDS) after endothelial cell damage and has discussed its role as a possible trigger of thrombogenesis. The aim of the present study is to elucidate the role and origin of this substance and to investigate the influence which inhibitors of platelet function (acetylsalicylic acid), coagulation (heparin), stimulation of fibrinolysis (streptokinase) and addition of factor VIII (AHF) have on AEDS.
ISSN:1424-8832
DOI:10.1159/000215559
出版商:S. Karger AG
年代:1987
数据来源: Karger
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9. |
Lack of Effect of Aspirin on Cigarette Smoke-Induced Increase in Circulating Endothelial Cells |
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Pathophysiology of Haemostasis and Thrombosis,
Volume 17,
Issue 1-2,
1987,
Page 66-69
James W. Davis,
Loretta Shelton,
David A. Eigenberg,
Charles E. Hignite,
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摘要:
A random-order, double-blind crossover study was done to compare the effects of placebo and two different doses of aspirin on the endothelial cell count of venous blood before and after smoking. Each of 17 male habitual smokers with coronary artery disease smoked two cigarettes during each of three 20-min periods separated by 2 weeks. Each patient was asked to take a tablet containing 150 mg of aspirin, 300 mg of aspirin or a placebo 12 h before each experimental smoking period and to abstain from smoking in the interim. Endothelial cell counts were determined by means of differential centrifugation and phase-contrast microscopy and nicotine by gas chromatography. After ingestion of placebo, the mean endothelial cell counts ( ± SD) were 2.7 ± 0.8 and 4.5 ± 0.9 per counting chamber before and after smoking respectively (p < 0.001). Endothelial cell counts and plasma nicotine concentrations were not significantly correlated. Neither the mean presmoking values nor smoking-induced changes in either variable were affected either dose of aspirin. The data suggest that smoking caused acute endothelial cell desquamation which was not prevented by aspir
ISSN:1424-8832
DOI:10.1159/000215560
出版商:S. Karger AG
年代:1987
数据来源: Karger
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10. |
Influence ofL-Ascorbic Acid, Blood Cells and Components on Protein Adsorption/Desorption on Polycarbonate |
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Pathophysiology of Haemostasis and Thrombosis,
Volume 17,
Issue 1-2,
1987,
Page 70-78
Chandra P. Sharma,
Thomas Chandy,
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摘要:
In a previous study we have shown that vitamin C has some effect on the polymer surface by adsorption to it, which would probably affect the protein adsorption and platelet adhesion. The present work has been extended to demonstrate the influence of vitamin C on the kinetics of protein-polymer interaction, using labeled proteins, in the presence and absence of red blood cells, platelets and white blood cells. It appears that vitamin C causes an increase in albumin surface concentration compared to bare substrate which seems to decrease slightly in the presence of blood cells. On the other hand, the infusion of vitamin C to the fibrinogen blood cells system dramatically inhibits the fibrinogen surface binding. The role of L-ascorbic acid to reduce the protein adsorption in the presence of blood cells is discussed by taking into account (a) the interaction of vitamin C with the polymer surface, (b) the interaction of vitamin C with the proteins and cellular membrane, and (c) the interaction of proteins and cells with the polymer itself. The effect of various blood components also seems to be important, and slight differences in the adsorption pattern of proteins are observed in the presence of urea, creatinine, bilirubin, Fe+++ ion and zinc at normal blood levels.
ISSN:1424-8832
DOI:10.1159/000215561
出版商:S. Karger AG
年代:1987
数据来源: Karger
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