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1. |
Heparin Infusion Facilitates ex vivo Spontaneous Platelet Aggregation in Patients with Acute Myocardial Infarction Who Have Undergone Thrombolytic Therapy |
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Pathophysiology of Haemostasis and Thrombosis,
Volume 23,
Issue 4,
1993,
Page 185-191
Patrizia Noris,
Giampiera Bertolino,
Mario Previtali,
Maurizio Ferrario,
Carlo L. Balduini,
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摘要:
We investigated ex vivo spontaneous platelet aggregation (SPA) in platelet-rich plasma in 37 patients with acute myocardial infarction. It occurred in about 50% of subjects receiving heparin after streptokinase treatment, while it rarely took place in patients who did not receive either streptokinase or heparin and in those treated with streptokinase alone. The study of patients receiving heparin for deep vein thrombosis suggested that SPA may derive from adenosine diphosphate released from platelets during sample handling. We suggest that heparin infusion may facilitate ex vivo platelet activation and that this mechanism is operative in patients with acute myocardial infarction who have undergone thrombolytic therapy.
ISSN:1424-8832
DOI:10.1159/000216874
出版商:S. Karger AG
年代:1993
数据来源: Karger
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2. |
Effect of Heparin-lnduced Extracorporeal Low-Density Lipoprotein Precipitation and Bezafibrate on Hemorheology and Clinical Symptoms in Cerebral Multiinfarct Disease |
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Pathophysiology of Haemostasis and Thrombosis,
Volume 23,
Issue 4,
1993,
Page 192-202
M. Walzl,
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摘要:
The effects of heparin-mediated extracorporeal low-density lipoprotein (total cholesterol, lipoprotein (a), triglycerides, fibrinogen) precipitation (HELP) and bezafibrate on fibrinogen, metabolic parameters, hemorheological patterns and clinical symptoms were studied in 40 patients suffering from cerebral multiinfarct disease. After a single HELP application, the patients were randomly assigned to two groups, either receiving sustained-release bezafibrate 400 mg (n = 21) or placebo (n = 19) over a period of 8 weeks. In all cases, HELP led to a statistically significant reduction of fibrinogen (p < 0.0001) and other parameters relevant to hemorheology, this effect, however, only being retained in the bezafibrate group. Parallel to this development, the Mathew scale revealed an improvement after HELP (p < 0.01 in each group) with a further improvement in the bezafibrate group (p < 0.05). The Mini Mental State Examination also showed improved results after HELP ( p < 0.0005 and p < 0.03, respectively), a further improvement being observed in the bezafibrate group (p < 0.05). Comparing the day after HELP treatment to that at the end of the study, the Activities of Daily Living Score showed a statistically significant difference in the fibrate group (p < 0.05). These results support the hypothesis that the improved hemorheologic property of blood is an important factor in clinical recovery as well as basic neurologic function.
ISSN:1424-8832
DOI:10.1159/000216875
出版商:S. Karger AG
年代:1993
数据来源: Karger
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3. |
Activation of Human Blood Platelets Induced by Nocloprost, a Stable Prostaglandin E2Derivative |
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Pathophysiology of Haemostasis and Thrombosis,
Volume 23,
Issue 4,
1993,
Page 203-211
E. Glusa,
M. Richter,
I. Amon,
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摘要:
Nocloprost, a 9β-chloro-16,16-dimethyl derivative of prostaglandin E2 (PGE2), belongs to the gastric cytoprotective agents that are used in the therapy of gastric ulcer. Since methylated derivatives of PGE2 0.1 μmol/l) caused aggregation with a biphasic course at higher concentrations. Aggregation induced by nocloprost (1 μmol/l) corresponded to that induced by adenosine diphosphate (ADP) (5 μmol/l). Activation of platelets by nocloprost was accompanied by formation of thromboxane A2 and an increase in cytosolic calcium in In do 1-loaded platelets. At 0.1 μmol/l it potentiated aggregation induced by low concentrations of ADP or adrenaline. The effect of nocloprost on platelets was blocked by iloprost, daltroban and indomethacin. PGE2, which was studied for comparison, at 0.1-1.0 μmol/l inhibited aggregation induced by 1 μmol/l nocloprost. The concentrations of nocloprost required for therapeutic use as antiulcer agent were lower by three orders of magnitude than those which induce human platelet aggre
ISSN:1424-8832
DOI:10.1159/000216876
出版商:S. Karger AG
年代:1993
数据来源: Karger
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4. |
Platelet Function in Patients with Chronic Coronary Heart Disease on Long-Term Anticoagulant Therapy: Effect of Anticoagulant Stopping |
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Pathophysiology of Haemostasis and Thrombosis,
Volume 23,
Issue 4,
1993,
Page 212-218
Juana Vallés,
Justo Aznar,
Teresa Santos,
Piedad Villa,
Angeles Fernández,
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摘要:
Plasma β-thromboglobulin (βTG), platelet procoagulant activity (PPA) and malondialdehyde were evaluated in a control group and in 59 patients with chronic coronary heart disease (CHD) undergoing long-term anticoagulant therapy (ACT) with acenocoumarol, and within 2 months after its termination. The patients were clinically stabilized after more than 1 year of an acute myocardial infarction. An increase in βTG and PPA was found in the patients, both with or without ACT, when compared to the control group. In addition, PPA was found to be higher in older and hypercholesterolemic patients on ACT. After ACT suppression, PPA activity increased significantly, particularly in younger and normocholesterolemic patients. The results of the present study suggest that CHD patients on ACT have some platelet hyperactivity and that the termination of ACT induces an increase in platelet function, particularly in P
ISSN:1424-8832
DOI:10.1159/000216877
出版商:S. Karger AG
年代:1993
数据来源: Karger
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5. |
Comparison of a Thromboxane Receptor Antagonist and Aspirin in Experimental Arterial Thrombosis |
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Pathophysiology of Haemostasis and Thrombosis,
Volume 23,
Issue 4,
1993,
Page 219-228
W.A. Schumacher,
C.L. Heran,
S. Youssef,
J.R. Megill,
I. Michel,
S.K. Durham,
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摘要:
The antithrombotic activities of aspirin, the thromboxane (Tx) A2/prostaglandin endoperoxide-receptor (TP-receptor) antagonist, SQ 30,741, and heparin were determined in anesthetized rats. Heparin (3 doses of 50, 300 U/kg), aspirin (1 and 10 mg/ kg), SQ 30,741 (1 mg/kg + 1 mg/kg/h), or the combination of SQ 30,741 and aspirin (10 mg/kg) was administered intravenously before inducing occlusive thrombosis with 0.1-mA stimulation of the intimal surface of the carotid artery. Light and electron microscopy revealed the thrombi to be composed predominately of platelets enmeshed in a fibrin network. Heparin (300 U/kg), SQ 30,741 and SQ 30,741 + aspirin decreased average thrombus weight by 54, 57 and 39%, respectively. These treatments also reduced the incidence of occlusion and improved carotid blood flow during thrombosis. In contrast, aspirin alone (1 and 10 mg/kg) and the lower heparin dose (50 U/ kg) did not significantly affect thrombus weight or carotid blood flow. To verify adequate drug dosage, pharmacological activities were characterized ex vivo in separate rats. Aspirin (10 mg/kg) inhibited maximum thromboxane (Tx) B2 10-fold). These experiments demonstrate the contribution of platelet and coagulation mechanisms to a thrombosis model which is sensitive to a TP-receptor antagonist, but not aspir
ISSN:1424-8832
DOI:10.1159/000216878
出版商:S. Karger AG
年代:1993
数据来源: Karger
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6. |
Haemostasis Unbalance in Pugh-Scored Liver Cirrhosis: Characteristic Changes of Plasma Levels of Protein C versus Protein S |
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Pathophysiology of Haemostasis and Thrombosis,
Volume 23,
Issue 4,
1993,
Page 229-235
Maurizio De Caterina,
Giovanni Tarantino,
Carmela Farina,
Amalia Arena,
Giosuè di Maro,
Pasquale Esposito,
Francesco Scopacasa,
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摘要:
Liver cirrhosis leads to a protido-synthetic impairment that alters the levels of blood clotting factors and haemostasis. The aim of this study was to assess the alterations of haemostatic parameters in the evolution of liver cirrhosis scored according to Child’s classification, with Pugh’s modifications. Thirty-seven patients suffering from alcoholic and non-alcoholic liver cirrhosis, representing stages A5, A6, B7, B8 and C10, were tested for the main blood clotting parameters, i.e. prothrombin time, factor VII, partial activated thromboplastin time, fibrinogen, plasminogen, α2-antiplasmin and physiological inhibitors [antithrombin III (ATIII), protein C (PC), protein S (PS)]. No variations were observed between substages A5 and A6 in any of the parameters, except for coagulation inhibitor levels. Most parameters showed a progressive decrease in stages B and C of the disease. The most significant alterations were found in the physiological coagulation inhibitors, with a sharper decrease in PC and AT III level and a lesser decrease in the level of PS through stages A5 and B8: this evidence could assume an important biological and diagnostic signific
ISSN:1424-8832
DOI:10.1159/000216879
出版商:S. Karger AG
年代:1993
数据来源: Karger
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7. |
Book Review |
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Pathophysiology of Haemostasis and Thrombosis,
Volume 23,
Issue 4,
1993,
Page 236-236
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ISSN:1424-8832
DOI:10.1159/000216880
出版商:S. Karger AG
年代:1993
数据来源: Karger
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