Heparin-induced platelet aggregation and its inhibition by antagonists of the thromboxane pathway.
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Aspirin↗
Biomedical subjects
E M Pogliani
Publications and source records attributed to E M Pogliani.
Diagnostic possibilities in megakaryoblastic transformation of chronic granulocytic leukemia.
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Aged↗
High fibrinopeptide A levels modified by heparin in acute nonlymphocytic leukemia.
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Fibrinogen↗
[Low-dose heparin in thoracic surgery].
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Dose-Response Relationship, Drug↗
Selective PF4 release in vitro induced by heparin and related glycosaminoglycans (GAGs)--correlation with beta-TG release and platelet aggregation.
We studied human platelet aggregation and beta-TG/PF4 release induced by heparin and related GAGs in vitro both in normal PRP and in PRP after aspirin. In our experimental conditions, heparin and related GAGs always caused PF4 release in vitro from normal platelets, whether or not there was measurable platelet aggregation in the aggregometer. Significant beta-TG release was induced only by the mucosal heparin preparation (which also induced platelet aggregation in some citrated PRP). Therefore, while beta-TG release in vitro seems to correlate with platelet aggregating activity of heparin, the selective PF4 release, caused by heparin and related GAGs also in conditions in which neither platelet aggregation nor beta-TG are measurable, is probably associated with the high affinity of PF4 for heparin. The degree of affinity of GAGs for PF4 (heparin greater than DeS greater than HS) seems to correlate with PF4 release. Moreover, the significant reduction in PF4 release in vitro after aspirin suggests that GAGs-induced PF4 release is related to a cyclooxygenase-dependent activation process.
Adenosine Diphosphate↗
Effects of porcine calcitonin on human platelet fuction.
The effects of different doses of porcine calcitonin (pCT) were tested in vitro and in vivo. In vitro, pCT at a concentration ranging from 0.1 to 5 M. R. C. Units/ml induced a dose-dependent inhibition of ADP (1.2 microM) and collagen- (2 micrograms/ml) induced platelet aggregation, showing a prevalent action on the second wave of ADP-induced aggregation and causing prolongation of the lag time and reduction of both maximum aggregation and slope in collagen-induced aggregation. 45Ca uptake by platelets in the presence of the ionophore A23187 and 14C-serotonin release were also inhibited in a dose-related fashion, using concentrations ranging from 1 to 10 M. R. C. Units of pCT. The in vivo tests, performed before and after a 7-day treatment with 2 different doses of pCT (1 and 160 M. R. C. Units/daily, i. m.) confirmed the inhibitory effect of pCT on ADP- and collagen-induced platelet aggregation. It should be stressed that the effect of 1 unit was stronger than that of 160 units. It is therefore postulated that in vitro and in vivo effects of pCT on platelet functions probably depend on different mechanisms of action.
Adult↗
[Low-dose calcium-heparin prophylaxis in thoracic surgery. Bleeding, changes in coagulation and fibrinolysis].
In a controlled, randomized study of patients undergoing thoracic surgery, calcium heparin prophylaxis is confirmed to prevent activation of the coagulation and fibrinolysis system, by determining plasmatic kallikrein, antitrombin III, and plasmin. In a further study calcium heparin, 5000 I.U. s.c. every 8 hr, is statistically proved not to increase post-operatory bleeding.
Adult↗
Non interference by heparin with the cytostatic effect of adriamycin: an in vitro study on a human promyelocytic leukaemia cell line.
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Cell Division↗
Primary shunt hyperbilirubinemia associated with Gilbert's syndrome.
A patient with primary shunt hyperbilirubinemia associated with Gilbert's syndrome is described. The laboratory findings of unconjugated hyperbilirubinemia, mild reticulocytosis, normoblastic erythroid hyperplasia of bone marrow, increased plasma iron turnover, and normal peripheral red blood cell survival were consistent with increased intramedullary hemolysis. Nevertheless, unconjugated bilirubin level exceeding 4 mg/100 mL, in the absence of appreciable anemia and of biochemical evidence of hepatic dysfunction, suggested the coexistence of defective hepatic bilirubin clearance. The mode of inheritance and the effect of fasting and phenobarbital on bilirubin concentrations were indicative of associated Gilbert's syndrome.
Adolescent↗
Platelet release reaction and prostaglandin pathway activation in angina patients during exercise: effect of indobufen.
Platelet 14C-serotonin release induced by collagen, and platelet malondialdehyde (M.D.A.) generation induced by thrombin were assessed in twenty patients with stable angina, before and after exercise with a bicycle ergometer. The patients received a single oral 200 mg dose of indobufen or placebo according to a crossover design in double-blind conditions. The M.D.A. concentration increased when exercise was carried out after placebo, whereas indobufen markedly inhibited M.D.A. production and 14C-serotonin release. These results suggest that effort may be an important factor in activation of the platelet prostaglandin pathway and that the use of antithrombotic drugs may be appropriate in patients with angina.
Adult↗
Intravenous urokinase in ischemia of lower limbs.
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Aged↗
Low-dose heparin in thoracic surgery: effect on blood coagulation and fibrinolysis system.
Plasma kallikrein, antithrombin III and antiplasmin were determined with chromogenic methods in 29 patients pre-, per- and post-operatively in a controlled, randomized study. 16 patients received calcium heparin, 5000 IU s. c. every 8 hr for 7 days, the first administration given 2 hr before surgical procedure. 13 control patients received saline. A significant reduction of kallikrein and antiplasmin in per- and post-operative periods was observed in the control patients compared with the heparin-treated patients, while there was a significant reduction of anti-thrombin III in the control patients compared with the treated patients only in the per-operative period. The results obtained suggest that activation of the coagulation and fibrinolysis system occurs in patients undergoing thoracic surgery, and that it is inhibited significantly by calcium heparin prophylaxis.
Adult↗
Abnormal platelet function in a case of megakaryoblastic leukaemia.
A platelet function study in a patient with megakaryoblastic leukaemia is reported. The abnormalities of the platelet function suggest a probable platelet membrane injury and a platelet release defect. The reduced platelet half-life and the non changing splenohepatic ratio confirm the clinical and histological features of the systemic disease.
Bleeding Time↗
Beta-thromboglobulin and platelet factor 4 plasma levels during haemodialysis: effect of indobufen.
The effect of a single dose of indobufen (100 mg i.v.) on the release of beta-thromboglobulin and of the platelet factor 4 was investigated during dialysis in 20 uraemic subjects by a within-subjects, single-blind, indobufen versus placebo study. Plasma levels were measured in baseline conditions and 15, 30, 60, 120 and 240 minutes after the beginning of dialysis. Pre-treatment with indobufen clearly inhibited beta-TG and PF 4 output. The difference from placebo was highly significant (p less than 0.01) from the 30-minute control up to the end of dialysis. No changes in platelet count before and after dialysis were observed.
Adult↗
Thrombolytic therapy for venous thrombosis in patients with gastro-intestinal diseases.
Venous thrombosis in 2 patients with gastro-intestinal diseases (chronic liver disease and ulcerative colitis) is reported. A good clinical improvement was obtained after thrombolytic (urokinase) therapy without any haemorrhagic side-effect. A decrease in the plasma of the fast-acting antiplasmin has been correlated with urokinase thrombolytic effect in vivo. These preliminary reports suggest that thrombolytic drugs are a safe tool for the treatment also of thromboembolic complications in patients with potential haemorrhagic diathesis.
Aged↗
Inhibition of human platelet function by parsalmide.
2-Propargyloxy-5-amino-N-butyl-benzamide (parsalmide), an antiinflammatory drug, inhibits human platelet function in vitro and ex vivo. The degree of inhibition of ADP- and collagen-induced platelet aggregation "in vitro" is dose-dependent and parsalmide shows a more marked effect than equal concentrations of acetylsalicylic acid (ASA) and indometacin. Moreover, malondialdehyde levels in human PRP after addition of thrombin were inhibited at the same degree by parsalmide, ASA and indometacin. In ex vivo experiments, the administration of 400 mg p.o. of parsalmide in arthropathic patients shows a significant inhibitory effect on ADP-induced platelet aggregation at 3 and 24 h after treatment, while a drop of malondialdehyde levels was observed only at 3 h after treatment. No significant inhibitory effect was observed in collagen-induced platelet aggregation.
Adenosine Diphosphate↗
Empiric treatment of infections in granulocytopenic patients with acute leukemia: a study on amikacin-carbenicillin-cotrimoxazole.
The amikacin-carbenicillin-cotrimoxazole combination was used as an empiric treatment for febrile episodes in patients with acute leukemia and severe granulocytopenia. The choice of drugs was based on the finding in our institute that the majority of infections are caused by gram-negative rods, particularly Pseudomonas, with high percentage of strains resistant to gentamycin and tobramycin. Granulocyte transfusions were given to the patients who did not show satisfactory clinical improvement 48 h after start of antibiotic therapy. There were cures in 84.6% of the febrile episodes treated with this antibiotic combination, including five of eight episodes of microbiologically confirmed bacteremia. Survival after 21 days of antibiotic therapy amounted to 89.1%. Renal toxicity occurred in 10.9% of the episodes treated. The prompt use of this antibiotic combination seems to be a safe and efficacious therapeutic tool for treating these high-risk patients.
Acute Disease↗
GAGs-potentiated inhibition of thrombin, factor Xa and plasmin in plasma and in a purified system containing antithrombin III - correlation with total charge density.
The ability of heparin and related glycosaminoglycans (GAGs) to accelerate the inhibition of thrombin, factor Xa and plasmin in plasma and in a purified system containing antithrombin III (At III) was studied using chromogenic peptide substrate assays. There was good correlation between the charge density of the mucopolysaccharides and the activities investigated. While the difference between potentiation of the antithrombin activity by GAGs in plasma and in the purified system was slight, the inhibition of factor Xa in plasma was more pronounced than in the presence of purified At III, indicating the mechanisms for GAGs-potentiated inhibition of thrombin and factor Xa are not identical. For the antiplasmin activity, there was a good correlation between the chemical structure and biological activity only in the pure system, confirming that the antithrombin-GAG complex plays a very limited role in the inactivation of plasmin in plasma.
Antithrombins↗