ABSTRACT
Pentoxifylline is an orally active agent for the treatment of peripherial and cerebral vascular diseases. Pentoxifylline increases the deformability of red blood cells in vitro, reduces blood viscosity and decreases platelet aggregation and thrombus formation. Depogen has shown antiaggregatory effect both in vitro and in ex vivo. The inhibitory effect of Pentoxifylline was about 3-5 times weaker than that of Depogen. IC50 = 900/micrograms/ml for Depogén and 3600/micrograms/ml for Pentoxifylline on human platelet rich plasma. Depogen has shown ex vivo antiaggregatory effect on anesthetised rabbits, ID50 = 7 mg/kg in case of iv. administration, and ID50 = 300 mg/kg in case of orally administration. Both compound inhibit the release of platelet precoagulation factor, but the effect of Pentoxifylline was slighter.
Subject(s)
Erythrocytes/drug effects , Leukocytes/drug effects , Papaverine/analogs & derivatives , Pentoxifylline/pharmacology , Platelet Aggregation Inhibitors/pharmacology , Platelet Aggregation/drug effects , Theophylline/analogs & derivatives , Animals , Cell Aggregation/drug effects , Drug Combinations , Drug Evaluation, Preclinical , Humans , Papaverine/pharmacology , Platelet Factor 3/antagonists & inhibitors , Rabbits , Theophylline/pharmacologyABSTRACT
Factor V inhibitors are uncommon, bleeding manifestations variable and recommendations for management are unclear. We present a patient with non-Hodgkins lymphoma who developed gastrointestinal bleeding and was found to have a Factor V inhibitor. The inhibitor was active against both plasma Factor V and platelet associated Factor V, and was associated with a five-fold increase in platelet associated IgG. Fresh frozen plasma was ineffective in preventing bleeding. Resolution of bleeding was associated with a fall in the levels of the inhibitor and of platelet associated IgG. The patient had no further bleeding episodes nor evidence of progression of his lymphoma, but six months later died as a result of metastatic adenocarcinoma.
Subject(s)
Blood Coagulation Disorders/complications , Blood Coagulation Factors/antagonists & inhibitors , Blood Platelets/metabolism , Factor V Deficiency/complications , Gastrointestinal Hemorrhage/etiology , Adenocarcinoma/secondary , Aged , Blood Coagulation Disorders/blood , Factor V Deficiency/blood , Gastrointestinal Hemorrhage/blood , Humans , Immunoglobulin G/metabolism , Leukemia, Lymphocytic, Chronic, B-Cell/complications , Male , Partial Thromboplastin Time , Platelet Factor 3/antagonists & inhibitors , Prothrombin TimeSubject(s)
Blood Coagulation Factors/antagonists & inhibitors , Ephedrine/analogs & derivatives , Epoprostenol/analogs & derivatives , Epoprostenol/pharmacology , Platelet Factor 3/antagonists & inhibitors , Adult , Blood Coagulation Tests , Collagen/pharmacology , Ephedrine/pharmacology , Humans , Platelet Aggregation/drug effects , Platelet Factor 3/physiologyABSTRACT
The effect of lomustin on platelet functions was investigated in vitro using a wide battery of tests. Lomustin was found to act as a specific inhibitor of platelet aggregation, release reaction and clot retraction and to induce acquired thrombocytopathy. Thus, impairment of platelet functions might play a role in hemorrhagic complications accompanying lomustin therapy in some cases.
Subject(s)
Blood Platelets/drug effects , Lomustine/pharmacology , Platelet Function Tests , Adenosine Diphosphate/pharmacology , Clot Retraction , Collagen/pharmacology , Epinephrine/pharmacology , Humans , Platelet Aggregation/drug effects , Platelet Factor 3/antagonists & inhibitors , Platelet Factor 4/antagonists & inhibitors , Serotonin Antagonists/pharmacologyABSTRACT
Lysine salt of acetylsalicylic acid (ASA) was given to ten patients by intravenous infusion. Blood samples taken at intervals during the infusion permitted the examination of the influence of the dose of ASA on platelet functions. Aggregation was significantly reduced when 50 mg ASA had entered circulation, while a diminution of PF3 and PF4 availability could only be demonstrated when the dose had reached 500 and 200 mg, respectively. In order to exclude a longer latency time for the diminution of PF3 and pf4 availability, a second series of ten patients received intravenous injections of 100 and 300 mg ASA, respectively. From these patients, blood was taken 1 h after the injection. The decrease of PF3 and PF4 availability in these cases was comparable to the results of the first group. In a third series of patients, a daily intravenous dose of 2,000 mg ASA was given. In these cases, a moderate decrease of factors II, VII, IX and X was observed. Since the appearance of a PIVKA effect could also be demonstrated, vitamin K antagonism was assumed when a high dose of AS
