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[Site of action of anticoagulant drugs].
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[Renal tolerance of an incremental dosage regimen of anturan in the aged with altered renal function]].
The aim of the study was to investigate renal tolerability of a flexible increasing dose-schedule of anturan (E), dependent on basal serum creatinine values. 12 male cardiovascular elderly patients (mean age: 75 years; SD: 5.5 years) suffering from mild chronic renal failure (serum creatinine between 2.00 and 4.00 mg/100 ml) entered an open study of 2-month duration. Starting dosage was 200 mg per day; daily dosage was then increased every 4 days of 200 mg, or kept constant for another 4 days, according to each patient's renal function, up to 800 mg per day. All the patients reached the maintenance dosage of 800 mg/day in 12 days, because renal function didn't worsen. Two patients were withdrawn: one at the end of the 1st month of E therapy because of exitus due to myeloma, the other one at the 24th day of E therapy for serum creatinine increase, possibly related to ongoing therapy. Creatinine clearance significantly increased, serum creatinine and uric acid significantly decreased at the end of E therapy. The other biochemical examinations didn't change and no patient complained of any undesired effect during the whole study. The obtained results seem to prove that anturan, if an incremental dose-schedule is followed at the beginning of therapy is well tolerated even in elderly azotemic patients.
Prevention of postoperative deep vein thrombosis by a combination of subcutaneous heparin with subcutaneous dihydroergotamine or oral sulphinpyrazone.
In a randomized clinical trial the effect of subcutaneous heparin alone or in combination with dihydroergotamine or sulphinpyrazone in preventing postoperative deep vein thrombosis (DVT) was studied. Sodium heparin (5000 IU) was administered subcutaneously twice daily; dihydroergotamine (1/2 mg) was also administered subcutaneously twice daily, and sulphinpyrazone (400 mg) was administered orally or intravenously twice daily. Administration occurred for at least 7 days. The diagnosis DVT was made with the radiofibrinogen uptake test. 358 patients undergoing major elective abdominal surgery were allocated to three treatment groups: heparin alone (Hep), heparin + dihydroergotamine (DHE-Hep) and heparin + sulphinpyrazone (Sulph-Hep). The frequency of DVT was 14/114 in Hep, 10/115 in DHE-Hep and 20/114 in Sulph-Hep. These differences were not significant. After application of the "logistic regression" procedure of Cox (1) it turned out that the major risk factors for developing DVT were age, sex, weight, type of operation and presence of diabetes mellitus. Also a significant treatment influence was observed (p = 0.001). This treatment effect was most probably due to improvement in the DHE-Hep group. The results in the Sulph-Hep group were not significantly different from those in the Hep group. A risk index was formulated on the basis of the above mentioned risk factors by which the chance of occurrence of DVT during heparin prophylaxis in an individual patient could be predicted. Patients that should receive additional prophylactic treatment can be defined by using this risk index.
Platelet sequestration during hypothermia in dogs treated with sulphinpyrazone and ticlopidine--reversibility accelerated after intra-abdominal rewarming.
During body cooling, a progressive thrombocytopenia is observed, with platelet sequestration mainly in the liver. Platelets return progressively to the circulation during rewarming. In this work the presence of platelet clumps is demonstrated by electron microscopy inside the hepatic sinusoids of dogs cooled to 20 degrees C by immersion in iced water. Such clumps were not found either before cooling or after body rewarming. Similar platelet clumps in the hepatic microcirculation were found in two other groups of dogs cooled and rewarmed as before, but previously treated with the antiaggregants sulphinpyrazone or ticlopidine. Another group of dogs was cooled and rewarmed by intra-abdominal circulation of physiological saline respectively at 4 degrees C and 40 degrees C. In these animals a similar decrease of circulating platelets was observed. However, just after rewarming was started, with the body temperature still at 22 degrees C, sequestered platelets came back abruptly to circulation. We conclude that hepatic platelet sequestration induced by hypothermia appears mainly due to local haemodynamic conditions.
Experimental papillary necrosis of the kidney. 3. Effects of reserpine and other pharmacologic agents on the lesion.
Reserpine is able to exert a pronounced inhibitory effect on the development of papillary necrosis following the administration of bromoethylamine hydrobromide to the rat. This inhibitory effect has been observed using light microscopy, histochemistry, indigo carmine excretion and urine output. These observations suggest that vasoconstriction may play a significant role in the pathogenesis of papillary necrosis, but the evidence for this is incomplete.
Modification of platelet adherence to protein-coated surfaces.
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Current concepts of hemostasis. Progress report on platelet aggregation.
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Platelet-surface reaction and thrombosis.
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[On a cell-free model system from rabbit-reticulocytes for the study of the effects of pharmaco on the proteinsynthesis].
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[Therapy and prevention of acute phlebothrombosis with heparin, coumarins and inhibitors of platelet function].
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Drugs in the treatment of hyperuricemia.
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[Biochemical studies on the action mechanism of phenylbutazone and a few derivatives].
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[Species specific difference in binding to plasma proteins].
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Zyloprim and other drugs in the management of gout.
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[How to treat gout].
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Interaction of non-steroidal antiinflammatory agents with corticosterone binding to plasma proteins in the rat.
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[Functional nephrography].
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