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PubMed1990

Sulphinpyrazone reduces endocardial injury and mural thrombosis.

STUDY OBJECTIVE: The aim of the study was to investigate the effectiveness of sulphinpyrazone, a drug which stabilises endothelial cell membranes, in reducing endocardial injury and mural thrombosis produced by lactic acid in the left ventricle. DESIGN: The left ventricular endocardium of isolated beating rat hearts, perfused via the aorta with oxygenated Krebs-Henseleit buffer, was exposed for up to 4 h to additional lactic acid (pH 6.4), with and without sulphinpyrazone (100 ng x ml-1). After flushing with buffer, passage of 10 ml blood, and further flushing, the hearts were fixed by coronary perfusion and the endocardium examined by scanning electron microscopy. EXPERIMENTAL MATERIAL: Hearts from 48 male albino Wistar rats, weight 270-380 g, were used. MAIN RESULTS: Morphometric analysis of the surface of the papillary muscles showed that lactic acid caused membrane injury in endothelial cells, up to 30% of which exfoliated. However when sulphinpyrazone was present, endothelial cell damage was reduced and there was up to 75% reduction in the area of exposed basal lamina or connective tissue. This was associated with a corresponding reduction in the extent of platelet adhesion (79%) and thrombus formation (94%). CONCLUSIONS: The results show that sulphinpyrazone has the potential to reduce the risk of mural thrombosis following endocardial injury.

Animals↗
PubMed1986

Evaluation of antiplatelet agents in the prevention of aorto-coronary bypass occlusion.

The cumulative occlusion rates of aorto-coronary artery venous bypass grafts average from 16 to 26% per distal anastomosis within 12 months and about 2% per following year. The potential benefit of oral anticoagulants and platelet inhibitor drugs has been tested to prevent graft occlusion and to retard the atherosclerotic process. Oral anticoagulants started on the third postoperative day do not significantly reduce graft occlusion after 6 months. Among the platelet inhibitor drugs, dipyridamole started before surgery, followed by dipyridamole and aspirin soon after surgery, was the drug regimen with the best results. More randomised double-blind clinical trials are highly desirable to confirm these findings and to resolve the question of relative efficacy and safety for the various drugs reported to have shown benefit when used in combination.

Administration, Oral↗
PubMedDate not supplied

Impairment of renal function due to sulphinpyrazone after coronary artery bypass surgery: a prospective double-blind study.

In this randomized, double-blind, placebo-controlled trial the renal function was studied in 60 patients recovering from coronary artery bypass surgery treated with a daily dose of 800 mg sulphinpyrazone (SP) or 880 mg acetylsalicylic acid (ASA) or placebo. Serum creatinine level increased (p less than 0.05) during the first 2 days of SP treatment, but returned to its baseline level within 4 days under maintained therapy; during ASA and placebo therapy no significant changes occurred. Serum urea levels decreased (p less than 0.01) during ASA and placebo treatments as time from surgery subsided; the decrease of serum urea level was delayed in the SP group compared with the ASA and placebo groups. Urinary excretion of prostaglandin E2 (PGE2) was significantly decreased (p less than 0.01) during ASA treatment; in the SP group, urinary PGE2 excretion tended also to decrease during the first days of treatment, the decrease being significant only on the 4th day (p less than 0.01). The urinary excretion of kallikrein decreased significantly only in the SP group (p less than 0.01), while the changes in the ASA and placebo group were not significant. We suggest that the rapidly reversible acute renal impairment during SP therapy was probably due to a transient renal ischemia caused by a drug-related decrease in urinary kallikrein excretion rather than by renal prostaglandin inhibition.

Clinical Trials as Topic↗
PubMed1980

Effect of sulphinpyrazone on human platelet aggregation, 5-hydroxytryptamine release and adhesion ex vivo: comparison with naproxen.

1 The effects of single doses of naproxen and sulphinpyrazone and of 4 and 8 days treatment with sulphinpyrazone on human platelet responsiveness were compared. 2 A single dose of sulphinpyrazone had no effect whereas a single dose of naproxen caused a five-fold depression in responsiveness to collagen. 3 Repeated administration of sulphinpyrazone led to a weak and equivocal inhibitory effect on collagen-induced aggregation, second phase aggregation in response to ADP and adhesion to collagen. There was no effect on ADP-induced first phase aggregation, adrenaline-induced second phase aggregation or platelet retention in glass bead columns. 4 It is concluded that the anti-aggregant activity of sulphinpyrazone is too weak to be a major factor in its reported effect on the incidence of cardiac death.

Adenosine Diphosphate↗
PubMed1981

Sulphinpyrazone metabolism during long-term therapy.

1 The plasma concentrations of sulphinpyrazone and four of its metabolites are reported together with the amounts excreted in urine. Eight insulin-requiring diabetics were investigated, all treated with sulphinpyrazone 600-800 mg day-1 for 2.5 years or more. 2 Blood samples were drawn before the first morning dose and 2 h later. The mean plasma concentrations were (t=0 h-t=2 h): sulphinpyrazone 7.1-16.0 microgram ml-1; sulphone 1.7-4.8 microgram ml-1; p-OH-sulphide 0.67-0.89 microgram ml-1; p-OH-sulphinpyrazone 0.10-0.16 microgram ml-1. Statistically significant correlations were found between the plasma concentrations at t=0 of the sulphide and the p-OH-sulphide and that of sulphinpyrazone. 3 In urine, a very wide range in excretion of unconjugated compounds was observed. Sulphinpyrazone were excreted in amounts corresponding to 1-30% of the daily dose. The metabolites were generally excreted to amounts corresponding to less than 1% of the daily dose; however, up to 3% was found as the sulphone. 4 Increases of the concentration of all compounds in urine were found after treatment with beta-glucuronidase indicating 0-conjugation with glucuronic acid. 5 Since both the sulphide and the sulphone were found more active as inhibitors of platelet function in vitro than their parent compound, they may together constitute the major part of the platelet inhibitory drug activity in plasma during long-term therapy with sulphinpyrazone.

Adult↗
PubMed1982

Pharmacokinetics of single doses of sulphinpyrazone and its major metabolites in plasma and urine.

1 High pressure liquid chromatographic assays for the estimation of sulphinpyrazone and its sulphide, sulphone and p-hydroxy metabolites in plasma and urine are described. 2 Five normal volunteers received 200 mg and 400 mg sulphinpyrazone orally. Sulphinpyrazone was rapidly absorbed and eliminated with a half-life of approximately 4 h irrespective of dose. Peak plasma concentrations and area under the plasma concentration-time curves (AUC) were consistent with linear pharmacokinetic behaviour. 3 Plasma concentrations of the sulphone were low and peaked before those of the sulphide; its mean half-life was 3.1 h. The sulphide, which may be the sulphinpyrazone metabolite with activity on platelets, was eliminated with a mean half-life of 13.4 h. The AUC increases with dose of both metabolites suggested non-linearity. 4 Approximately 45-50% of the administered dose was eliminated in the urine as unchanged drug or as sulphone or p-hydroxy-sulphinpyrazone. The sulphide metabolite was not detected in the urine. The renal clearance of sulphinpyrazone was approximately 18 ml min-1 and that for the sulphone was similar. Sigma minus plots of the urinary excretion yielded half-lives of 3.5 h for the sulphone and 1 h for p-hydroxy-sulphinpyrazone.

Adult↗
PubMed1982

The effect of prolonged treatment with sulphinpyrazone on thromboxane A2 and prostacyclin in man.

We studied the effect of 3 weeks' treatment with 4 x 200 mg of sulphinpyrazone daily (six healthy volunteers) on proaggregatory thromboxane A2 (TxA2) and antiaggregatory prostacyclin (PGI2). Platelet TxA2 production was evaluated by measuring its stable metabolite, immunoreactive thromboxane B2, from serum, and vessel wall PGI2 production by measuring its stable metabolite, immunoreactive 6-keto-prostaglandin F1 alpha in plasma. The TxA2 production (initially 209.0 +/- 27.1 ng/ml, mean +/- s.e. mean) decreased to about 30% from the second day of the treatment onwards, and it recovered in three days after the discontinuation of the treatment. PGI2 (initially 33.6 +/- 3.6 pg/ml) did not change. The shift of the balance between TxA2 and PGI2 to the dominance of antiaggregatory PGI2 during sulphinpyrazone treatment may be involved with the efficacy of the drug in the secondary prevention of myocardial infarction.

Adult↗
PubMed1983

Evidence for a dual action of sulphinpyrazone on drug metabolism in man: theophylline-sulphinpyrazone interaction.

The effects of sulphinpyrazone administration on the metabolic and renal clearances of theophylline in man were investigated. Sulphinpyrazone increased total plasma theophylline clearance by 22%. This was the sum of increases in metabolic clearances by 3-demethylation (32%), 1-demethylation (30%) and 8-oxidation (22%) and of a decrease in renal clearance (27%). It is proposed that sulphinpyrazone has differential effects on at least two forms of cytochrome P-450 inhibiting one enzyme or group of enzymes which metabolises tolbutamide, phenytoin and S(-)warfarin and inducing a form (or forms) which metabolises theophylline, antipyrine and R(+)warfarin.

Adult↗