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At least 775 records · Page 43Linked to original sources
PubMed1986

Sulphinpyrazone and the platelet serotoninergic mechanism in ischaemic heart disease.

A double blind study in 25 patients with ischaemic heart disease and 20 matched healthy controls examined the effect of sulphinpyrazone on the uptake of serotonin by platelets and the basal concentrations of serotonin in platelets. Uptake was measured using tritium labelled serotonin and basal concentrations estimated spectrophotofluorometrically. Serotonin uptake was significantly increased both in the patients with chronic stable angina of effort and in those with a history of myocardial infarction six months or more previously. Sulphinpyrazone reduced serotonin uptake from 94.25 (SE 8.65) to 57.86 (5.37) cpm/10(8) platelets after 24 weeks of treatment in the group with stable angina and from 137.45 (16.26) to 68.08 (8.38) cpm/10(8) platelets in the myocardial infarction group. Raised basal concentrations in the two groups were also reduced by sulphinpyrazone. Placebo had no effect on serotonin uptake or basal concentrations in either group of patients. The ability of sulphinpyrazone to inhibit uptake and reduce basal concentrations of serotonin in patients with ischaemic heart disease may be yet another mechanism through which this drug exerts its beneficial antiplatelet effect.

Adult↗
PubMed1969

Effect of drugs on urate binding to plasma proteins.

The effect of various drugs on urate binding to plasma proteins was investigated in normal subjects. Whereas allopurinol, aspirin, phenylbutazone, probenecid, and sulphinpyrazone all significantly reduced plasma urate concentrations, only aspirin, phenylbutazone, and probenecid significantly impaired urate binding. Colchicine and indomethacin in the doses administered had no significant effect on plasma urate concentrations or binding. In the case of aspirin, urate binding was reduced to 25% of normal, and this effect was quickly abolished after cessation of therapy. Phenylbutazone reduced urate binding to 56% and probenecid to 46% of normal; this impairment was still detected four days after cessation of therapy. Drugs may impair urate binding by competition for plasma protein binding sites, with displacement of bound urate. Impairment of urate binding in vivo by administration of certain drugs may be relevant to the precipitation of acute gouty arthritis, to the formation of gouty tophi, and to the augmentation of uricosuria. Furthermore, the role of drugs must be seriously considered during all studies on urate binding in patients with gout.

Adult↗
PubMed1981

Transient cerebral ischaemic attacks--management and prognosis.

Fifty patients who had recently had a transient ischaemic attack took part in a double-blind cross-over trial of sulphinpyrazone 200 mg 4 times daily against placebo. Each treatment was given for 4 months. The incidence of recurrences was much greater in the initial 4 months but there was no difference between the 2 treatments. A follow-up of 39 of the patients showed that 2 years later 90% of those who had not had a recurrence during the 8 months had suffered no further neurological events whereas of those who did have a recurrence during the study only 47% had no further neurological events.

Aged↗
PubMed1987

A serial study of platelet reactivity throughout the first six months after myocardial infarction: its modification by sulphinpyrazone.

Platelet reactivity was studied immediately after and throughout the first 6 months following myocardial infarction. Its modification by sulphinpyrazone was observed. Out of 65 consecutive patients admitted to the coronary care unit, ten did not meet the protocol criteria. Fifty five received either placebo or sulphinpyrazone in a double-blind trial for 6 months, treatment being started within 6 days of infarction. Forty four patients completed the study (19 on placebo and 25 on sulphinpyrazone). An additional ten patients commenced treatment within one day of infarction and were studied daily for one week. Platelet hyper-reactivity was demonstrable in all patients at presentation and persisted throughout the 6 months in the control group. This effect was reversed by sulphinpyrazone, the modification of reactivity being established by the third day of treatment.

Adult↗
PubMed1977

Urate excretion.

Explore the source record for details and available documents.

Acetohexamide↗
PubMed1980

Prostaglandins and platelets.

Release of arachidonate from cell membrane phospholipids by activation of phospholipase A1 is a key step in the formation of prostaglandins and thromboxanes. In platelets PGH2 and TXA2 are formed from arachidonate and can cause aggregation and the release of granule contents; in vascular tissue, PGI2 is formed instead and, by increasing platelet cAMP, inhibits platelet reactions. There is considerable interest in inhibitors of the enzymes in these pathways as drugs to modify thrombus formation. Results of the clinical trials, however, indicate that drugs which inhibit cyclo-oxygenase may not have a major effect on the thromboembolic complications of arterial disease.

Arachidonic Acids↗
PubMed1983

Therapeutical aspects of cerebrovascular disease.

Treatment of hemorheologic alterations in patients with CVD must be directed to reduce enhanced platelet and red cell aggregation, to improve reduced red cell deformability, and to control plasmatic hypercoagulability.

Aspirin↗
PubMed1987

Electrophysiologic and antiarrhythmic actions of sulphinpyrazone and its sulfide metabolite G25671.

In anesthetized dogs, the cumulative intravenous administration of 1.0-40.0 mg/kg sulphinpyrazone failed to alter the ventricular excitation threshold, ventricular refractory period and ventricular fibrillation threshold determined during nonobstructed coronary blood flow. Sulphinpyrazone, however, did attenuate the reduction in the ventricular fibrillation threshold occurring during transient myocardial ischemia. G25671, the sulfide metabolite of sulphinpyrazone, failed to alter ventricular refractoriness and 'nonischemic' ventricular fibrillation thresholds, and was minimally effective in reducing the decrease in 'ischemic' fibrillation thresholds when administered in cumulative intravenous doses of 5.0-20.0 mg/kg. In conscious dogs in the subacute phase of anterior myocardial infarction, the administration of a cumulative 10.0-40.0 mg/kg sulphinpyrazone failed to alter the mode of induction, rate or morphology of ventricular tachyarrhythmias initiated by programmed ventricular stimulation. These data suggest that neither sulphinpyrazone nor its sulfide metabolite possess primary electrophysiologic properties which might contribute directly to significant antiarrhythmic or antifibrillatory activity.

Animals↗