Quantitative assay of sulphinpyrazone in plasma and urine by high-performance liquid chromatography

Lecaillon, J.B.; Souppart, C.

doi:10.1016/s0021-9673(00)85018-9

Cited by 27 publications

(12 citation statements)

References 3 publications

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“…Using a mean measured plasma level of SP of 270+40 (SD) ,ug/ml, which was found in samples obtained 20 min after drug administration (n = 3; method according to ref. 14), and assuming no essential immediate extravasation or destruction of fMLP, a rough estimation of the dissociation constant for the antagonist (&d) (15) around a value of 21 ,uM can be obtained.…”

Section: Resultsmentioning

confidence: 99%

Receptor-directed inhibition of chemotactic factor-induced neutrophil hyperactivity by pyrazolon derivatives. Definition of a chemotactic peptide antagonist.

Dahinden¹,

Fehr²

1980

J. Clin. Invest.

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A B S T R A C T The two pyrazolon derivatives, phenylbutazone and sulfinpyrazone, selectively inhibit chemotactic peptide-induced effects on neutrophils. As they antagonize the induction of acute neutropenia in vivo and of cellular hyperadhesiveness, lysosomal enzyme release, hexose monophosphate shunt activity, and superoxide production in vitro, these effects occur with a specificity not shared with other prostaglandin biosynthesis inhibitors. Inhibition by these drugs resembles the competitive type ofantagonism and occurs at concentrations attainable in vivo under clinical conditions. The locomotory machinery, the directionfinding mechanisms, and the basic metabolic machinery ofthe cell are unaffected. These drugs interfere with specific binding of the formylpeptide to its receptor on neutrophils.

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Section: Resultsmentioning

confidence: 99%

Receptor-directed inhibition of chemotactic factor-induced neutrophil hyperactivity by pyrazolon derivatives. Definition of a chemotactic peptide antagonist.

Dahinden¹,

Fehr²

1980

J. Clin. Invest.

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“…Blood was collected before and 2,5,10,20,30, and 45 min, and 1, 2,3,4,6,8,12,24,28,32, and 48 hr after the dose.…”

Section: Methodsmentioning

confidence: 99%

Sulfinpyrazone kinetics after intravenous and oral administration

Lecaillon

Souppart

Schoeller

et al. 1979

Clin Pharma and Therapeutics

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Sulfinpyrazone kinetics has been investigated after intravenous and oral doses. They may be described by a 3-compartment open model. In the body about half the drug is in the plasma or in interstitial fluids, which equilibrated with plasma. Most of the rest is in an extravascular compartment, from which it easily diffuses back to the plasma. About 3% of the dose is still in the body after 24 hr and is located mainly in a deep compartment. After oral administration, sulfinpyrazone is quickly absorbed, largely from the stomach.

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“…Plasma sulfinpyrazone levels were also measured serially following oral ingesrion of the drug on two different occasions before the animals were killed. Determinations were carried out by CIBA-Geigy Biopharmaceutical Research Center, Cedex, France, by means of liquid chromatography (Lecaillon and Souppart, 1976).…”

Section: Baboon Homocysteine Vascular Modelmentioning

confidence: 99%

Effect of sulfinpyrazone on homocysteine-induced endothelial injury and arteriosclerosis in baboons.

Harker¹,

Harlan²,

Ross³

1983

Circulation Research

236

108

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The effect of sulfinpyrazone on endothelial injury induced by homocysteine has been studied both in vitro, using cultured human umbilical vein endothelial cells, and in vivo, using a primate model of homocysteine-induced arteriosclerosis. Oral sulfinpyrazone (250 mumol/kg body weight per day in three divided doses) in eight chronically homocystinemic baboons (0.14 +/- 0.04 mM plasma homocystine) decreased the extent of aortic endothelial injury as measured morphometrically by silver staining techniques, compared with six untreated comparably homocystinemic animals (denuded surface averaged 0.5% with range 0-2.1 vs 7.7 +/- 1.6%, respectively; P less than 0.001). Sulfinpyrazone therapy to homocystinemic baboons also normalized platelet survival and turnover measurements (5.1 +/- 0.4 days and 70,000 +/- 11,000 platelets/microliter per day vs. 2.8 +/- 0.6 days and 179,000 +/- 19,000 platelets/microliter per day in untreated homocystinemic controls; P less than 0.001). Sulfinpyrazone therapy also reduced the size and frequency of homocysteine-induced intimal lesion formation (P less than 0.001). Although sulfinpyrazone reduced the amount of specific 51Cr release from cultured human umbilical vein endothelial cells induced by 10 mM homocysteine after 24 hours of co-incubation, no effect was observed in assays of endothelial cell detachment when sulfinpyrazone (10(-5) M) or its thioether metabolite were pre- or co-incubated during 24 hours with homocysteine (2.5-10 mM). These data suggest that sulfinpyrazone may protect endothelial cells from injury in vivo by some apparently indirect mechanism.

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Quantitative assay of sulphinpyrazone in plasma and urine by high-performance liquid chromatography

Cited by 27 publications

References 3 publications

Receptor-directed inhibition of chemotactic factor-induced neutrophil hyperactivity by pyrazolon derivatives. Definition of a chemotactic peptide antagonist.

Receptor-directed inhibition of chemotactic factor-induced neutrophil hyperactivity by pyrazolon derivatives. Definition of a chemotactic peptide antagonist.

Sulfinpyrazone kinetics after intravenous and oral administration

Effect of sulfinpyrazone on homocysteine-induced endothelial injury and arteriosclerosis in baboons.

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