Quantitation of prostanoids in biological fluids by gas chromatography/triple stage quadrupole mass spectrometry.
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Dinoprostone↗
Biomedical subjects
H Schweer
Publications and source records attributed to H Schweer.
Determination of prostaglandin E2, prostaglandin F2 alpha and 6-oxo-prostaglandin F1 alpha in urine by gas chromatography/mass spectrometry and gas chromatography/tandem mass spectrometry: a comparison.
Electron impact fragmentation of methyl ester/methyloxime/trimethylsilyl ether derivatives of prostaglandin E2 and 6-oxo-prostaglandin F1 alpha and the methyl ester/trimethylsilyl ether derivative of prostaglandin F2 alpha is followed by argon collision-activated dissociation in a triple quadrupole mass spectrometer. Daughter ion chromatograms of prostaglandin derivatives show an enormous increase of selectivity compared to the multiple ion detection chromatograms of the same samples in single quadrupole mode.
6-Ketoprostaglandin F1 alpha↗
Determination of peripheral plasma prostanoid concentration: an unreliable index of 'in vivo' prostanoid activity.
Plasma concentrations of PGE2, PGF2 alpha, 6-keto-PGF1 alpha and TxB2 were determined in 4 healthy volunteers by gas chromatography-negative ion chemical ionization mass spectrometry. TxB2 concentrations in all volunteers increased with time during blood collection, increases occurred more sporadically in the case of PGE2, PGF2 alpha and 6-keto-PGF1 alpha. Rapid changes in plasma prostanoid concentrations within a sampling series were unpredictable and were inexplicable. The measured plasma prostanoid concentrations apparently depended on the sampling conditions, which could not be adequately standardized and controlled. However, very short term changes in plasma prostanoid levels cannot be excluded.
6-Ketoprostaglandin F1 alpha↗
Indomethacin for prevention of intraventricular hemorrhage in low birth weight infants.
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Cerebral Hemorrhage↗
Simultaneous determination of prostanoids in plasma by gas chromatography-negative-ion chemical-ionization mass spectrometry.
A method for simultaneous determination of prostaglandin E2 (PGE2), prostaglandin F2 alpha (PGF2 alpha), 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), and thromboxane B2 (TxB2) in plasma was developed. After acidification and addition of 2H- and 3H-labelled internal standards, plasma prostanoids were extracted by reversed-phase cartridges and purified by normal-phase high-performance liquid chromatography. The pentafluorobenzyl, methoxime, trimethylsilyl derivatives were formed. Negative-ion chemical-ionization mass spectra with methane as reagent gas show one intense peak at m/z (M - pentafluorobenzyl). This ion was used for selective-ion monitoring. Prostanoid plasma concentrations (pg/ml) in five healthy volunteers were: PGE2 2.0-10.4, PGF2 alpha 2.2-9.8, 6-keto-PGF1 alpha 0.6-1.8, and TxB2 3.0-45.3. However, there is evidence that the TxB2 values may frequently be falsely high because of ex vivo production during the sampling procedure.
6-Ketoprostaglandin F1 alpha↗
Congenital hypokalemia with hypercalciuria in preterm infants: a hyperprostaglandinuric tubular syndrome different from Bartter syndrome.
A congenital hypokalemic tubular disorder is described with many features resembling Bartter syndrome. Additional features include prenatal onset with polyhydramnios and premature labor; failure to thrive; episodes of fever, vomiting, diarrhea, and renal electrolyte and water wastage; hypercalciuria; nephrocalcinosis; and osteopenia. Unlike Bartter syndrome, there is no defect in tubular reabsorption of chloride. Urinary levels of prostaglandin E2 and 7 alpha-hydroxy-5,11-diketotetranorprosta-1,16-dioic acid are selectively elevated, indicating marked stimulation of renal and systemic PGE2 production. Chronic suppression of PGE2 activity by indomethacin corrects most of the abnormalities, and there is an immediate decompensation of the disease on indomethacin withdrawal. We conclude that these preterm infants have a distinct variety of hypokalemic tubular disorders rather than a variant of Bartter syndrome, because renal and systemic hyperprostaglandinism ranks high in the pathogenic chain of events, and the suppression of PGE2 hyperactivity is associated with significant improvement in the development (and probably in the prognosis) of the affected children.
Bartter Syndrome↗