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At least 19 recordsLinked to original sources

PubMed1991

Determination of 6-keto-PGF1 alpha, 2,3-dinor-6-keto-PGF1 alpha, thromboxane B2, 2,3-dinor-thromboxane B2, PGE2, PGD2 and PGF2 alpha in human urine by gas chromatography-negative ion chemical ionization mass spectrometry.

A method for quantification of 6-keto-PGF1 alpha, 2,3-dinor-6-keto-PGF1 alpha TXB2, 2,3-dinor TXB2, PGE2, PGD2 and PGF2 alpha in human urine samples, using gas chromatography-negative ion chemical ionization mass spectrometry, is described. Deuterated analogues were used as internal standards. Methoximation was carried out in urine samples which were subsequently applied to phenylboronic acid cartridges, reversed-phase cartridges and thin-layer chromatography. The eluents were further derivatized to pentafluorobenzyl ester trimethylsilyl ethers for final quantification by gas chromatography-mass spectrometry. The overall recovery was 77% for tritiated 6-keto-PGF1 alpha and 55% for tritiated TXB2. Urinary levels of prostanoids were determined in a group of six volunteers before and after intake of the thromboxane synthase inhibitor Ridogrel, and related to creatinine clearance.

6-Ketoprostaglandin F1 alpha↗

PubMed1991

[Thrombogenic factors in the elderly. Evaluation of the plasma concentrations of thromboxane B2 and antithrombin III].

The aim of this study is to prove the existence of a major tendency of platelet aggregation in elderly patients compared to medium-aged adults and, also, to detect whether it is affected by the presence of diabetes mellitus. Plasmatic concentrations of B2 thromboxane (TXB2) and antithrombin III (AT III) were determined in 73 elderly patients of both sexes; 56 without metabolic disease known (Group a) and 17 diabetic patients, 7 type I (Group bI) and 10 of type II (Group bII); and 12 healthy adults (control group). Medium plasmatic concentration of TXB2 was significantly higher (p less than 0.001) in Group a (55 +/- 14 ng/ml) compared to the control group (37 +/- 9 ng/ml) and there was no difference between Group bI (53 +/- 19 ng/ml) and bII (57 +/- 15 ng/ml). No variations were noted in ATIII concentration between the adults (27.4 +/- 2.3 mg/dl) and elderly patients (a = 29.6 +/- 4.4, bI = 29 +/- 2.6, bII = 31.2 +/- 5.9 mg/dl). In elderly patients, there appears to be a state of platelet pro-aggregation without influence of any risk factor, such as diabetes. This could explain the thrombogenic tendency of this age group.

Aged↗

PubMed1977

Electron capture gas chromatographic detection of thromboxane B2.

An electron capture gas chromatographic method is described for the detection of thromboxane B2. Thromboxane B2 is esterified with diazomethane, followed by treatment with pentafluorobenzylhydroxylamine hydrochloride and silylation with BSA. In pyridine, the free aldehyde form of the acetal ring is favored allowing rapid formation of a novel thromboxane B2 pentafluorobenzyloxime. The method has been applied to detect thromboxane B2 formation during aggregation of washed platelets. It must be emphasized that by ordinary analytical standards, the derivatization reproducibility from 50-375 nanograms is poor (+/- 11% - +/- 42%); however, the improved selectivity of the method and its ability to detect nanogram levels of thromboxane B2 make it a useful complement to commonly employed bioassay techniques.

Arachidonic Acids↗

PubMed1978

Metabolism of thromboxane B2 in the monkey.

[3H8]Thromboxane B2 was biosynthesized and infused into an unanesthetized monkey. Several urinary metabolites were isolated and their structures elucidated using gas chromatography-mass spectrometry. In addition to the major urinary metabolite, dinor-thromboxane B2, a series of metabolites resulting from dehydrogenetion of the alcohol group at C-11 were identified: 11-dehydro-thromboxane B2, 11-dehydro-15-keto-13,14-dihydro-2,3-dinor-thromboxane B2, and 11-dehydro-15-keto-13,14-dihydro-19-carboxyl-2,3,4,5-tetranor-thromboxane B2. 6-(1,3-dihydroxypropyl)-7-hydroxy-10-oxo-3-pentadecaenoic acid was also identified. Three mono-O-ethylated metabolites were formed from thromboxane B2, which in this study was infused in an ethanolic solution. A small quantity of thromboxane B2 was excreted unchanged into the urine.

Animals↗

PubMed1991

A chemiluminescent immunoassay for urinary thromboxane B2.

Because of the vasoactive properties of thromboxane A2 and other related prostaglandins, much research has been conducted on drugs which alter their levels. Urinary levels of thromboxane B2 and 2,3-dinor thromboxane B2 (major urinary metabolite of thromboxane B2) are used as an indication of thromboxane production in-vivo. In order to accurately measure urinary TXB2 levels of subjects on investigative drugs which lower TXA2 and subsequently TXB2, a simple and sensitive analytical tool becomes necessary. We have thus developed a non-radioisotopic (chemiluminescent) assay for urinary TXB2. Sensitivity has been demonstrated to 5 pg/ml. The method correlates well with gas chromatography/mass spectrometry (the accepted reference method) even without column chromatographic purification prior to the conduct of the chemiluminescent assay (r = 0.96). In addition, we have demonstrated feasibility for a chemiluminescent assay to measure urinary 2,3-dinor TXB2.

Acridines↗

PubMed1977

Identification of the major urinary metabolite of thromboxane B2 in the monkey.

Thromboxane B2 (TxB2) was biosynthesized from prostaglandin endoperoxides (PGG2, PGH2) using guinea pig lung microsomes and infused into an unanesthetized monkey. Urine was collected and TxB2 metabolites were isolated by reversed phase partition chromatography and high performance liquid chromatography. A major metabolite (TxB2-M) was found to be excreted in greater than two-fold abundance relative to other metabolites. Its structure was determined by gas chromatography-mass spectrometry to be dinor-thromboxane B2. In vitro incubation of TxB2 with rat liver mitochondria yielded a C18 derivative with a mass spectrum identical to that of TxB2-M, substantiating that the major urinary metabolite of TxB2 in the monkey is a product of a single step of beta-oxidation.

Animals↗

PubMed1979

Structure and quantitative determination of the major urinary metabolite of thromboxane B2 in the guinea pig.

2,3-Dinor-thromboxane B2 was the major urinary metabolite of thromboxane B2 in the guinea pig. The structure was assessed mainly by mass spectrometric analysis of a number of derivatives of the metabolite and by chemical degradation by oxidative ozonolysis. A method for quantitative determination of 2,3-dinor-thromboxane B2 in guinea pig urine based on multiple ion analysis and octadeuterated 2,3-dinor-thromboxane B2 as internal standard was developed. The basal excretion of the metabolite was 65 +/- 36 (S.D.) ng/kg x 24 h (n = 19; range 19--140 ng). This level corresponded to an endogenous synthesis of 543 +/- 300 ng of TXB2. No increase in the excretion was seen after anaphylaxis, in contrast to what has earlier been reported for PGF2 alpha.

Anaphylaxis↗

PubMed1977

Metabolism of thromboxane B2 in the cynomolgus monkey.

[5,6,8,9,11,12,14,15-3H8]-Thromboxane B2 was injected into the saphenous vein of female cynomolgus monkeys, and blood samples were withdrawn from the contralateral saphenous vein. The compound was eliminated from the circulation with a half-life of about 10 min after an initial rapid disappearance. Some more polar products appeared with time, and also small amounts of material less polar than thromboxane B2; however, the dominating compound in all blood samples was unconverted thromboxane B2. About 45% of the given dose of tritium was excreted into urine in 48 hrs. Several metabolites of thromboxane B2 were found. The major urinary metabolite was identified as dinorthromboxane B2 (about 32% of urinary radioactivity). Unconverted thromboxane B2 was also found in considerable amounts (13% of urinary radioactivity). It is concluded that 1) dehydrogenation at C-12 is not a major pathway in the degradation of this compound, in contrast to metabolism at the corresponding C-15 alcohol group of prostaglandins; 2) after having gained access to the circulation, thromboxane B2 is the main circulating compound; however, assay of thromboxane B2 in plasma will be complicated or precluded by large artifactual production of the compound by platelets during sample collection.

Animals↗

PubMed1992

The change of urinary 11-dehydro-thromboxane B2 and 2,3-dinor-6-keto-prostaglandin F1 alpha in arteriogenic impotence.

Thromboxane A2 is a potent vasoconstrictor and a stimulus of platelet aggregation, which may contribute to hypercoagulability. The prostacyclin, prostaglandin I2, has exactly the opposite effect. Measurement of the major urinary metabolites, 11-dehydro-thromboxane B2 and 2,3-dinor-6-keto-prostaglandin F1 alpha (prostaglandin F1 alpha) by radioimmunoassay can accurately reflect in vivo the biosynthesis of thromboxane A2 and prostaglandin I2, respectively. Group 1 consisted of 60 patients less than 50 years old. The mean urinary 11-dehydro-thromboxane B2 level of 3 patients with arteriogenic impotence was significantly greater than that of the 57 control volunteers: 2.66 +/- 0.65 versus 1.74 +/- 0.56 (plus or minus standard deviation) ng./mg. creatinine (p = 0.008). The prostaglandin F1 alpha levels for the patients and controls were 32.74 +/- 8.45 and 37.58 +/- 16.55 ng./mg. creatinine, respectively, which was not significantly different (p greater than 0.05). Group 2 consisted of 96 patients 50 years old or older. The 11-dehydro-thromboxane B2 concentration in the urine was 1.83 +/- 0.58, 2.54 +/- 1.12 and 1.91 +/- 0.73 ng./mg. creatinine in the 47 normal control volunteers, 20 patients with arteriogenic impotence and 29 with arteriogenic impotence plus intracavernous injection of 20 micrograms prostaglandin E1, respectively. The arteriogenic impotence group showed the significantly highest level among the 3 groups (p = 0.0025). Also, the urinary prostaglandin F1 alpha levels in these patients were 45.71 +/- 36.3, 57.71 +/- 35.53 and 59.30 +/- 45.08 ng./mg. creatinine, respectively, which was not significantly different (p greater than 0.05). For the 13 patients with arteriogenic impotence (group 3) we compared the urinary 11-dehydro-thromboxane B2 and prostaglandin F1 alpha levels before and after intracavernous injection of prostaglandin E1 by using a paired t test. The results showed that the change in 11-dehydro-thromboxane B2 levels was 2.78 +/- 1.09 versus 1.99 +/- 0.75 ng./mg. creatinine, which was significantly different (p = 0.005), whereas that for prostaglandin F1 alpha was 62.30 +/- 40.41 versus 58.86 +/- 44.26 ng./mg. creatinine, with no significant difference (p greater than 0.05). Our findings suggest that urinary 11-dehydro-thromboxane B2 may have an important role in the diagnosis and treatment of arteriogenic impotence.

6-Ketoprostaglandin F1 alpha↗

PubMed1976

A method for measuring the unstable thromboxane A2: radioimmunoassay of the derived mono-O-methyl-thromboxane B2.

A radioimmunoassay was developed for a mono-O-methyl derivative of thromboxane B2. The antibodies showed high specificity for this compound and cross reacted only 1.2% with thromboxane B2 and less than 0.1% with prostaglandins and prostaglandin metabolites. The method had a sensitivity of 7 picog. The radioimmunoassay was employed in studies where thromboxane A2 was generated in human platelets and immediately converted into mono-O-methyl thromboxane B2 by treatment of the sample with a large volume of methanol. In some of the experiments, thromboxane B2 was simultaneously measured by a separate radioimmunoassay. Using these two assays it was demonstrated that thromboxane A2 could be detected only during the earlier stages of the platelet aggregation, whereas thromboxane B2 rapidly reached a constant level. In a separate experiment, the half-life of thromboxane A2 in buffer was found to be 32.5 + 2.5 (S.D.) sec at 37 degrees C; the compound was more stable at lower temperatures. The t1/2 for thromboxane A2 was also considerably longer in plasma.

Antibody Specificity↗

PubMed1978

Chemotactic activity of thromboxane B2, prostaglandins and their metabolites for polymorphonuclear leucocytes.

(1) The chemotactic activities of thromboxane B2 (TxB2), PGE2, PGF2alpha, the 15-oxo, 15-oxo-13,14-dihydro and 13,14-dihydro metabolites of PGE2, PGF2alpha, and a metabolite of TxB2 for polymorphonuclear leucocytes (PMN) have been investigated. (2) Thromboxane B2 increased the directional migration of rat peritoneal PMN at a concentration of 2.0 micrograms/ml and of human peripheral neutrophils at a concentration of 0.5 microgram/ml. (3) Neither PGE2, PGF2alpha nor their metabolites showed chemotactic activity for rat peritoneal PMN. (4) PGF2alpha and 15-oxo-13,14-dihydro-thromboxane B2 showed no chemotactic activity for human peripheral PMN. (5) The possible role of thromboxane B2 in inflammation is discussed.

Animals↗

PubMed1977

The effects of thromboxane B2 and 6-ketoprostaglandin F1alpha on cultured fibroblasts.

The effects of thromboxane B2 and 6-ketoprostaglandin F1alpha on the synthesis of DNA, RNA and hexosamine-containing substances were studied. Thromboxane B2 (1 microgram/ml) added to cultures in the stationary phase caused the initiation of DNA synthesis and cell proliferation in a small proportion of cells. The same amount of thromboxane B2 also increased [3H]uridine incorporation into acid-insoluble fraction by 50% in 24 h, and stimulated the production of hexosamine-containing substances 2.5 fold over the control during the first 6 h. On the other hand, 6-ketoprostaglandin F1alpha was essentially inactive on these indexes except slight stimulation of DNA synthesis.

Cell Division↗

PubMed1991

[Elevation of 11-dehydro-thromboxane B2 levels in unstable angina].

To evaluate in vivo platelet activation, 11-dehydro-thromboxane B2 levels in plasma and urine were measured in 9 patients with unstable angina and 11 with stable angina using radioimmunoassay modified by the extraction method of Kawano et al. The 2 groups were matched for age, sex, coronary risk factors, medications or atherosclerotic lesions in coronary angiography. Although there was no difference in the plasma level between the 2 groups in the usual state, urinary 11-dehydro-thromboxane B2 amount in unstable angina was significantly increased compared to the stable angina group (865.5 +/- 238.7 vs 535.9 +/- 177.4 pg/mg creatinine (mean +/- SD), p < 0.01). There was no correlation between the 11-dehydro-thromboxane B2 level and the degree of coronary atherosclerosis in either group. The plasma level increased during the attacks in 2 patients with unstable angina. The amount of urinary 6-keto-PGF1 alpha did not differ between the 2 groups. These findings suggest that platelet activation in vivo is more pronounced in unstable angina than in stable angina, and that the measurement of urinary 11-dehydro-thromboxane B2 may be useful for evaluating and treating angina.

Angina Pectoris↗

PubMed1977

Metabolism of thromboxane B2 in man. Identification of the major urinary metabolite.

One and five-tenths milligrams of [3H8]thromboxane B2 (12.2 Ci/mol) was infused at a maximum rate of 6.4 microgram/min into a healthy male volunteer. Seventy-four per cent of the infused radioactivity was recovered in the urine within 13 h. Urinary metabolites of thromboxane B2 were isolated by reversed phase partition chromatography and high performance liquid chromatography. The major urinary metabolite was found to represent approximately 16.8% of the total radioactivity in the urine. The structure of this metabolite was shown by gas chromatography-mass spectrometry to be 2,3-dinor-thromboxane B2, the product of a single step of beta-oxidation. The rate of excretion of infused radioactivity and the relative percentage represented by 2,3-dinor-thromboxane B2 in the urine of man are very similar and the major urinary metabolite identical to that previously found by us in the non-human primate.

Animals↗

PubMed1977

Synthesis of thromboxane B2 and prostaglandins by bovine gastric mucosal microsomes.

Bovine gastric mucosal microsomes synthesize prostaglandins from arachidonic acid but thromboxane B2 is the principal product. Thromboxane B2 synthesis occurs at an appreciable rate from endogenous precursor but more rapidly with added arachidonate. Nonsteroidal antiinflammatory drugs inhibited synthesis of prostaglandins and thromboxanes with the following decreasing order of potency: indomethacin, fenoprofen, acetylsalicylic acid, phenylbutazone, sulfinpyrazone, and acetaminophen.

Animals↗

PubMed1992

Association between total cholesterol and thromboxane B2 levels in offspring of parents suffering from premature coronary artery disease.

Relationship between plasma thromboxane B2 concentration and serum total cholesterol level was studied in 129 healthy 3 to 18 years old children, 77 girls and 52 boys, without any family history of premature coronary artery disease and in 181 offspring, 105 girls and 76 boys, of parents suffering from acute myocardial infarction before the age of 45. It was identified an enhancement in serum total cholesterol level of endangered children, and an elevated release of thromboxane A2 in affected girls. A significant negative correlation was found between serum total cholesterol concentration and plasma thromboxane B2 level in healthy girls. However, there was no correlation between serum total cholesterol level and plasma thromboxane B2 concentration in the children whose parents had premature coronary artery disease. It appears, from our results, that this in an alteration of thromboxane A2 release of platelets in children of families with high risk of cardiovascular diseases.

Adolescent↗

PubMed1979

Cardiovascular and pulmonary effects of thromboxane B2 in the dog.

The hemodynamic properties of thromboxane B2 (TxB2), a product of prostaglandin endoperoxide metabolism, have not been thoroughly described. TxB2 is a bronchoconstrictor, but its effects on the systemic circulation and circulating platelets are unknown. Its precursor, thromboxane A2(TxA2), is a potent vasoconstrictor as well as a platelet-aggregating agent. Using intact anesthetized dogs, we investigated the effects of TxB2 on pulmonary artery pressure (PAP), airway pressure (AP), systemic arterial pressure (SAP), and myocardial contractility (MC). Vascular responses were evaluated in relation to changes in platelet population and aggregability. Intravenous TxB2 (25 and 50 micrograms/kg) increased AP (mean 62% and 69%) and PAP (50% and 86%), respectively, whereas SAP and MC responses were inconsistent. Left ventricular injections (25 micrograms/kg) also increased AP (36%) and PAP responses were inconsistent. Left ventricular injections (25 micrograms/kg) also increased AP (36%) and PAP (36%). Intraventricular administration of TxB2 produced a consistent elevation of SAP (10%) with a concomitant fall in MC (11%). These vascular responses were not consistent with alterations in platelet number or aggregability. A tachyphylactic response to TxB2 developed in AP and PAP at both dose levels and with both routes of administration. Intravenous and intraventricular TxB2 (25 micrograms/kg) produced a parallel decreasing response in PAP, suggesting the possible saturation of TxB2 binding sites or the depletion of a catabolic enzyme in the lung.

Animals↗

PubMed1978

Production of thromboxane B2 by the intra-uterine tissues from late pregnant Rhesus monkeys (Macaca mulatta) in vitro.

The rates of production of thromboxane B2 in vitro by intra-uterine tissues obtained from late pregnant monkeys by Caesarean section have been determined. The general quantitative order of rates of production was decidua basalis = decidua parietalis greater than placenta greater than chorion greater than amnion = myometrium. Myometrial production of thromboxane B2 was greater at term than during late pregnancy; no other tissue showed a significant trend with advancing gestation. These data demonstrate that the production of thromboxane B2 by intra-uterine tissues from late pregnant monkeys is both qualitatively and quantitatively different from the production of prostaglandins described previously. It is suggested that prostaglandins rather than thromboxanes are more intimately involved in the onset of labour in the rhesus monkey.

Amnion↗