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At least 109 records · Page 6Linked to original sources
PubMed1990

Influence of an alpha-1-adrenoceptor antagonist, nicergoline, on placental prostanoid production in streptozotocin-induced diabetic pregnant rats.

The aim of this study was to determine if placental prostanoids could mediate the vasodilating action of an alpha-1-adrenoceptor antagonist, nicergoline (400 micrograms/kg i.p.), during late pregnancy in streptozotocin-induced diabetic rats (40 mg/kg i.v.). Placental prostanoid concentrations were evaluated by radioimmunoassay. Prostaglandin E2 levels showed a highly significant increase in diabetic and nondiabetic rats treated with nicergoline (p less than 0.001). 6-Keto-PGF1 alpha concentrations were slightly increased in diabetic rats compared to controls, and this increase was reversed by both nicergoline and insulin treatments. In all groups studied thromboxane B2 levels were comparable. It is concluded that prostaglandin E2 could mediate the vasodilating action of nicergoline on the placental irrigation and, therefore, improved the hemodynamic state of this organ in diabetic rats.

6-Ketoprostaglandin F1 alpha↗
PubMed1988

Effects of cimetidine on prostanoid production in the gastric corpus specimens from rats.

In order to examine the effect of cimetidine on the production of prostanoids in the stomach mucosa, the amounts of prostaglandin (PG) E2, F1 alpha and thromboxane (TX) B2 were determined after the specimens from the rat stomach corpus were incubated in the presence of cimetidine. Cimetidine significantly stimulated the production of PGE2 in the specimens at a concentration of 10 microM, but did not significantly affect the production of PGF1 alpha and TXB2 at concentrations of 1 to 100 microM.

Animals↗
PubMed1976

Radioimmunoassays for prostaglandin metabolites.

Radioimmunoassays were developed for the main plasma and urinary metabolites of PGF2alpha in the human, viz., 15-keto-13,14-dihydro-PGF2alpha and 5alpha, 7alpha-dihydroxy-11-ketotetranorprosta-1,16-dioic acid. The methods allowed assay of unextracted samples and had a sensitivity of 5 pg and 2 pg, respectively. The assays were evaluated by comparison with mass spectrometric data. Normal levels of these metabolites were estimated in a number of subjects. Levels in plasma and urine of the metabolites were followed after injection or during infusion of PGF2alpha and during administration of various antiinflammatory drugs.

Epitopes↗
PubMed1984

Use of a homologous internal standard for the quantification of the major metabolite of prostaglandin F2 alpha in human urine by multiple ion analysis.

A gas chromatographic-mass spectrometric method for quantitative determination of 9 alpha, 11 alpha-dihydroxy-15-oxo-2,3,4,5,20-pentanor-19-carboxyprostanoic acid, the major urinary metabolite of prostaglandin F2 alpha (PGF-M), was developed. The metabolite was analyzed as the dimethyl ester-O-methyloxime-bis-trimethylsilyl ether derivative. The internal standard consisted of a mixture of diethyl ester + monoethyl ester-delta-lactone of PGF-M. Those two species were converted to the 1-methyl-20-ethyl ester derivative during the analytical process. Linear standard curves were developed in the range 0 to 100 ng of injected prostaglandin. The method comprised extraction with Amberlite XAD-2, methylation, chromatography over octadecasilyl-silica, delactonization, remethylation, and chromatography over silicic acid and Lipidex-5000, followed by methoximation, trimethylsilylation, and instrumental analysis. Interassay coefficient of variation, for the analysis of four identical urine specimens, was 7% and intraassay coefficient of variation, when each sample was injected four times, ranged from 3.2 to 6.0%. Specificity, accuracy, and precision of the method were verified by recovery of the metabolite from two different urine pools. The recovery of authentic, underivatized PGF-M added to urine was 99.1 +/- 2.4% (mean +/- SE, N = 6). The plot of recovered versus added metabolite followed the equation y = 0.936 x + 25.8, with r = 0.9918.

Biotransformation↗
PubMed1985

Prostanoid modulation (mediation?) of certain behavioral effects of ethanol.

Prostaglandin E1 (PGE1) and prostanoid precursor fatty acids enhance the acute sedative effects of ethanol in mice, and reduce the intensity of withdrawal after chronic exposure to ethanol. Aspirin, and other inhibitors of prostanoid synthesis, attenuate ethanol's sedative effects, and interfere with the beneficial effects of prostanoid precursors (but not of PGE1 itself) in withdrawal. Neither aspirin nor indomethacin administered alone affect withdrawal behavior. In contrast, ethanol impairment of rotorod behavior is not affected by prostanoid precursors nor by aspirin. These findings support a role for prostanoids as modulators (? mediators) of certain direct effects of ethanol and a role for prostanoid deficiency in the pathogenesis of withdrawal behavior.

Alcoholism↗
PubMed1980

Prostaglandin F2 alpha metabolites in plasma and urine during pseudopregnancy in the rabbit.

Two prostaglandin (PG) F2 alpha metabolites, 13,14-dihydro-15-keto PGF2 alpha (dhkPGF2 alpha) in blood and 5 alpha, 7 alpha-dihydroxy-11-keto tetranorprostane 1,16-dioic acid (PGF2 alpha UM) in urine, were measured in the pseudopregnant rabbit by radioimmunoassay. During pseudopregnancy, marked increases in the two PGF2 alpha metabolites were demonstrated at about the time of luteal regression. Hysterectomy and intrauterine administration of indomethacin prolonged the life span of corpora lutea in the pseudopregnant rabbit by 8 and 5 days, respectively, with no elevation of PGF2 alpha UM excretion. The findings indicate that PGF2 alpha is a uterine luteolysin in the pseudopregnant rabbit, as in other animal species.

Animals↗
PubMed1984

Synthesis of [17,18-3H] trans-13-azaprostanoic acid. A labeled probe for the PGH2/TXA2 receptor.

Because of its highly unstable nature, TXA2, produced by platelet metabolism of arachidonic acid, does not lend itself to use as a receptor probe for its own receptor. As such, the stable TXA2/PGH2 antagonist, trans-13-azaprostanoic acid (trans-13-APA, 12b), was prepared as the [17, 18 3H] derivative [( 3H] trans-13-APA, 12c) to study this receptor and to better evaluate the mechanism of action of these azaprostanoids. Tritiated trans-13-APA, 12c, was prepared in nearly theoretical specific activity (57 Ci/mmole) from (17Z)-trans-13-azaprost-17-enoic acid (11b) by catalytic tritiation. The unsaturated 11b was prepared by condensation of cis-7-amino-3-heptene (8) with 2-(6-carboxyhexyl) cyclopentanone (9), NaBH4 reduction, chromatography, and hydrolysis of the trans isomer so isolated. The olefins 11a and b were also of biochemical interest because of the unsaturation in the lower side chain. The presence of similar unsaturation in PGH3(4) and TXA3 (3) renders these prostaglandins inactive as proaggregatory agents. Evaluation of the antiaggregatory activity of 11a and b indicated it to be about the same potency in inhibiting human platelet aggregation as the parent cis and trans-13-APAs, suggesting that introduction of a double bond at the 17 position in platelet prostaglandin antagonists is unlikely to result in enhanced antiplatelet activity.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1985

Eicosanoids in health and in disease: an appraisal.

Oxygenation of the 20-carbon polyunsaturated fatty acid, arachidonic acid, which is found in most body cells of all domestic animals, leads to the formation of a group of compounds possessing biological activity. These compounds, collectively known was eicosanoids, currently receive considerable attention owing to their involvement in a wide variety of physiological and pathophysiological processes. Particular interest has been focussed in recent years on the role and control of prostanoids and leukotrienes in inflammatory and allergic conditions in animals and man. Arachidonic acid metabolites are also recognised to be intimately involved in reproductive and perinatal processes; with platelet aggregation and vascular homeostasis; kidney function; fever; certain tumours and many other normal and disease conditions. Eicosanoid research in veterinary medicine is still at a relatively early stage in many respects and in this review an attempt is given to highlight some of the functions of this important series of compounds both in health and in disease. As more evidence comes to light, it is possible that veterinary surgeons may have to consider revising their clinical approach to the treatment of certain disease states where eicosanoids are implicated or where chemotherapy may interfere with their normal physiological activities.

Animals↗
PubMed2000

Significant increase in prostaglandin E-main urinary metabolite by laxative administration: comparison with ulcerative colitis.

OBJECTIVE: To assess the production of prostaglandin E(2), an important chemical mediator in diarrhea induced by laxative administration, a prostaglandin E-main urinary metabolite (7alpha-hydroxy-5,11-diketotetranor-prosta-1,16-dioic acid, PGE-MUM) was measured in healthy volunteers and compared with the values of patients with ulcerative colitis. METHODS: PGE-MUM was determined by a simplified immunoassay of bicyclic PGE-MUM and analyzed for the influence of laxative administration and active/remission phases of ulcerative colitis. RESULTS: Administration of laxatives induced a significant increase in PGE-MUM in healthy volunteers. A significant elevation was also found in the active as compared with the remission phase of ulcerative colitis. The PGE-MUM levels were significantly correlated with our modified Talstad scores, clinical disease activity indices in ulcerative colitis. It was confirmed by time course studies of individual patients that changes in PGE-MUM correlated well with colitis activity. CONCLUSION: Laxative administration induces production of prostaglandin E(2) as one of the chemical mediators, although its production grade is relatively low as compared with ulcerative colitis in the active phase.

Aged↗
PubMed1984

Mechanical trauma to bladder epithelium liberates prostanoids which modulate neurotransmission in rabbit detrusor muscle.

Transitional epithelium of the rabbit urinary bladder has been implicated as a major site of prostanoid production and various studies have indicated that prostanoids have significant influences in muscle activity and neurotransmission in the bladder. We have examined the possibility that mechanical irritation of the epithelium could release diffusable substances which could influence neuromuscular function in the bladder. Epithelium was dissected from muscle strips of rabbit urinary bladder and the two components were incubated in separate chambers. Krebs' solution bathing epithelium was transferred to the bath in which the muscle was being field stimulated. Increases in the basal tension and spontaneous activity of the muscle as well as in the electrically evoked responses were observed after transfer and were related to the intensity of the irritation given the epithelium sample. The effects were mimicked by prostaglandins E1 E2, F2 alpha and I2 and the transfer effect was reduced significantly by pretreatment of the epithelium, but not the muscle, with indomethacin (10 microM) or ibuprofen (100 microM). Transfer of solution bathing-irritated epithelium also raised basal tension but not the maximum response to bethanechol. Finally, radioimmunoassay was used to demonstrate that irritation of epithelium samples caused the appearance of prostaglandin and 6-oxo-prostaglandin F1 alpha in the bathing medium and that this appearance was profoundly depressed by indomethacin (10 microM). It is plausible, therefore, that mechanical irritation of the bladder epithelium could result in changes in neuromuscular function in the underlying muscle layers and that these changes would be consistent with the symptoms associated with mechanical trauma of urothelium.

6-Ketoprostaglandin F1 alpha↗
PubMed1984

Effect of cimetidine on human gastric and duodenal prostanoid synthesis.

In 13 patients with endoscopically proven duodenal ulcer, biopsies were obtained from the stomach body and antrum and from the duodenal bulb before and, in 10, after 4 weeks of cimetidine treatment (1 g/day). The specimens were organ-cultured for 90 min, and prostanoid accumulation in the medium was determined by radio-immunoassay. After 4 weeks of cimetidine treatment, prostaglandin E2 and 6-keto-prostaglandin F1 alpha synthesis by cultured specimens obtained from the body of the stomach (1304 +/- 197 and 497 +/- 124, no. +/- 10) was significantly higher than their respective synthesis before therapy (734 +/- 90 and 222 +/- 26; no. = 13) (X +/- SE, pg/mg wet wt/90 min). Prostanoid synthesis by cultured specimens from the antrum and duodenum was not significantly different before and after cimetidine treatment. It is therefore suggested that cimetidine, in addition to its antisecretory effects, accelerates ulcer healing also by induction of endogenous gastric prostanoid synthesis.

6-Ketoprostaglandin F1 alpha↗
PubMed1987

Production of prostanoids by rheumatic synovial cells in vitro: effects of anti-inflammatory drugs on arachidonic acid metabolism.

To evaluate the role of prostanoids in rheumatoid arthritis the effects of anti-inflammatory drugs on prostanoid concentrations and their ratios were studied in a primary culture of adherent synovial cells from patients with rheumatoid arthritis. Cells from rheumatoid synovium have a great capacity for prostanoid production. PGE2 is the main prostanoid but synovial cells are also capable of producing 6-keto-PGF1 alpha and PGF2 alpha. There were also very low TxB2 concentrations in the culture medium after incubation. All nonsteroidal anti-inflammatory drugs used (diclofenac, indomethacin and tolfenamic acid) reduced markedly, in concentrations achieved therapeutically (greater than or equal to 0.13 mumol/l), the production of all the prostanoids from endogenous substrate. There were no differences in the efficacity of the drugs. Hydrocortisone was needed for higher concentrations to inhibit PGE2, 6-keto-PGF1 alpha and PGF2 alpha production. TxB2 formation remained almost unaltered. After the drug incubation there were also clear alterations in the ratios between these prostanoids, which may have therapeutic importance. It is suggested that this kind of synovial cell culture can be used for testing the effects and mechanisms of different anti-inflammatory drugs in standardized cell culture conditions.

6-Ketoprostaglandin F1 alpha↗