Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Prostanoic Acids”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 91 records · Page 5Linked to original sources
PubMed1982

Prostacyclin potentiates 13-azaprostanoic acid-induced platelet deaggregation.

The specific thromboxane A2/prostaglandin H2 (TXA2/PGH2) antagonist 13-azaprostanoic acid (13-APA) reverses platelet aggregation stimulated by TXA2/PGH2 and the prostaglandin endoperoxide analog U46619. The present report demonstrates that the deaggregatory properties of 13-APA are potentiated by prostacyclin (PGI2). Human platelet-rich plasma was aggregated with U46619. Deaggregation was induced 2 min subsequent to the addition of the aggregating agent. Concentrations of 13-APA or PGI2 which induced 20 percent deaggregation were determined. Simultaneous addition of half of these concentrations resulted in 60 percent deaggregation, demonstrating that the observed response was supraadditive. Measurement of cyclic adenosine 3':5' monophosphate (cAMP) in resting or deaggregating platelets demonstrated that 13-APA itself did not stimulate cAMP production nor did 13-APA facilitate PGI2-induced increases in cAMP. In separate studies PGI2 and 13-APA were added to PRP prior to the induction of aggregation by U46619. Under these conditions, additive inhibition of aggregation was observed. Thus, it is clear that the pharmacological interaction between PGI2 and 13-APA depends upon the relative state of platelet activation.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1984

Prostanoids and hemodynamics in man before and during cardiopulmonary bypass.

The plasma concentration of 6-keto-PGF1 alpha, the stable degradation product of prostacyclin, was similar in the radial and pulmonary arteries and in the coronary sinus before and after the induction of the anesthesia in patients undergoing coronary artery bypass surgery. After the beginning of the mechanical ventilation and anesthesia the pulmonary vascular resistance decreased although no changes were detected in the plasma levels of 6-keto-PGF1 alpha or TXB2. During the prebypass period after the sternotomy and cannulation of the large vessels the plasma level of 6-keto-PGF1 alpha was increased similarly in the radial and pulmonary arteries and even more in the coronary sinus. During the cardiopulmonary bypass the concentration of 6-keto-PGF1 alpha remained at the increased level as compared to the values before the anesthesia. This indicates that pulmonary circulation is perhaps not the main source of prostacyclin in man. The plasma level of TXB2 was increased during the prebypass period significantly only in the coronary sinus, but during the bypass also in the radial artery. The concentration ratio of 6-keto-PGF1 alpha/TXB2 was increased significantly during the prebypass period in the radial and pulmonary arteries. At the same time the pulmonary vascular resistance was, however, returned to the preanesthesia level and was thus not decreased. The vascular resistance in the systemic circulation was increased during the prebypass period. The plasma level of 6-keto-PGF1 alpha or TXB2 in the radial and pulmonary arteries did not correlate significantly with the total vascular resistance in the systemic and pulmonary circulation, respectively. The vascular resistance in the coronary circulation did not correlate significantly with TXB2 level in the radial artery or coronary sinus. There was, however, a slight positive correlation between the blood flow and the concentration of TXB2 in the coronary sinus (r = 0.76, P less than 0.01). Coronary sinus flow did, however, not correlate with the plasma level of 6-keto-PGF1 alpha in the radial artery or coronary sinus. These results indicate that the detected plasma concentrations of prostacyclin and thromboxane A2 have no significant effects on the total vascular resistance in vivo.

6-Ketoprostaglandin F1 alpha↗
PubMed1985

Long term 'marine diet' in Eskimos is not associated with altered urinary excretion of total tetranor prostaglandin metabolites.

The total urinary excretion of tetranor prostaglandin metabolites, measured as tetranorprostanedioic acid (TPD), was quantified in traditionally living Greenland Eskimos (E) and compared with that in Caucasian Danes (D). TPD excretion (microgram/24h) was not significantly different between both groups, neither for males (331 +/- 62.4 (E) vs. 331 +/- 25.7 (D), mean +/- SEM, n = 9 and 10) nor for females (190 +/- 31.7 (E) vs. 264 +/- 27.4 (D), n = 11 and 10, P2 greater than 0.05). Since urinary prostaglandin metabolites are thought to reflect the total prostaglandin turnover in vivo, these results suggest that a long-term intake of relatively large amounts of polyunsaturated fatty acids of the (n-3) family does not alter total prostaglandin turnover in vivo. This is in contrast to stimulated prostanoid formation in vitro, and thus suggests a different regulatory role of dietary and tissue fatty acids for 'stimulated' and 'basal' prostaglandin production.

Adult↗
PubMed1984

The effects of 9-hydroxy-19,20-bis-norprostanoic acid on mucus, acid and gastrin secretion in duodenal ulcer patients.

The effects of 9-hydroxy-19,20-bis norprostanoic acid (rosaprostol, IBI), a new prostaglandin analogue, on gastric secretion and gastrin release were studied in 15 patients with duodenal ulcer. In acute experiments, rosaprostol lowered pentagastrin-stimulated acid secretion by 27-36%, whereas after chronic administration there were no changes in acid secretion or gastrin release (fasting and oxo-stimulated) but N-acetylneuraminic acid (NANA)-glycoproteins increased significantly. Our results indicate that the antisecretory and mucopoietic activities of 9-hydroxy-19,20-bis-norprostanoic acid are the basis of its healing effect in duodenal ulcer patients.

Adolescent↗
PubMed1987

Preparation and biological evaluation of a potential photoaffinity label for the prostaglandin H2/thromboxane A2 receptor.

Two aromatic azides (24 and 26) were prepared as potential photoaffinity probes for the PGH2/TXA2 receptor. The compounds are based on the well-characterized PGH2/TXA2 receptor antagonist 13-azaprostanoic acid, with the terminus of its lower side chain replaced with phenoxy (24) or benzyl (26) azide functionality. The two compounds were shown to irreversibly inhibit platelet function after photolysis and resuspension. However, of the two aromatic azides, only the benzyl derivative 26 appeared to be selective for the prostaglandin pathway. The latter compound was also prepared as the aromatic 125I (29) derivative, which may ultimately prove useful as a labeled probe for the identification and isolation of the putative TXA2/PGH2 receptor.

Adenosine Diphosphate↗
PubMedDate not supplied

[Cytoprotective effect of rosaprostol during treatment with non-steroidal anti-inflammatory agents in arthrorheumatic pathologies].

A clinico-endoscopic study has been carried out in a group of 22 patients treated with 1 g of naproxene + 2 g of rosaprostol compared in a blind situation with another group of 19 patients treated with a similar dose of naproxene + placebo in order to evaluate the cytoprotective action of rosaprostol. Analysis of the results showed a high correlation between intake of rosaprostol and low onset of algico-dyspeptic disturbances and mucosal lesions of some gravity, although the problem of the monitoring of patients undergoing long-term treatment with NSAID remains unsolved.

Adult↗
PubMedDate not supplied

[Effect of 7-aza- and 13-aza-prostanoids on platelet aggregation].

The effects of 11 new analogues of 7-aza- and 13-azaprostanoic acid on platelet aggregation of the rat were studied in vitro and ex vivo. The analogues of 13-azaprostanoic acid in vitro (10(-7)-10(-8) mol/l) were found to exhibit the antiaggregation activity in the blood. The compounds containing five-member cycle are more active antiaggregants. They decrease by 70-80% the degree of platelet aggregation stimulated by thrombin and ADP. The modification of omega-chain of these analogues (alkyl, phenyl) exerts no effect on the antiaggregation activity. The antiaggregation action of these compounds in ex vivo condition (5-10 micrograms/kg) does not preserve. 7-azaprostanoids possess the proaggregation activity in vitro.

Adenosine Diphosphate↗
PubMedDate not supplied

Anti-aggregatory prostanoids. Part I.

Properties of several products of cyclo-oxygenation of polyunsaturated fatty acids: prostacyclin, prostaglandins 6-keto E1, E2, D2, D3 are reviewed in relation to their antiplatelet activity.

Alprostadil↗
PubMed1983

Reduced excretion of the main urinary metabolite of prostaglandin F1 alpha and F2 alpha in psoriatic patients.

Twenty-four hour excretion of main urinary metabolite of prostaglandin F1 alpha and F2 alpha (PGF-MUM) in 18 patients with stable psoriasis (9 males and 9 females) and 18 almost age-matched healthy subjects (9 males and 9 females) was examined. The mean excretion level of PGF-MUM in male psoriatic patients (15.2 +/- 4.0 micrograms/day) was significantly lower than that in male healthy subjects (22.8 +/- 3.3 micrograms/day) (p less than 0.01). A similar tendency was observed between female psoriatic patients (10.6 +/- 3.0 micrograms/day) and female healthy subjects (13.3 +/- 2.4 micrograms/day) although the difference in the excretion level was not so remarkable (p = 0.05) compared with male subjects. These results suggest an altered endogenous prostaglandin synthesis in psoriatic patients.

Adolescent↗
PubMed1984

The role of prostaglandins in cercarial (Schistosoma mansoni) response to free fatty acids.

In examining the structure-activity relationship of a diverse group of chemicals reported to prevent cercarial penetration after topical application, we noticed a moiety that was common to free fatty acids and prostaglandins. Because unsaturated fatty acids have been reported to stimulate cercarial penetration, we hypothesized that cercarial stimulation by skin and fatty acids may invoke prostaglandin mechanisms in cercariae, skin, or both. Thus we compared the stimulation of cercariae by a series of essential and nonessential fatty acids and demonstrated an inhibition of this response by ibuprofen and aspirin, known cyclo-oxygenase inhibitors, and by 13-azaprostanoic acid, a potent antagonist of the thromboxane/endoperoxide receptor. These data led us to postulate a major role for prostaglandins in the cercarial penetration response.

Animals↗
PubMed1988

Phospholipid profile and production of prostanoids by murine colonic epithelium: effect of dietary fat.

Dietary fat and abnormal production of various prostanoids have been linked to various disease states of the large bowel, including cancer of the colon. Studies were conducted to determine the effect of dietary fat (beef tallow or corn oil) on the lipid composition and prostanoid production of the murine colon. Female C57BL/6J mice were fed high-fat (HF) diets (47% of calories as fat) or low-fat (LF) diets (10% of calories as fat). After four wk of dietary treatment, the mucosa was scraped, and lipids were extracted from the mucosal and muscle layers. The fat content of the diets did not significantly alter the amount of phospholipid (PL) or neutral lipid in the colonic tissue. However, the HF affected the PL profile of the colonic mucosa. For example, the ratio of phosphatidylcholine (PC) to phosphatidylethanolamine (PE) was significantly higher for both the HF groups compared with that of the two LF groups (0.76 +/- 0.15 and 0.80 +/- 0.13 vs 0.31 +/- 0.20 and 0.34 +/- 0.18). Production of 13,14-dihydro-15-keto-PGE2 (measured as bicyclic PGE2) and TXB2 (a stable metabolite of TXA2) and PGF1 alpha (a stable metabolite of PGI2) was unaffected by the dietary treatments. The muscle had a different PL profile (PC:PE is 2.6 +/- 0.1) than the mucosa and contributed a larger proportion of the prostanoids formed. This study demonstrates that the phospholipid polar head group composition of normal colonic mucosa is altered by dietary fat, but the ability of the mucosa to synthesize metabolites of PGE2, TXA2 and PGI2 is not affected.

Animals↗
PubMed1983

Quantitative analysis of 11 alpha-hydroxy-9,15-dioxo-2,3,4,5,20-pentanor-19-carboxyprostanoic acid, the major urinary metabolite of E prostaglandins in man.

A system for the assay of the major metabolite of E prostaglandins (PGE-M) in human urine was developed. The metabolite, as the dimethyl ester-bis(O-methyloxime)-trimethylsilyl ether derivative, was quantified by gas chromatography-mass spectrometry with selected ion monitoring. The internal standard was the diethyl ester analog. A linear response ratio over the range 10 to 300 ng of injected prostaglandin was demonstrated in calibrations with authentic material. The 20-ml specimens of urine were extracted with Amberlite XAD-2, methylated, chromatographed over octadecasilyl-silica, silicic acid, and Lipidex-5000, and then methoximated, trimethylsilylated, and instrumentally analyzed. The interassay coefficient of variation, for analysis of four identical urine specimens, was 11% and the intraassay coefficient of variation ranged from 1 to 5%. Specificity, accuracy, and precision of the method were verified by recovery of PGE-M from four different 80-ml urine pools. Each pool was divided into four equal portions, and different amounts of PGE-M were added to three. The recovery of authentic, underivatized PGE-M added to urine was 103.2 +/- 3.3% (mean +/- SE, N = 12). The plot of recovered versus added PGE-M followed the equation y = 1.003x + 1.83, with R = 0.9974.

Fatty Acids↗
PubMed1983

Antagonism of platelet aggregation by 13-azaprostanoic acid in acute myocardial ischemia and sudden death.

The effects of 13-azaprostanoic acid (13-APA) were studied during acute myocardial ischemia in cats and in rabbit sudden death induced by sodium arachidonate (Na-Ar). To more clearly define the mechanism of action of 13-APA, we also examined its effects on isolated cat and rabbit coronary arteries, in vitro aggregation of cat and rabbit platelet-rich plasma (PRP) and circulating rabbit platelet count measured in vivo. 13-APA provided minimal protection during myocardial ischemia in cats, partially reversing ischemia-induced ST segment elevations by 3-5 hours after coronary artery occlusion. However, 13-APA was ineffective in inhibiting the rise in plasma creatine kinase (CK) activity or the loss of CK from ischemic myocardial tissue. 13-APA (1.0 - 100 microM) did not inhibit contraction of cat coronary arteries produced by a stable thromboxane A2 analog. However, 13-APA (100 microM) inhibited aggregation of cat PRP induced by AA (1.0 microM). 13-APA also provided significant protection against sudden death induced by Na-Ar in rabbits. While this agent was ineffective in reducing vasoconstriction of rabbit coronary arteries or inhibiting platelet aggregation in response to 500 microM AA, aggregation of rabbit PRP by 250 microM AA was completely inhibited. AA injection produced a significant decrease in circulating platelet count in vehicle-treated rabbits. However, 13-APA reduced the decrease in circulating platelet count in rabbits which survived AA injection during the 13-APA infusion. These results indicate that antagonism of thromboxane A2 receptors in platelets may be an important feature in protecting against sudden death. The difference in sensitivities of vascular and platelet thromboxane receptors as well as the accessability of 13-APA to these receptors may explain the lack of protection of 13-APA in myocardial ischemia.

Animals↗