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Biomedical subjects

I Ramis

Publications and source records attributed to I Ramis.

17 recordsLinked to original sources
PubMed1992

Solid-phase extraction of prostanoids using an automatic sample preparation system.

A commercial automated solid-phase extraction system for cyclooxygenase arachidonic acid metabolites in urine samples has been evaluated. Comparison of manual and automatic batch (36 samples) extraction procedures for tritium labelled prostanoids added as tracers to urine samples has shown equivalent results with recoveries greater than 90% for prostaglandins E2, F2alpha and 6-keto prostaglandin F1alpha as well as thromboxane B2. Analyte stability is not affected by the automated procedure, which uses less solvents and has a faster overall processing time than the manual method. The automated system has been applied to the extraction of prostanoids in urine samples from workers exposed to dichloroethane.

Arachidonic Acids↗
PubMed1992

In vivo transformation of arachidonic acid into 12-hydroxy-5,8,10,14-eicosatetraenoic acid by human nasal mucosa.

A method for the determination of 12-hydroxy-5,8,10,14-eicosatetraenoic acid (12-HETE) by gas chromatography-mass spectrometry (GC-MS) in samples obtained from healthy subjects by nasal lavage is presented. HETEs were extracted from samples obtained by nasal lavage using C18 solid-phase cartridges. The purification of 12-HETE and 5-HETE was carried out in two consecutive steps of purification by reversed-phase high-performance liquid chromatography. Methylated and trimethylsilylated fractions were separated by GC-MS with electron-impact ionization. The production of 12-HETE by human nasal mucosa was confirmed by GC-MS.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1992

Human and experimental studies on renal eicosanoid response to long-term cadmium exposure.

In order to assess the effects of long-term exposure to cadmium (Cd) on the renal metabolism of eicosanoids, the urinary excretion of 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), prostaglandin E2 (PGE2), prostaglandin F2 alpha (PGF2 alpha), and thromboxane B2 (TXB2) was determined in 37 workers exposed to Cd and in female Sprague-Dawley rats given 100 ppm Cd in drinking water for 10 months. Urinary output of sodium and calcium was also determined. The Cd-exposed workers showed an increased urinary concentration of 6-keto-PGF1 alpha, PGE2, sodium, and calcium. The rise of 6-keto-PGF1 alpha was related to Cd levels in blood and weakly correlated with urinary sodium. Calcium in urine was not related to the concentration of the metal in blood and urine. A slight elevation in urinary TXB2 was also observed in workers with blood Cd higher than 5 micrograms/liter. After 10 months of exposure to Cd, female Sprague-Dawley rats presented an enhanced urinary excretion of albumin, transferrin, beta 2-microglobulin, sodium, and PGE2 in urine. The latter was significantly correlated with albuminuria and transferrinuria. In conclusion the results show that chronic exposure to Cd induces changes in the urinary excretion of some eicosanoids. The possible relation of these changes to Cd-induced kidney dysfunction are discussed.

6-Ketoprostaglandin F1 alpha↗
PubMed1992

Oxidative metabolism of N-phenyllinoleamide by human nasal polyps.

N-phenyllinoleamide (NPLA), the anilide of linoleic acid, has been associated with the epidemiology of Toxic Oil Syndrome, but no data are available on its metabolism. On account of the similarity in chemical structure between the linoleic acid and NPLA, the aim of this study has been to investigate the oxidative metabolism of this xenobiotic by the human nasal polyp, a tissue with elevated 15-lipoxygenase activity. For this purpose, tissue homogenates have been incubated for 2 h with NPLA (0.1 mM) spiked with either N-(ring G-3H)PLA (0.2 microCi/ml) or N-P(1-14C)LA (0.05 microCi/ml). Gas chromatographic/mass spectrometric analysis of the high performance liquid radiochromatographic fractions shows that the 9,12,13-trihydroxy, 12,13-epoxy-11-hydroxy and 13-hydroxy NPLA derivatives are the major metabolites. These results revealed that NPLA metabolites are chemical structures related to the linoleic acid derivatives, some of which may show biological activity.

Anilides↗
PubMed1992

Release of peptide leukotriene into nasal secretions after local instillation of aspirin in aspirin-sensitive asthmatic patients.

Although the mechanism of aspirin-induced asthma and rhinitis is unknown, it has been suggested that adverse nasal and bronchial reactions are caused by an increased production of lipoxygenase products. In examining this hypothesis we have measured the release of peptide leukotrienes (PeptLTs), 15-HETE, and prostaglandins in nasal fluids obtained by nasal lavages after instillation of acetylsalycilic acid (ASA) and placebo (saline). Ten ASA-sensitive asthmatics, 10 ASA-insensitive asthmatics, and seven healthy subjects were challenged in a double-blind study with normal saline and 12 mg of ASA. Twelve mg were administered based on the results of a previous study that showed that this dose caused minor to moderate symptoms in ASA-sensitive patients. PeptLTs, LTB4, 15-HETE, PGE2, PGF2 alpha, and PGD2 were measured by radioimmunoassay methods. Significant levels of PeptLTs were detected in sensitive asthmatic patients 60 min after nasal challenge. This change was associated with a significant increase in symptoms. No increase in PeptLTs levels were found, however, in either insensitive patients or healthy subjects. Inhibition of PGE2 and PGF2 alpha release was detected in the three groups after ASA administration. ASA also inhibited PGD2 release in insensitive asthmatic patients but not in both sensitive patients and healthy subjects. These results suggest that an abnormal release of PeptLTs in ASA-sensitive asthmatic patients contributes to nasal and bronchial adverse reactions. The lack of effects on PGD2 release suggests that mast cells from ASA-insensitive patients are more sensitive to ASA than those from sensitive asthmatic patients and healthy subjects.

Administration, Intranasal↗
PubMed1992

Systemic prostacyclin in cirrhotic patients. Relationship with portal hypertension and changes after intestinal decontamination.

The total body production of prostacyclin was shown to be increased in cirrhotic patients, suggesting that its synthesis by blood vessels of the systemic circulation is enhanced. However, the mechanism by which the synthesis of systemic prostacyclin is stimulated is not known. The present study investigated the urinary excretion of 2,3-dinor-6-keto-PGF1 alpha, an index of total body prostacyclin synthesis, first, in cirrhotics with portal hypertension (n = 19) as compared with cirrhotics with reduced portal pressure after portacaval shunt surgery (n = 18) and with control noncirrhotic subjects (n = 11), and; second, in cirrhotics before and after intestinal decontamination by oral nonabsorbable antibiotics (n = 9 antibiotic treated patients, n = 10 control nontreated cirrhotics). Control noncirrhotic subjects showed lower urinary excretion of 2,3-dinor-6-keto-PGF1 alpha than both groups of cirrhotics (P less than 0.001). Interestingly, urinary excretion of 2,3-dinor-6-keto-PGF1 alpha was significantly higher in cirrhotics with portacaval shunt than in those with portal hypertension (P less than 0.01). The urinary excretion of 2,3-dinor-6-keto-PGF1 alpha decreased significantly after intestinal decontamination in the antibiotic-treated group (580.1 +/- 232.4 vs. 431.2 +/- 219.2 pg/mg creatinine; P less than 0.05) but not in nontreated patients (543.9 +/- 214.4 vs. 581.2 +/- 281.4 pg/mg creatinine; P = NS). These data suggest that the increased urinary excretion of 2,3-dinor-6-keto-PGF1 alpha observed in cirrhotics is not directly related to portal hypertension itself but to portal blood factors that bypass the liver. Some such factors may be of intestinal bacterial origin.

6-Ketoprostaglandin F1 alpha↗
PubMed1991

Cyclooxygenase and lipoxygenase arachidonic acid metabolism by monocytes from human immune deficiency virus-infected drug users.

Prostaglandin E2, thromboxane B2 and leukotriene B4 monocyte production have been determined in human immune deficiency virus (HIV)-infected drug users (n = 36) and healthy subjects (n = 29). Eicosanoids were extracted from the incubates using C18 solid-phase cartridges and determined by radioimmunoassay. An enhanced production of prostaglandin E2 and thromboxane B2 was detected in monocytes from HIV-positive drug users whether or not they had been previously stimulated with zymosan. Concomitant leukotriene B4 increases were not observed. The results reported in this paper indicate that altered cyclooxygenase arachidonic acid metabolism in monocytes from HIV-infected drug users is associated with the severe cellular immunodysfunction characteristic of AIDS. In contrast, leukotriene B4 does not seem to play a role in AIDS-associated immunosuppression.

Acquired Immunodeficiency Syndrome↗
PubMed1991

Mast cells in the rat gastric mucosa are not primarily responsible for PGD2 generation.

The present study investigates the contribution of gastric mast cells on PGD2 generation in rat gastric mucosa. Cold-restraint induced stress or i.v. carbachol injection methods were used for gastric mast cell degranulation. In 19 stressed, 15 carbachol-infused and 14 control rats, gastric mast cell counts and gastric mucosa PGD2 assay were performed. Gastric mucosal content of PGF2 alpha was also determined in carbachol infused and control rats. The mean number of gastric mast cells was significantly lower in stressed and carbachol infused than in control rats. Despite these differences in gastric mast cell counts, neither PGD2 or PGF2 alpha contents in the gastric mucosa were significantly different in mast cells degranulated rats than in control animals. These results suggest another source of PGD2 in the rat gastric mucosa other than mast cells.

Animals↗
PubMed1991

In vivo release of 15-HETE and other arachidonic acid metabolites in nasal secretions during early allergic reactions.

The purpose of this study is to examine the "in vivo" release of 15-HETE and other arachidonic acid metabolites in nasal secretions following a challenge with "Dermatophagoides Pteronyssinus" in patients with allergic rhinitis and non-allergic controls. In addition, we examine the effects of a membrane stabilizer, such as sodium cromoglycate, on these metabolites. Thirteen allergic subjects and seven healthy controls are studied. 15-HETE, peptide leukotrienes, LTB4, PGD2, PGE2 and PGF2 alpha levels are evaluated before and after nasal challenge in sodium cromoglycate treated and untreated subjects. This study provides "in vivo" evidence that the pathophysiological responses to nasal antigen challenge could be related to the release of 15-HETE as well as other arachidonic acid metabolites, mainly arising from the lipoxygenase pathway.

Adolescent↗
PubMed1990

Simultaneous reversed-phase extraction of lipoxygenase and cyclooxygenase metabolites of arachidonic acid in nasal secretions: methodological aspects.

An improved analytical method for the simultaneous solid-phase extraction of arachidonic acid metabolites in biological samples is described. The major aim of the work was to define the cause of the different recoveries reported in the literature for leukotrienes and hydroxyeicosatetraenoic acids. We used nasal lavages to carry out a comparative study of solid-phase extraction parameters of practical importance in securing good recoveries of leukotrienes and hydroxyeicosatetraenoic acids from biological samples. We evaluated the influence of the pH of the sample, the pH of the water used to wash the extraction cartridge before elution of the adsorbed analytes, the comparative behaviour of commercially available octadecyl adsorbents and the influence of the concentration-evaporation step on final recoveries. Data thus obtained show that there is no significant difference in results when the samples and the water used to wash the cartridge before analyte elution are adjusted to pH values ranging between 4.0 and 7.4. Below pH 4.0, losses may be significant. Furthermore, recoveries can be very much dependent on the type of solid-phase cartridge material and on the eluent evaporation method, especially with regard to aqueous phase removal.

Arachidonic Acid↗
PubMed1990

Cyclooxygenase products of metabolism of arachidonic acid in mouse macrophages exposed to N-phenyllinoleamide from toxic oil samples.

N-phenyllinoleamide (NPLA), one of the major extraneous constituents of Spanish toxic oil samples, appears to enhance the cyclooxygenase metabolic pathway of arachidonic acid by peritoneal mouse macrophages. Results reported herein show an increased biosynthesis of 6-oxo-PGF1 alpha and TXB2 by macrophages exposed to NPLA. However, light and electron microscopy failed to show cellular alterations in macrophages incubated with NPLA for two hours at 27 degrees C. These data suggest a possible involvement of cyclooxygenase arachidonic acid metabolism in the etiopathogenesis of the Spanish Toxic Oil Syndrome.

6-Ketoprostaglandin F1 alpha↗
PubMed1990

Recovery of nasal prostaglandin production after inhibition by aspirin.

We have investigated the duration of the inhibitory effects of aspirin in eight healthy volunteers after oral administration of a single 500 mg dose. Prostaglandin E2, D2 and leukotriene C4 levels in nasal lavage fluid were measured by radioimmunoassay without purification by high performance liquid chromatography. The inhibitory effects of aspirin on eicosanoid synthesis were maximum between 1 h to 24 h, showing total recovery within 3-5 days. LTC4 synthesis was not modified by aspirin.

Adult↗
PubMed1989

Modern high-performance liquid chromatographic-radioimmunoassay strategies for the study of eicosanoids in biological samples.

An evaluation of the most recent literature on the determination of eicosanoids by immunoassay methods confirms that owing to the inherent lack of specificity of many of the antibodies used for this purpose, immunological assays (radioimmunoassay or enzyme immunoassay) are often preceded by solid-phase extraction followed by further purification of the antigens of interest by routine reversed-phase high-performance liquid chromatographic methods. In this way the analytical potential of radioimmunoassay is remarkably enhanced and accuracy and precision of the assay are ensured.

Animals↗
PubMed1989

Increased synthesis and production of prostaglandin E2 by monocytes from drug addicts with AIDS.

We analysed the production of prostaglandin E2 (PGE2) by monocytes in 11 drug addicts with AIDS and opportunistic infections and in 13 controls. In three patients and six controls we isolated the PGE2 fraction from culture supernatants of purified monocytes (greater than 95%) incubated in medium containing (3H) arachidonic acid, using silicic acid columns. In two of three patients PGE2-fraction values (21.9 and 21.6 pmol/g protein) were significantly higher than controls (10 +/- 4). In eight AIDS patients and seven controls, PGE2 levels were determined by high-performance liquid chromatography and radioimmunoassay (HPLC and RIA). In three out of eight patients PGE2 levels were markedly higher (736, 419 and 208 pg/ml) than the mean + 2 s.d. values from controls (73 +/- 51). We tested the effect of PGE2 on the production of interleukin-2 by normal phytohemagglutinin-stimulated peripheral blood lymphocytes (PBL). There was a significant suppression of interleukin-2 production by PGE2 released from AIDS monocytes. PGE2 may be one of the factors involved in the severe immune dysfunction associated with AIDS.

Acquired Immunodeficiency Syndrome↗