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Biomedical subjects

O Bulbena

Publications and source records attributed to O Bulbena.

At least 73 records · Page 4Linked to original sources
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↗
PubMed1990

Zinc acexamate inhibits gastric acid and pepsinogen secretion in the rat.

Pretreatment with zinc acexamate (25-100 mg kg-1 i.p.) inhibited acid and pepsinogen secretion in the pylorus-ligated rat. Zinc acexamate (5-50 mg kg-1 p.o.) also inhibited the increases in acid secretion induced by carbachol (10 micrograms kg-1) and 2-deoxy-D-glucose (200 mg kg-1) in the perfused stomach of the anaesthetized rat. A delayed antisecretory effect was observed with this drug on histamine induced responses. High concentrations of zinc acexamate (10(-5) - 10(-2) M) did not modify the in-vitro activity of pepsin. Administration of zinc acexamate resulted in an increase in the presence of pepsinogen at the mucosal level. A morphological examination of the gastric mucosa confirmed an accumulation of zymogen-containing granules in the gastric chief cells of zinc acexamate-treated rats (50 mg kg-1 p.o.). These results indicate that zinc acexamate decreases acid and pepsinogen secretion in-vivo, and this may explain its antiulcer activity.

Aminocaproates↗
PubMed1990

Effect of zinc acexamate and ranitidine on chronic gastric lesions in the rat.

Using the rat as an experimental model we have studied the healing of chronic gastric lesions and the modifications of these lesions by antiulcer agents. Gastric injuries were induced by submucosal injection of 0.05 ml of 5% acetic acid. Placebo, ranitidine (RNT) or zinc acexamate (ZAC) were administered orally. The evolution of gastric injuries was macro- and microscopically evaluated at 6, 12 and 21 days after acetic acid injection. The administration of either RNT (30 mg/kg) or ZAC (200 mg/kg) was followed by a marked improvement of the healing process with respect to control groups. The size of experimental ulcers at 21 days was 3.1 +/- 0.8 mm2 for the control group, 1.8 +/- 1.1 mm2 for RNT-treated animals and 0.3 +/- 0.6 mm2 for ZAC-treated rats (p less than 0.05, vs. control). A similar tendency was observed when lesions were microscopically analyzed. Indices of microscopical lesions (0-6) at 21 days were 3.8 +/- 0.8 for the control group, 3.0 +/- 0.8 for rats receiving RNT and 2.3 +/- 0.4 for rats receiving ZAC (p less than 0.05, vs. control). The statistical analysis of the distribution of microscopical indices of lesions showed significant differences in favour of ZAC at days 6 (p less than 0.01) and 21 (p less than 0.05). Our study indicates that the evolution of gastric damage induced by acid acetic injection was consistently better in rats treated with ZAC than in those receiving RNT. Data obtained in our experiments suggest that the blockade of H2 receptors does not guarantee the optimal healing of chronic gastric lesions induced in rats.

Acetates↗
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

Effects of zinc acexamate on blood flow and prostanoid levels in the gastric mucosa of the rat.

The effects of the new antiulcer compound zinc acexamate on blood flow and prostanoid levels in the gastric mucosa have been studied. Zinc acexamate (30 and 300 mg/kg) dose-dependently prevents the reduction induced by the perfusion of noradrenaline (3.5 micrograms/kg.min, 30 min) in gastric mucosal blood flow, as measured by 3H-aniline clearance. Zinc acexamate pretreatment also increases the levels of prostaglandin E2 in the gastric mucosa of the rat, both under control conditions and after infusion with noradrenaline. The levels of thromboxane A2 and prostacyclin were not modified by zinc acexamate. These results confirm the importance of microcirculation in pathogenesis and the idea that the antiulcer activity of zinc acexamate is due in part to its action in increasing the mechanism which defend the gastric mucosa against aggression.

Aminocaproates↗
PubMed1989

Zinc acexamate reduces gastric damage induced by platelet-activating factor.

We have tested the ability of zinc acexamate (ZAC) to prevent platelet-activating-factor (Paf) induced gastric damage in rats. Lesions were characterized by a vascular congestion affecting the entire mucosa, oedema, haemorrhage and frequent necrosis of the more superficial areas. The gastric damage appearing after Paf was accompanied by degranulation of gastric mast cells. Leukocytes were often seen at the submucosal level. Oral pretreatment with ZAC reduced in a dose-dependent manner both gastric damage and mast cell degranulation observed after Paf. ZAC administered orally at a dose of 100 mg kg-1 statistically inhibited (p less than 0.01) gastric damage and mast cell degranulation. ZAC did not affect the hypotension induced by Paf confirming that gastric damage and hypotension appearing in rats after Paf administration are two independent phenomena. The present findings indicate that the inhibitory effect of ZAC upon gastric lesions induced by Paf may be related to the different protective actions exhibited by this zinc compound in a wide variety of experimental models of gastric ulcer.

Aminocaproates↗
PubMed1989

Zinc compounds as therapeutic agents in peptic ulcer.

Zinc acexamate (ZAC) is the first zinc compound developed and marketed for use in the therapy of peptic ulcer. ZAC is active in several ulcer experimental models. This action is secondary to an effect on both aggressive and defensive mucosal factors. ZAC reduces acid and peptic secretion, increases mucus secretion, protects mucosa from disruption by aspirin and reverses the reduction of blood flow caused by noradrenaline. Clinically, ZAC has proven to be a useful drug in the healing of peptic ulcer. Reduction of inflammatory associated processes of peptic ulcer, which has not been seen with H2-blockers, suggests that ZAC may be highly effective in preventing ulcer relapse. These properties, together with its good safety profile, indicate that ZAC would be an interesting option in the treatment of peptic ulcer.

Humans↗
PubMed1989

Zinc compounds, a new treatment in peptic ulcer.

Effects of zinc in gastric ulcer have been reviewed through investigations carried out on zinc acexamate (ZAC). ZAC is an organic compound that has been shown to possess an experimental antiulcer effect and a wide therapeutic index, making it a useful drug in the treatment of peptic ulcer disease. ZAC protects from ulceration in several experimental models such as pylorus occlusion, reserpine-induced ulcer, necrotizing agents, PAF-induced ulcer and cold-restraint stress. ZAC first reduces the gastric acid output by inhibiting the mast cell degranulation, an action likely to be mediated through a membrane stabilizing action. Secondly, it enhances the mucosal protection factors by increasing mucus secretion, inhibiting the H+ retrodiffusion and improving microcirculation. ZAC is also effective in acetic acid-induced chronic ulcer, restoring the continuity of the damaged mucosa. Several clinical trials have shown the usefulness of ZAC in acute and maintenance treatment of both gastric and duodenal ulcers. Endoscopic studies showed that ZAC reduced the inflammatory processes (gastritis and duodenitis) associated with ulcer healing. This reduction was statistically significant and not observed with other comparative treatments (H2-antagonists). The observed side-effects were minimal and affected less than 2% of treated patients. The pharmacological profile, clinical effectiveness and good tolerance of ZAC suggest this compound as an interesting option in the treatment of peptic disease.

Aminocaproates↗
PubMed1989

Gastrointestinal surface changes: interpretation problems and indexing possibilities (a review).

The purpose of this review on state-of-the-art and new perspectives on the use of scanning electron microscopy (SEM) in gastrointestinal pathology is to discuss the possibility of developing an index for quantitatively grading mucosal epithelial injury. This topic is reviewed within the framework of ulcer indices previously developed for gross lesions, where analogous problems exist, and in relation to the transmission electron microscope staging of epithelial cell pathology. If such an index could be developed it would increase objectivity and standardization of data analysis from laboratory to laboratory, and would allow for quantitative and statistical analysis of morphometric data. It is concluded that an index is possible based upon fields of injured cells rather than upon the grading of individual cell injury progression. An example of a useful SEM lesion index is presented. There are definite limitations to development of such an index, and guidelines are provided to help minimize some of the numerous complicating factors. These guidelines include comments on magnification, tissue contour, cell versus tissue analysis, morphometric considerations, sources of error, and other factors.

Animals↗
PubMed1988

Determination of oxidation products of N-phenyllinoleamide: Spanish toxic oil syndrome studies.

The early identification of fatty acid anilides in suspect oils directed attention to their possible role in the Spanish toxic oil syndrome. These anilides or their oxidized derivatives could have been spontaneously formed during the handling and/or storage of the oil. The exact cause of the intoxication is still unknown but free radical and peroxidative mechanisms have been implicated in its etiology. Epoxy-hydroxylated derivatives from linoleic acid anilide were obtained using a model of accelerated oxidation. Their mass spectral patterns agree with the trimethylsilyl ethers of N-phenyl-9,10-epoxy-11-hydroxy-12-octadecenamide and N-phenyl-12,13-epoxy-11-hydroxy-9-octadecenamide, respectively. These compounds were also identified is rapeseed oil samples supplemented with N-phenyl-linoleamide and submitted to the reported accelerated oxidation method.

Anilides↗
PubMed1988

Thermospray liquid chromatography/mass spectrometry of prostaglandin methyl ester derivatives: application to the determination of prostaglandins E2 and D2 in rat gastric mucosa.

Methyl ester derivatives of 6-keto prostaglandin (PG) F1 alpha, PGF 2 alpha, PGE2 and PGD2 as well as methyl oximes of 6-keto PGF1 alpha, PGE2 and PGD2 have been analysed by thermospray high-performance liquid chromatography mass spectrometry. These compounds are eluted in a gradient of ammonium acetate buffer-acetonitrile at pH 3.4 using a 5 micron ODS-2 reversed-phase column. The mass spectral patterns of the PG derivatives are discussed relative to those of non-derivatized PGs. In general, the methyl ester derivatives show better characteristics than the non-derivatized PGs for the analysis of these compounds in a biological matrix, both from a chromatographic as well as from a mass spectrometric standpoint. Detection limits between 100 and 600 pg on-column can be achieved. Response curves in the selected ion monitoring mode for PGF2 alpha, PGE2 and PGD2 are linear in the range from 100 pg to 10 ng. The technique has been applied to the analysis of PGE2 and PGD2 in rat gastric mucosa.

Animals↗
PubMed1988

Effects of zinc acexamate on gastric mucosal production of prostaglandin E2 in normal and stressed rats.

Changes in PGE2 levels induced by zinc acexamate (ZAC) at gastricmucosal level were assessed in a rat model. Experiments were performed in normal rats and rats subjected to cold-restraint stress and in experimental conditions in which prostaglandins (PGs) synthesis was inhibited by prior administration of indomethacin. Gastric injuries after different treatments were quantified macro and microscopically. Total amount of PGE2 and mucus material recovered from gastric mucosa were increased after ZAC treatment. Indomethacin aggravated gastric damage secondary to stress and inhibited PGE2 and mucus increase appearing after ZAC treatment. These data confirm the relation between PGE2, mucus production and gastric protection. ZAC 200 mg/kg was able to reduce the gastric damage induced by stress. This decrease was also evident in the group receiving indomethacin before ZAC administration. These experiments indicate that ZAC exhibits its antiulcer action by increasing prostaglandins but other mechanisms independent of PGs synthesis are also involved.

Aminocaproates↗
PubMed1988

Prostaglandin levels in infertile patients affected by asthenozoospermia and prostatitis.

19-hydroxy-prostaglandins and prostaglandins of the E series (19-OH PGEs) were estimated in the seminal plasma of asthenozoospermic patients (n = 15) and individuals affected by prostatitis (n = 10) and compared to controls (n = 13) and secretory azoospermic patients (n = 8). All of them were free from infections (except individuals affected by prostatitis), biochemical and ultrastructural problems. The results indicate that endogenous prostaglandin levels (19-OH PGEs and PGEs) bear no correlation either to motility or absence of spermatozoa. Significant increases of PGEs were observed in patients affected with prostatitis. Surprisingly PGE levels showed no correlation with the levels of 19-OH PGEs.

Adult↗
PubMed1987

Effect of cold-restraint stress and zinc acexamate on gastric mucus production in intact glands.

Gastric mucus content was morphometrically evaluated in gastric glands of normal and cold-restraint stressed rats. Variations induced by treatment with zinc acexamate (200 mg/kg p.o.) were also investigated. Stress decreased the glycoprotein content in glands located in areas of injury. However, in intact glands from the same animals, the glycoprotein content was increased and the proportion of sulphated macromolecules greatly augmented. Zinc acexamate reduced the severity of damage in stressed rats. Although it augmented mucus content it prevented the modification in sulphated macromolecules in these rats. These findings are discussed in relation to the role of gastric mucus in preventing gastric damage.

Aminocaproates↗
PubMed1987

Anti-ulcer and membrane stabilizing actions of zinc acexamate.

The effects of zinc acexamate on stress and reserpine ulcers as well as on gastric mast cells degranulation and membrane stability were evaluated in the rat. Zinc acexamate (100 mg/kg) has demonstrated an inhibitory effect on cold-restraint stress and reserpine-induced ulcer in a dose-dependent manner. Pretreatment of rats, prior to cold restraint stress, reduced gastric mast cell degranulation. Zinc acexamate (10(-4) M) inhibits Triton X-100 release of beta-glucuronidase in isolated hepatic lysosomes. These observations suggest that ulcer protective actions of zinc acexamate may be exerted in part through enhancing gastric mucosal resistance by stabilizing biological membrane integrity.

Aminocaproates↗