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At least 919 records · Page 51Linked to original sources
PubMed1994

A device for automatic measurement of writhing and its application to the assessment of analgesic agents.

A device was developed for automatically measuring writhing in mice so as to be applied to the assessment of analgesic agents. The device was composed of a specially designed container equipped with a detector, namely, a mechanoelectro transducer for writhing. The detector was made up of units of a string, two plates, and two strain gauges. In the unit, each end of the string was connected to either of the plates to which either of the strain gauges was attached. The change in tension of the string due to writhing was converted into the mechanical strain of the plates and then the resistance change of the strain gauges. The resistance change was amplified by a Wheatstone bridge circuit that was connected to a differential amplifier, a high-pass filter, comparator(s), and a monostable multivibrator to obtain the electrical signal for writhing. Using this device, writhing was continuously measured, and evaluation of various types of analgesic agents was performed. The result suggests that this device has sufficient accuracy both for the detection of writhing and the evaluation of analgesics. It has the advantage of automatic measurement of writhing in contrast to the conventional visual observation method.

Acetates↗
PubMedDate not supplied

[The effect of non-steroid antiphlogistic drugs on the number of antibody-forming cells during the primary immune response].

In mice immunized with sheep erythrocytes introduction of acetylsalycilic acid (250 mg/kg), sodium salicylate (100 mg/kg) and mephenamic acid (100 mg/kg) exerted an inhibitory effect on the synthesis of antibody-forming cells and the titre of hemagglutinines in immunized animals. The acetylsalicylic acid and sodium salicylate are more effective on the 3--5th post-immunization day; the maximal effect of the mephenamic acid becomes apparent on the 7th day and its action is more lasting.

Animals↗
PubMedDate not supplied

[Mefenaminic acid binding by blood plasma and organ homogenates].

Concerns the spectrophotometric method for microdetermination of total and unbound mefenaminic acid in biological material. The method has been developed on the basis of stained complex formation. Mefenaminic acid binding to plasma proteins and organ homogenates has been studied in vitro and in vivo experiments and by the methods of equilibrium dialysis and fluorescence. The rate of drug binding to plasma proteins amounts to 75 +/- 5%. The highest binding capacity is shown by the plasma, liver and kidneys. In the plasma, mefenaminic acid is chiefly bound to albumin in whose molecule there have been established two monotypic sites of binding with an association constant of approximately (1.23-1.68) . 10(5) M-1. In vivo experiments show variations in the relative indices of plasma bound mefenaminic acid as dependent on the dose and route of administration. In vitro evidence correlates with the results obtained in experiments made in vivo.

Animals↗
PubMed1993

Transport, distribution space and intracellular concentration of the anti-inflammatory drug niflumic acid in the perfused rat liver.

Transport and distribution space of niflumic acid in the perfused rat liver were investigated employing the multiple-indicator dilution technique with constant infusion of the drug (step input). Niflumic acid permeated the cell membrane in both directions at very high rates and its distribution in the cellular space was flow-limited; at least at 37 degrees, the rates of influx and efflux could not be measured. Dissociation of the niflumic acid-albumin complex also occurred at very high rates. The apparent space of distribution of niflumic acid in the liver depended on the concentration of the drug and varied between 4.37 (1 mM) and 43.5 (10 microM) times the water space; even with 90% extracellular binding to albumin, the apparent space of distribution of niflumic acid was 5.1 times greater than the water space. The high apparent spaces of distribution reflected the high intracellular concentrations. The ratio of intracellular bound plus free concentration to the extracellular bound plus free concentration (Ci/Ce) varied between 6.62 (1 mM portal niflumic acid) and 71.0 (10 microM portal niflumic acid). Metabolic transformation depended on the concentration of the free form. Intracellular binding is probably the major reason for the high concentration of the drug in the hepatic tissue.

Animals↗
PubMed1999

Randomised controlled trial of educational package on management of menorrhagia in primary care: the Anglia menorrhagia education study.

OBJECTIVE: To determine whether an educational package could influence the management of menorrhagia, increase the appropriateness of choice of non-hormonal treatment, and reduce referral rates from primary to secondary care. DESIGN: Randomised controlled trial. SETTING: General practices in East Anglia. SUBJECTS: 100 practices (348 doctors) in primary care were recruited and randomised to intervention (54) and control (46). INTERVENTIONS: An educational package based on principles of "academic detailing" with independent academics was given in small practice based interactive groups with a visual presentation, a printed evidence based summary, a graphic management flow chart, and a follow up meeting at 6 months. OUTCOME MEASURES: All practices recorded consultation details, treatments offered, and outcomes for women with regular heavy menstrual loss (menorrhagia) over 1 year. RESULTS: 1001 consultation data sheets for menorrhagia were returned. There were significantly fewer referrals (20% v 29%; odds ratio 0. 64; 95% confidence interval 0.41 to 0.99) and a significantly higher use of tranexamic acid (odds ratio 2.38; 1.61 to 3.49) in the intervention group but no overall difference in norethisterone treatment compared with controls. There were more referrals when tranexamic acid was given with norethisterone than when it was given alone. Those practices reporting fewer than 10 cases showed the highest increase in prescribing of tranexamic acid. CONCLUSIONS: The educational package positively influenced referral for menorrhagia and treatment with appropriate non-hormonal drugs.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1984

Inhibition of histamine-induced protein leakage in rat skeletal muscle by blockade of prostaglandin synthesis.

The effects of two prostaglandin synthesis blockers, indomethacin and mefenemic acid, on both histamine-induced extravasation of albumin and arteriole dilation were studied using intravital fluorescent microscopy. Sprague-Dawley rats (140-180 g) were anesthetized with pentobarbital (50mg/Kg) and the cremaster muscle was positioned in a Krebs bath (pH = 7.4, PCO2 = 40 mm Hg, PO2 = 35 mm Hg, temp = 34 degrees). Fluorescein isothiocyanate-labeled albumin was injected intravascularly and the fluorescent image of the cremaster microcirculation was produced by illumination from an argon laser (488 nm). Videotape analysis of the experiments showed that increasing concentrations of histamine in the bath produced both a concentration-dependent arteriole dilation and a concentration-dependent leakage of labeled albumin into the interstitium. Adding indomethacin (10 or 100 micrograms/ml) or mefenemic acid (10 micrograms/ml) to the Krebs bath significantly diminished the protein leakage induced by histamine but did not alter the arteriole dilation. These results indicate that prostaglandins may be directly involved in the histamine-induced increase in vascular permeability to macromolecules but not in the arteriole dilation histamine produces.

Animals↗
PubMed1984

[Use of interferon inducers in treating viral diseases].

The results obtained in the experimental and clinical study of the preparations of mephenamine acid and levamisole with respect to their interferonogenic and interferon-stimulating action and their therapeutic effectiveness in influenza and virus hepatitis are presented. The study has revealed that mephenamine acid, along with its capacity for stimulating the processes of interferon formation in the body, produces a pronounced curative effect, prevents the development of postinfluenza complications much more effectively than levamisole and remantadin and accelerates the processes of reparation in virus hepatitis.

Adolescent↗
PubMed1976

[Role of bioenergetic changes in the mechanism of action of nonsteroid anti-inflammatory agents].

In experiments on rats the antiphlogistic action of sodium mephenaminate and salicylate was found to be more pronounced under conditions of ovalbumin than that of dextran inflammation. The antiphlogistic effect of sodium salicylate was greater than that of mephenaminate in ovalbumin inflammation; this correlated with a more marked drop in the content of lactic acid in the blood and with a more complete elimination of uncoupling of oxidative phosphorylation in the hepatic mitochondria than in case of mephenaminate injection. It is supposed that lowering the macroerg level by the principle of feed back action leads to intensification of phosphorylation; this provides elimination of inflammatory disturbances and can explain the antiphlogistic effect of the drugs.

Adenosine Diphosphate↗
PubMed2004

[Acute renal failure--"a well meant present from a friend"].

Acute allergic interstitial nephritis (AIN) due to non-steroidal anti-inflammatory drugs (NSAID) is a well known but rare adverse drug event. Here, we describe the case of a 70 year old woman with recurrent episodes of acute renal failure. A first episode of (AIN) occurred after the intake of mefenaminic acid tablets. A second episode of AIN occurred two years later, this time after transdermal application of diclofenac. Our case illustrates cross-reactivity between NSAIDs and shows that transdermally applied medication can cause systemic adverse events as well. Patients do not mention ointments because they often do not realize that ointments contain active substances, and physicians forget to ask.

Acute Kidney Injury↗
PubMedDate not supplied

Antiproliferative effect of nonsteroidal antiinflammatory drugs against human colon cancer cells.

Several lines of evidence suggest that nonsteroidal antiinflammatory drugs may be effective in preventing colorectal cancer. These include animal experiments, case-control studies, and clinical experience with sulindac in promoting the regression of adenomatous colon polyps in adenomatous polyposis coli. We determined the antiproliferative activity of various nonsteroidal antiinflammatory drugs, including two sulindac derivatives, against human colon cancer cells in vitro. Ht-29, SW480, and DLD-1 cells were continuously incubated with serial drug dilutions for 6 days prior to fixation. Cell number was determined using the sulforhodamine B assay, and drug concentrations which inhibited cell growth by 50% were estimated for each agent by interpolation. All drugs exhibited antiproliferative activity against Ht-29 and DLD-1 cells, and most inhibited SW480 cells. For Ht-29 cells, the 50% inhibitory concentration varied from 55 microM for diclofenac to 2100 microM for 5-aminosalicylic acid, with three drug groups of high, intermediate, and low potency evident. Inhibition of cell growth by sulindac sulfide was reversible following drug removal. Nonsteroidal antiinflammatory drugs exert an antiproliferative effect against human colon cancer cells with a wide range of potencies. A cytostatic response was demonstrated with sulindac sulfide. These data further support the potential role of these agents for chemoprevention of colorectal neoplasia.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1982

High-performance liquid chromatographic assay of indomethacin and its application in pharmacokinetics in healthy volunteers.

A new sensitive high-performance liquid chromatographic method for indomethacin from plasma on a reversed-phase column (C18) has been developed. The method involves precipitation of plasma with perchloric acid followed by diethyl ether extraction. The assay is quantitative down to 0.25 microgram ml-1 from a 200-microliters aliquot of plasma with a detection limit of 0.1 microgram ml-1 and a recovery of approximately 90%. The method was applied to single-dose studies with volunteers under various dietary restrictions. The results of these studies indicated that intrasubject variability within these regimens may be as important a factor as the intersubject variability already documented for this drug. These results have important implications in the determination of bioavailability and pharmacokinetic parameters of this drug.

Chromatography, High Pressure Liquid↗
PubMedDate not supplied

Human metabolism of tolfenamic acid. II. Structure of metabolites and C-13 NMR assignments of fenamates.

Metabolites of tolfenamic acid appearing in human urine have been isolated and their structures determined by C-13 nuclear magnetic resonance and gas chromatography-mass spectrometry. Comparative studies on tolfenamic, mefenamic, and flufenamic acids in conjunction with the metabolites have permitted complete C-13 NMR assignments for this series of compounds. Five metabolites identified included three that were monohydroxylated, one that was both methoxylated and hydroxylated, and another in which the methyl group was oxidized to a carboxyl group. The information presented on the fenamate standards and the metabolites represents an excellent basis for structural elucidation of other fenamates and their metabolites.

Biotransformation↗
PubMedDate not supplied

Anti-inflammatory agents and inducibility of hepatic drug metabolism.

Two rat liver cytosolic aldehyde dehydrogenases, ALDH1 and ALDH3c, are of particular interest because they are inducible by different classes of xenobiotics. ALDHI is mainly increased by phenobarbital-type inducers; polycyclic aromatic hydrocarbons (PAHs), such as 3- methylcholanthrene (3MC), increase ALDH3c enzyme activity in all rat species currently tested. In addition, ALDH3c has been found to reflect the subfamily CYPIA of cytochrome P-450, as well as other enzymes functionally related to the aryl hydrocarbon receptor (the "Ah-receptor enzyme battery"), which is activated by the same type of inducers. In the present study we investigated whether the induction of ALDH3c might be connected with a chemically produced aseptic inflammation of the hepatocyte. To answer this question, we examined the relationship between the induction of ALDH3c by 3MC and the arachidonic acid cascade. Different non-steroid anti-inflammatory drugs (NSAIDs) were tested in combination with 3MC and in post-treatment. The 3MC-induced ALDH3c activity was significantly diminished by the co-administered anti-inflammatory agents. Two microsomal enzyme activities (ethoxyresorufin-O-deethylase, EROD; aryl-hydrocarbon-hydroxylase, AHH) were also decreased. Similar results were obtained with NSAIDs administered to animals pre- treated with 3MC, as far as the ALDH3c activity was concerned, but not for the microsomal enzyme activity (EROD and AHH). In conclusion, the induction of ALDH3c, after PAH treatment, may be related to an aseptic inflammation of the hepatocytes. This effect is reduced by commonly used steroid and non-steroid anti- inflammatory drugs, and although the mechanism of inhibition has not yet been elucidated, it appears likely that ALDH3c and CYP1A activities are associated with the "acute phase" response.

Aldehyde Dehydrogenase↗
PubMed1995

[Segmental small intestine lesions after taking non-steroidal antirheumatic drugs].

Over a period of 7 months a 51-year-old diabetic took mefenamine acid (up to 500mg 20 times daily), diclofenac and, more rarely, paracetamol for lumbosacral pain. In addition, dexamethasone (4 mg three times daily) was prescribed later. For 4 weeks he had colicky abdominal pain which then started acutely to radiate into the flanks. Pressure and rebound pain in the left epi- and mesogastrium, as well as the results of biochemical tests, suggested an acute abdomen. Abdominal X-rays, selective contrast examination of the small intestine and computed tomography demonstrated changes within some segments of the jejunum (thickened wall, irregular wall surface). Laparoscopy showed brown discoloration of the loops of the small intestine. In consequence of these findings a 10 cm long segment of the jejunum was resected. Histological examination showed extensive ulcers at the tip of the rugae with granulating inflammation and bifringent foreign bodies with giant-cells. The villi were extensively atrophied, the blood vessel were congested and the submucosa fibrosed. The patient was discharged after 9 days and, no longer taking NSAIDs, has been free of abdominal symptoms.

Abdominal Pain↗
PubMed1992

Therapy of symptomatic patent ductus arteriosus in preterms using mefenemic acid and indomethacin.

Mefenemic acid (MA) was given in three doses of 2 mg/kg/dose at 12 hourly intervals in 16 cases clinically suspected of having symptomatic patent ductus arteriosus (PDA). All babies were 35 weeks gestation (mean 30.1 weeks) and weighed less than or equal to 1700 g at birth (mean 1320 g), the mean age of administration of MA being 16 days. Of the 16 cases, two did not respond to therapy. One non-responder was subsequently shown to have an endocardial cushion defect without PDA on 2-D Echo and Doppler study. The other was 29 days old at the initiation of therapy. In once case, the ductus reopened after an initial closure, however, it closed on repeating a second course of the drug. Thirty preterms (less than or equal to 34 weeks) who were earlier treated with three doses of indomethacin (0.25 mg/kg/dose) formed the comparative study group. The closure rate of PDA on treatment with indomethacin was 70% and that with MA was 93.3% (p greater than 0.05). Two neonates treated with MA and two treated with indomethacin had feeding intolerance and vomiting, perhaps attributable to the drug therapy. We recommend the use of MA for closure of symptomatic PDA in preterms, especially in those cases where indomethacin is not tolerated or when minute titration of its dosage is impracticable.

Ductus Arteriosus, Patent↗
PubMed1985

Stress by restraining potentiates morphine catalepsy in rats.

Restraint-induced stress potentiated morphine catalepsy in rats. This potentiation was partially antagonized by pharmacologic treatments decreasing central serotonin, acetylcholine, prostaglandins and by naloxone. Selective increase in central dopamine also inhibited the potentiation.

5,6-Dihydroxytryptamine↗