PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Mefenamic Acid”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

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

At least 775 records · Page 43Linked to original sources
PubMed1994

Effects of non-steroidal anti-inflammatory drugs on polymorphonuclear leukocyte functions in vitro: focus on fenamates.

Prostanoid-independent anti-rheumatic effects of non-steroidal anti-inflammatory drugs (NSAIDs) are a matter of debate. The aim of the present study was to compare the effects of chemically different NSAIDs (diclofenac, indomethacin, ketoprofen, paracetamol, piroxicam and four fenamates: flufenamic, meclofenamic, mefenamic and tolfenamic acids) on human polymorphonuclear leukocyte (PMN) functions, i.e. calcium ionophore A23187-triggered degranulation, leukotriene B4 (LTB4) release, platelet-activating factor (PAF) production and migration towards LTB4. The four fenamates caused a dose-dependent inhibition of each of the PMN functions tested. Flufenamic, meclofenamic and tolfenamic acids were about equipotent to inhibit PMN degranulation (IC50S 21-32 microM) and LTB4 release (IC50s 21-25 microM) whereas mefenamic acid achieved similar effects at somewhat higher drug concentrations. Tolfenamic and meclofenamic acids were the most potent fenamates to inhibit PAF synthesis (IC50s 37 and 51 microM) as well as migration towards LTB4 (IC50s 61 and 92 microM). Out of the other NSAIDs, diclofenac (which is chemically related to fenamates) suppressed degranulation as well as LTB4 and PAF production. Indomethacin inhibited LTB4 and PAF synthesis whereas ketoprofen reduced degranulation. The inhibitory effects of the non-fenamate NSAIDs occurred only at drug concentrations far higher than those achieved clinically. Paracetamol and piroxicam (up to 300 microM) did not influence the PMN functions tested. We conclude that NSAIDs with a fenamate structure differ from other NSAIDs by inhibiting PMN functions induced either by receptor-mediated stimulus (LTB4) or calcium ionophore (A23187) at micromolar drug concentrations.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1975

Simple analgesics.

A number of drugs are available that act fairly specifically as "mild" analgesics, although this description by no means implies that their clinical effectiveness is limited to the relief of slight pain and trivial disability. They are effective by mouth and their action is mediated peripherally. Among the possible mechanisms of action, the inhibition of prostaglandin synthesis is currently regarded as most likely to be relevant. Some centrally acting drugs of the narcotic analgesic type, such as codeine and dextropropoxyphene are effective orally; they are usable in the same way as other mild analgesics and may be preferable for some types of pain. Many problems arise in the assessment and comparison of mild analgesics, both experimentally and clinically. Subjective assessments may be made on a pain scale by the patient himself, or by a trained observer. Individual variations are all-important, and the limitations of controlled trials need to be remembered. Alternative drugs and mixtures have little advantage over aspirin, but specific drug tolerance, in the long term, varies from patient to patient. Gastric irritation is most likely to occur with aspirin in the presence of chronic dyspepsia or acute precipitating causes such as alchoholic gastritis. Allergy also occurs in some susceptible individuals. The risk of renal damage with phenacetin is increasingly appreciated, and the possibility of hepatic damage from paracetamol is now recognised. Other side-effects and interactions are summarized in the review, and some notes are given on therapeutic and non-therapeutic use.

Acetaminophen↗
PubMed2006

Second-order calibration of excitation-emission matrix fluorescence spectra for the determination of N-phenylanthranilic acid derivatives.

A spectrofluorimetric method has been developed for the quantitative determination of mefenamic, flufenamic, and meclofenamic acids in urine samples. The method is based on second-order data multivariate calibration (unfolded partial least squares (unfolded-PLS), multi-way PLS (N-PLS), parallel factor analysis (PARAFAC), self-weighted alternating trilinear decomposition (SWATLD), and bilinear least squares (BLLS)). The analytes were extracted from the urine samples in chloroform prior to the determination. The chloroform extraction was optimized for each analyte, studying the agitation time and the extraction pH, and the optimum values were 10 minutes and pH 3.5, respectively. The concentration ranges in chloroform solution of each of the analytes, used to construct the calibration matrix, were selected in the ranges from 0.15 to 0.8 microg mL-1 for flufenamic and meclofenamic acids and from 0.25 to 3.0 microg mL-1 for mefenamic acid. The combination of chloroform extraction and second-order calibration methods, using the excitation-emission matrices (EEMs) of the three analytes as analytical signals, allowed their simultaneous determination in human urine samples, in the range of approximately 80 mg L-1 to 250 mg L-1, with satisfactory results for all the assayed methods. Improved results over unfolded-PLS and N-PLS were found with PARAFAC, SWATLD, and BLLS, methods that exploit the second-order advantage.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1975

Relationship of inhibition of prostaglandin biosynthesis by analgesics to asthma attacks in aspirin-sensitive patients.

Eleven patients with asthma and aspirin hypersensitivity have been challenged with eight non-steroidal anti-inflammatory drugs. Each drug was given by mouth in at least three different doses and the patients' symptoms and peak expiratory flow (PEF) rates were observed over a three-hour period. Indomethacin 5 mg caused bronchoconstriction in all patients. Therapeutic doses of mefenamic or flufenamic acid caused bronchoconstriction in most patients. Phenylbutazone 200-400 mg induced a moderate fall in PEF. There were no reactions to therapeutic doses of salicylamide, paracetamol, benzydamine, and chloroquine. Microsomal prostaglandin synthetase, activity was inhibited by aspirin, indomethacin, mefenamic acid, flufenamic acid, and phenylbutazone. The other four drugs had no inhibitory effect. We suggest that precipitation of attacks in asthmatic patients hypersensitive to certain anti-inflammatory drugs is related to drug's ability to inhibit prostaglandin biosynthesis.

Adult↗
PubMed1992

Intracellular Ca2+ release by flufenamic acid and other blockers of the non-selective cation channel.

We report in this paper using measurement of intracellular free Ca2+ with fura-2, that flufenamic acid and several related blockers of the 25 pS Ca(2+)-activated non-selective cation channel cause release of Ca2+ from an intracellular store other than the endoplasmic reticulum, possibly from mitochondria. A new compound, 4'-methyl-DPC, is found to be as effective in blocking non-selective cation channels as other flufenamate analogs but, like the parent compound, the non-selective cation channel blocker DPC, it does not cause release of Ca2+ from intracellular stores. DPC and 4'-methyl-DPC are thus the most suitable of the available blockers of non-selective cation channels for use in studies on the role of these channels in normal cell function.

Animals↗