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PubMed1981

Effect of nonsteroidal anti-inflammatory drugs on the hypoxic rat heart.

The influence of the nonsteroidal anti-inflammatory drugs indomethacin (10 microgram/ml), mefenamic acid (10 ng/ml) and acetylsalicylic acid (50 microgram/ml) were investigated for their effects on hypoxically perfused rat hearts. Hypoxia-induced mechanical cardiodepression was attenuated to varying degrees by most drugs, although only mefenamic acid reduced the degree of bradycardia. All the agents reduced in some measure the rise in resting tension produced by hypoxic perfusion and enhanced the functional activity of the myocardium upon reoxygenation of hearts made hypoxic for 10 min only. The degree of contracture after reoxygenation was substantially attenuated by all three drugs. Although coronary flow decreased dramatically during prolonged hypoxia, this phenomenon was significantly prevented by the nonsteroidal anti-inflammatory drugs. Cellular Na content of hypoxic hearts treated with mefenamic acid was elevated, whereas no other significant electrolyte changes were observed. The presence of mefenamic acid results in a reduced extracellular space size, whereas cellular water content was increased by both mefenamic acid and acetylsalicylic acid. Calcium transport of isolated mitochondria from hypoxically or normoxically perfused hearts was not modified by any treatment. Indomethacin, acetylsalicylic acid and mefenamic acid all significantly inhibited prostaglandin release from the heart. These results suggest that various nonsteroidal anti-inflammatory drugs may offer some protective influence on hypoxic rat hearts particularly with respect to coronary artery patency during hypoxic perfusion.

Animals↗

PubMed1980

Control of pain resulting from endodontic therapy: a double-blind, placebo-controlled study.

The efficacy of mefenamic acid, aspirin, and a placebo for control of postendodontic pain was compared in a double-blind, randomized study of 150 patients. Medication was begun immediately prior to the endodontic therapy and continued for a total of eight doses. The results were analyzed in terms of the patients' assessments of postendodontic pain, the need for additional analgesic medication, and the patients' and investigator's evaluations of drug efficacy. The results indicate that mefenamic acid was well tolerated. Mefenamic acid was equal to, or exceeded, aspirin in ability to control postendodontic pain in every comparison made. The converse was never true. Mefenamic acid was statistically superior to placebo in every comparison made. Aspirin was not consistently superior to the placebo. Under the conditions of this trial, it can be stated that, for control of pain following simple endodontic therapy, mefenamic acid rather than aspirin is the drug of choice.

Adolescent↗

PubMed1995

Choice of antipyretic in children.

The objective of this study was to evaluate the relative efficacy of 3 commonly used antipyretics viz. mefenamic acid, ibuprofen and paracetamol. The subjects were randomized to 3 groups to receive either paracetamol 10 mg/kg or ibuprofen 7 mg/kg or mefenamic acid 6.5 mg/kg. Axilla temperature was recorded just prior to drug administration and at hourly intervals for 4 hrs. The mefenamic acid group (n = 29) showed a drop of 3.5 degrees F at the end of 4 hours as compared to the paracetamol group (n = 29) (drop 2.44 degrees F) and ibuprofen group (n = 20) (drop 2.79 degrees F). Analysis of the area under the mean temperature vs. time curve showed that mefenamic acid demonstrated significantly better antipyretic activity compared to paracetamol (P < 0.05) over the entire period of observation and ibuprofen (P < 0.05) in the 2 to 4 hour range. Mefenamic acid continued to show antipyretic activity at the end of 4 hours in contrast to ibuprofen and paracetamol. Since the period of observation was restricted to 4 hours, we were unable to quantify the precise duration of its extended antipyretic efficacy.

Acetaminophen↗

PubMed2004

Inhibition of human liver and duodenum sulfotransferases by drugs and dietary chemicals: a review of the literature.

Sulfotransferase catalyzes the transfer of sulfate, donated by 3'-phosphoadenosine-5'-phosphosulfate, to an acceptor substrate that may be a hydroxy group or an amine group. Man is exposed daily to drugs and dietary chemicals that can inhibit sulfotransferase activity. The aim of this study was to review the literature concerning the inhibition of sulfotransferases by drugs and dietary chemicals in the human liver and duodenum. The IC50 value of mefenamic acid for human liver phenol sulfotransferase (SULT 1A1) was 0.02 microM and for human liver catechol sulfotransferase (SULT1A3) 76 microM with a SULT 1A3/SULT1A1 ratio for the IC50 of 3,800. Mefenamic acid is therefore a potent and selective inhibitor of human liver SULT1A1. The IC50 values of mefenamic acid for the sulfation rates of (-)-salbutamol and (-)-apomorphine were 4 orders of magnitude greater in the human duodenum than in the liver. Salicylic acid inhibited the sulfation of (-)-apomorphine in human liver with an IC50 of 54 gM but did not inhibit the sulfation of (-)-apomorphine in human duodenum. Quercetin, a flavonoid present in edible fruit, vegetable and wine, was a potent inhibitor of human liver SULT1A1 and estrogen sulfotransferase (EST) activities and the sulfation of resveratrol. Quercetin inhibited the sulfation of dopamine, (-)-salbutamol, minoxidil and paracetamol and the IC50 values were 1 - 2 orders of magnitude greater in human duodenum than in the liver. In conclusion, mefenamic acid, salicylic acid and quercetin inhibit SULT1A1 whereas SULT1A3 is relatively resistant to the inhibition by these compounds. Under particular circumstances, human duodenum sulfotransferase is more resistant than liver sulfotransferase to the inhibition by mefenamic acid, salicylic acid and quercetin.

Anti-Inflammatory Agents, Non-Steroidal↗

PubMed1990

Management of cyclical menorrhagia with prostaglandin synthetase inhibitor.

A well controlled double blind prospective trial was undertaken to determine the efficacy of mefenamic acid in the treatment of menorrhagia. Eighty patients who had unexplained cyclical menorrhagia with secretory endometrium received mefenamic acid orally in a dose of 500 mg 8 hourly or a placebo tablet thrice daily starting from day-one of the cycle for 5 days or till cessation of menses. Mefenamic acid administration caused a statistically significant reduction in the number of days of bleeding from 9.7 +/- 3.1 days before treatment to 4.1 +/- 0.6 days after treatment. It also brought about significant reduction in the amount of bleeding in terms of number of pads used per day, that is from 15.2 +/- 3.1 before treatment to 6.5 +/- 0.02 after treatment. Eighty-six percent patients in the treatment group had control of menorrhagia with the drug compared to 20% in the control group without drugs and this difference was statistically significant. Mefenamic acid proved to be a potent and efficacious agent in the control of unexplained menorrhagia.

Adult↗

PubMed1998

Ca2+ resting current and Ca2+-induced Ca2+ release in insect neurosecretory neurons.

The effect of a Ca2+ resting current on spiking and intracellular Ca2+ concentration [Ca2+]i of isolated cockroach dorsal unpaired median neurons was investigated by combining microfluometry (Fura2) with patchclamping. The resting current was reduced by 10 microM 5-nitro-2-(3-phenylpropylamino)benzoic acid (NPPB) and 10 microM mefenamic acid, which caused slower spiking of cells. Up-modulation of the resting current by neurohormone D (NHD, 100 fM to 10 pM) transiently increased [Ca2+]i. This Ca2+ transient was largely reduced by the ryanodine receptor antagonist dantrolene (10 microM) but it was not reduced by the IP3-receptor antagonist heparin which indicates Ca2+-induced Ca2+ release. The NHD-effect on [Ca2+]i was strongly attenuated by NPPB and mefenamic acid. Thus, NHD caused Ca2+-induced Ca2+ release by enhancing the Ca2+ resting current.

Action Potentials↗

PubMed1991

Interactions between oleic acid and drug competitors influence specific binding of thyroxine in serum.

Long chain nonesterified fatty acids and various drugs may share albumin-binding sites in common. We questioned whether serum binding of T4 could be indirectly influenced by displacement of drug competitors from these sites by nonesterified fatty acids. The influence of oleic acid on drug-induced inhibition of [125I]T4 binding was measured by equilibrium dialysis, using undiluted serum in order to avoid dilution-related artefacts. Oleic acid (1 mmol/L) alone did not inhibit serum protein binding of T4, but this concentration augmented the inhibitory effects on T4 binding of diflunisal, mefenamic acid, meclofenamic acid, and aspirin. This effect increased with increasing concentrations of mefenamic acid, meclofenamic acid, and furosemide. The T4-displacing effect of fenclofenac was not augmented by oleic acid. The mechanism of these interactions was studied by examining 1) oleic acid effects on drug binding, and 2) drug effects on oleic acid binding in undiluted serum. Increments in added oleic acid (0.5-2.0 mmol/L) progressively increased the mean unbound fractions of [14C]aspirin, [14C] diflunisal, and [14C]furosemide, but did not displace [14C]fenclofenac. At the relevant total and free drug concentrations, the inhibitory effect of oleic acid on drug binding and its influence on drug-induced displacement of T4 were concordant in the order: meclofenamic acid greater than aspirin greater than mefenamic acid greater than diflunisal greater than furosemide greater than fenclofenac. In contrast, drug-induced increases in the unbound fraction of [14C]oleic acid did not correlate with augmentation of T4 displacement. We conclude that synergistic effects of oleic acid and drugs on T4 binding result from drug displacement by oleic acid, rather than the reverse effect. Hence, substances that increase the unbound concentration of a competitor by displacing it from albumin can increase its T4-displacing potency. Interactions between various ligands may exert a greater hormone-displacing effect than the sum of each alone.

Anti-Inflammatory Agents, Non-Steroidal↗

PubMed1987

The effect of diphenylamine derivatives on arachidonic acid metabolism in rat peritoneal macrophages.

The effect of diphenylamine derivatives such as diclofenac sodium, mefenamic acid and lobenzarit disodium on arachidonic acid metabolism in rat peritoneal macrophages was examined. Lobenzarit disodium has no effect on prostaglandin E2 production as measured by radioimmunoassay although two other diphenylamine derivatives have a potent inhibitory activity. Three diphenylamine derivatives have no effect on Ca2+ ionophore-stimulated release of radioactivity from (3H)arachidonic acid-labeled macrophages. HPLC analysis revealed that lobenzarit disodium had no effect on the synthesis of lipoxygenase products as observed in diclofenac sodium and mefenamic acid. It is concluded that lobenzarit disodium, although its fundamental chemical structure resembles diclofenac sodium and mefenamic acid, has no inhibitory activity on arachidonic acid metabolism, suggesting that immunomodulatory activities of lobenzarit disodium are manifested without interfering with arachidonic acid metabolism.

Aniline Compounds↗

PubMed2006

L-364,373 fails to activate the slow delayed rectifier K+ current in canine ventricular cardiomyocytes.

Activators of the slow delayed rectifier K+ current (I(Ks)) are promising tools to suppress ventricular arrhythmias originating from prolongation of action potentials. A recently synthesized compound, L-364,373, was shown to activate I(Ks) in ventricular cells isolated from guinea pigs and rabbits. Due to the interspecies differences known to exist in the properties of the delayed rectifier K+ currents, the effect of L-364,373 on I(Ks) was studied and compared with that of another I(Ks) activator mefenamic acid in canine ventricular myocytes. Mefenamic acid (100 microM) significantly increased the amplitude of the fully activated I(Ks) current, as well as the I(Ks) current tails, by shifting the voltage dependence of its activation towards negative voltages and increased the time constant for deactivation. In contrast, L-364,373, up to concentrations of 3 microM, failed to augment I(Ks) at any membrane potential studied, but slightly increased the time constant of deactivation. It is concluded that human studies are required to evaluate the therapeutically beneficial effects of I(Ks) activators. Rodent cardiac tissues are not suitable for this purpose.

Animals↗

PubMed1998

Contribution of cAMP to the inhibitory effect of non-steroidal anti-inflammatory drugs in rat uterine smooth muscle.

1. The effect of the non-steroidal anti-inflammatory drugs naproxen, mefenamic acid, phenylbutazone, piroxicam and tolmetin on the vanadate (0.3 mM)-induced tonic contraction, as well as the modifications of these effects by the G-protein inhibitor pertussis toxin, and the inhibitors of protein kinase A, Rp-cAMPS (Rp-Adenosine 3',5'-cyclic monophosphothioate triethylamine salt) and protein kinase C, H-7 [1(5-isoquinolynilsulfonyl)-2-methyl-piperazine], have been assayed to study the possible nature of intracellular mediators contributing to the inhibitory effects of NSAIDs in rat uterine smooth muscle incubated in medium lacking calcium plus EDTA. The effect of phorbol 12,13-dibutyrate on vanadate contraction and its modification with H-7 has also been examined. 2. Naproxen (6-600 microM), mefenamic acid (6-300 microM), phenylbutazone (6-300 microM), piroxicam (6-600 microM) and tolmetin (6-600 microM) produced concentration-dependent relaxation of vanadate-induced tonic contraction. The potency order, in accordance with their respective IC50 values was: phenylbutazone > or = mefenamic acid > or = naproxen > tolmetin > or = piroxicam. 3. The relaxant effects of naproxen, phenylbutazone, piroxicam and tolmetin were significantly antagonized with pertussis toxin (50 ng ml-1), Rp-cAMPS (100 microM) and H-7 (1 microM). However, the effect of mefenamic acid was unmodified by the three drugs. This suggests that the effect of mefenamic acid and other NSAIDs occur by different mechanisms. 4. Phorbol 12,13-dibutyrate relaxed the vanadate contraction but the maximal relaxation achieved (54.8 +/- 8.3%, n = 4) was lower than those induced with the NSAIDs. On the other hand, H-7 (1 microM) did not modify the relaxant effect of phorbol 12,13-dibutyrate. This suggests that H-7 behaves as a PKA, but not a PKC inhibitor, under the present experimental conditions. 5. The relaxation by naproxen, phenylbutazone, piroxicam and tolmetin is presumably produced by increasing cAMP because the effects of these are antagonized with Rp-cAMPS and H-7, and by pertussis-toxin-sensitive mechanisms.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗

PubMed1983

The mechanism of inhibition of mitochondrial oxidative phosphorylation by the nonsteroidal anti-inflammatory agent diflunisal.

The anti-inflammatory agent diflunisal was found to induce a progressive loss of respiratory control in tightly coupled rat liver mitochondria, starting at low concentrations (3.3 microM). This loss of control was accompanied by a stimulation of state 4 respiration in the presence of either succinate or glutamate plus malate as the respiratory substrate. The inhibition of state 3 respiration by oligomycin was released by diflunisal. Mitochondrial ATP hydrolysis was stimulated by diflunisal over the same concentration range that affected state 4 respiration: the stimulation was inhibited by oligomycin. It was concluded that diflunisal was acting as an uncoupler of mitochondrial oxidative phosphorylation. An identical action was found in mitochondria isolated from the livers of mice, rabbits and guinea-pigs. Potencies similar to diflunisal were found with flufenamic acid and mefenamic acid, but other anti-inflammatory agents were either less potent or inactive.

Adenosine Triphosphatases↗

PubMed1986

Converting enzyme activity in sow oviducts at different stages of the sex cycle. Influence of inhibitors of prostaglandin synthesis and its possible role in the inotropic effects of bradykinin.

The existence of angiotensin I converting enzyme (CE) activity in isolated sow Fallopian tubes and the "in vitro" influences of exogenous bradykinin (BK) on the spontaneous motility of sow oviducts, were explored. Independently of the stage of the sex cycle, the ampullary region of sow Fallopian tubes presented a higher basal CE activity than the isthmic one. On the other hand a greater CE activity was found in the isthmus at estrus and metestrus than at proestrus. Acetylsalicylic acid and mefenamic acid, two inhibitors of prostaglandin synthesis, reduced the CE activity only in ampullary segments obtained at metestrus. BK (0.06 microgram.ml-1) stimulates the spontaneous contractions of isthmic and ampullary tubal segments, triggering tonic responses. The positive inotropism had a longer duration in the isthmus than in the ampulla; presented at estrus a higher magnitude than at proestrus and was enhanced by captopril (50 microgram.ml-1). The data suggest that the low CE activity found in the isthmic tubal region could be subserving the positive inotropic action of BK in the isthmus, long lasting in comparison to that evoked in the ampulla. Moreover, at metestrus some tissue eicosanoid might be modulating the CE activity of ampullary tubal segments. Alternatively the foregoing results could be explained assuming the presence of a carboxy-peptidase different than CE in one region of the oviducts and not in the other, i.e., either one with different sensitivity towards sex hormones and prostaglandin synthesis blockers.

Animals↗

PubMed1992

Blockers of platelet-derived growth factor-activated nonselective cation channel inhibit cell proliferation.

In serum-deprived G(o)-arrested cells, the addition of serum or growth factors initiates a cascade of events that culminates in DNA synthesis and mitosis. Recently, we showed that in mouse L-M(TK-) fibroblasts a 28-pS nonselective cation channel (NS channel) becomes quiescent at G(o) arrest and rapidly active within seconds of platelet-derived growth factor (PDGF) or serum addition, placing this response very early in the postreceptor signaling cascade. However, lack of specific channel blockers hindered determination of whether channel activation was necessary for mitogenesis. Derivatives of N-phenylanthranilic acid (DCA) have been reported to block a pancreatic nonselective channel. Therefore, using single-channel analysis, we examined the effect of these agents on the L-M(TK-) NS channel. Flufenamic acid and mefenamic acid rapidly produced reversible channel block with an inhibitory constant (Ki) approximately 10 microM. Furthermore, the component of the macroscopic K+ efflux shown to be mediated by the NS channel was blocked with a similar Ki value. DCA effects on cell proliferation were tested by measuring cloning efficiency and growth rate. Both were inhibited over the range of concentration that affected channel activity, and a 50% inhibitory dose of 50-100 microM was determined. This observation further substantiates the hypothesis that NS channel activation forms a necessary component in the transduction of the mitogenic signal from the PDGF receptor.

Animals↗

PubMed1977

[Studies of sulfhemoglobin formation by various drugs (3) (author's transl)].

Sulfhemoglobin (SHb) and methemoglobin (MHb) formations by various compounds were examined by single and three consecutive intraperitoneal administrations to mice. With a single administration, methemoglobinemia was induced by diphenylamine (DPA), 1-naphthylamine (NA), phenylnaphthylamine (PNA), N-(1-naphthyl) anthranilic acid (N1) and N-(1'-naphthyl)-2-aminophenylacetic acid (IG240), and was not observed with phenylanthranilic acid (PAA), N-benzoyl-N'-phenyl-2, 6-diaminobenzoic acid (BPAA), flufenamic acid (FA), mefenamic acid (MFA), N-(2-6-dichlorophenyl) anthranilic acid (CPAA), N-(2', 6'-dichlorophenyl)-2-aminophenylacetic acid (CPPA), nine derivatives of N1 and two derivatives of IG240. On the other hand, sulfhemoglobinemia, with a single administration, was found to be induced by NA. Furthermore, with three consecutive administrations, such was induced by DPA, PAA, BPAA and FA even though SHb was not demonstrated with a single administration, and was not observed with MF, CPAA, CPPA and various derivatives of N1 and IG240.

1-Naphthylamine↗

PubMed2004

Benefits and risks of pharmacological agents used for the treatment of menorrhagia.

Menorrhagia affects the lives of many women. The assessment of menstrual flow is highly subjective and gauging the severity of the condition by objective assessment of menstrual blood loss is impractical. In treating menorrhagia, the primary aim should be to improve quality of life. Women are willing to undergo quite invasive treatment in order to achieve this. Drug therapy is the initial treatment of choice and the only option for those who wish to preserve their reproductive function. Despite the availability of a number of drugs, there is a general lack of an evidence-based approach, marked variation in practice and continuing uncertainty regarding the most appropriate therapy. Adverse effects and problems with compliance also undermine the success of medical treatment. This article reviews the available literature to compare the efficacy and tolerability of different medical treatments for menorrhagia. Tranexamic acid and mefenamic acid are among the most effective first-line drugs used to treat menorrhagia. Despite being used extensively in the past, oral luteal phase norethisterone is probably one of the least effective agents. Women requiring contraception have a choice of the combined oral contraceptive pill, levonorgestrel-releasing intrauterine system (LNG-IUS) or long-acting progestogens. Danazol, gestrinone and gonadotropin-releasing hormone analogues are all effective in terms of reducing menstrual blood loss but adverse effects and costs limit their long-term use. They have a role as second-line drugs for a short period of time in women awaiting surgery. While current evidence suggests that the LNG-IUS is an effective treatment, further evaluation, including long-term follow up, is awaited. Meanwhile, the quest continues for the ideal form of medical treatment for menorrhagia--one that is effective, affordable and acceptable.

Anti-Inflammatory Agents, Non-Steroidal↗

PubMedDate not supplied

Study of an anaphylactoid reaction to acetaminophen.

Generalized itching, urticaria and anaphylactic shock developed in a 9-year-old girl on two separate occasions after she ingested acetaminophen. She was admitted to our hospital for observation during oral challenge. Total eosinophil counts, total serum IgE, IgA, IgG, IgM, C3, and C4, specific IgE antibodies to six common allergens, and skin prick tests to purified acetaminophen and acetylsalicylic acid (aspirin) were unremarkable. No reaction occurred on open challenge with acetylsalicylic acid and mefenamic acid. However, urticaria and itching sensation occurred 45 min after ingesting 50 mg of purified acetaminophen. Dizziness, shivering, tachycardia and fainting also developed later. These symptoms resolved after treatment with a diphenhydramine injection and intravenous infusion of normal saline. There was a marked increase in the blood histamine level after challenge. In vitro histamine release before oral challenge was also abnormally as high as 50%. In summary, she had an immediate allergic reaction to acetaminophen but was tolerant to acetylsalicylic acid.

Acetaminophen↗

PubMed1976

Effect of some antirheumatics on connective tissue components.

The effects of a number of classical and modern antirheumatics on the biosynthesis of glycosaminoglycans and collagen were studied comparatively. The experimental results indicate that the antirheumatics deeply affect the metabolism of the main components of connective tissue. With regard to the methods used for testing, it may be stated that phenylbutazone, flufenamic acid, ibuprofen, mefenamic acid and trimetazone belong to the most effective of the entire series of antirheumatics tested.

Animals↗

PubMedDate not supplied

The influence of copper-dextran complex (C-79), non-steroid anti-inflammatory drugs and bacterial pyrogen on stabilization of rabbit erythrocyte membrane.

We investigated the effect of copper-dextran complex (C-79), acetylsalicylic acid (ASA), mefenamic acid (MEFA) and indomethacin (IND), alone or combined with E. coli lipopolysaccharide (LPS) on osmotic fragility of rabbit erythrocytes. It has been found that LPS in combination with ASA, MEFA, and IND did not change the stabilizing effect of the antipyretics on rabbit erythrocyte membrane. C-79 in doses of 0.4-0.8 mg Cu/kg iv stabilized the erythrocyte membrane for several hours. In lower doses, the compound produced a weak stabilizing effect, and an opposite effect was induced by a dose of 1.6 mg Cu/kg. After administration of C-79 and LPS in combination, the duration of LPS-induced fever was shortened and the erythrocyte stabilization by C-79 was weaker. A combination of ASA with C-79 depressed the body temperature in normothermic animals, while the stabilizing effect of both compounds on the erythrocyte membrane was non-additive.

Animals↗