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At least 811 records · Page 45Linked to original sources
PubMed1979

Fenamates may antagonize the actions of prostaglandin endoperoxides in human myometrium.

1 The prostaglandin endoperoxide analogue U-46619 potently contracted human isolated myometrium, suggesting that prostaglandin H2 (PGH2) may be a major stimulant of myometrial contractions. 2 Sodium mefenamate, flufenamate or meclofenamate 2 microgram/ml greatly reduced contractions of the myometrium induced by the PGH2 analogue. 3 Flufenamate, but not the other two drugs, also significantly inhibited contractions to acetylcholine. 4 Sodium meclofenamate 2 microgram/ml did not consistently antagonize contractions to PGF2alpha. 5 The relief of dysmenorrhoea by fenamates may be explained both by inhibition of PG synthesis, and by antagonism of contractions to PGH2 produced by incompletely blocked PG synthesis.

Acetylcholine↗
PubMed1990

Salicylate, mefenamate, meclofenamate, and quinine on cochlear potentials.

The perilymphatic spaces of guinea pig cochleae were perfused with artificial perilymph, with and without drug, at a rate of 2.5 microliters/minute for 10 minutes. The compound action potential of the auditory nerve, cochlear microphonics, and the summating potential evoked by 10 kHz tone bursts of varying intensities were recorded from a wire inserted in the basal turn scala vestibuli. The endocochlear potential was recorded from the scala media. Sodium salicylate (1.25 to 10 mmol/L) reduced the magnitude of the compound action potential evoked by low-sound intensities without affecting the compound action potential evoked by high-sound intensities. Sodium salicylate also reduced cochlear microphonics and had no effect on summating potential. Cochlear perfusions of prostaglandin synthesis inhibitors, mefenamate (200 mumol/L), and meclofenamate (200 mumol/L), had no effect on the cochlear potentials. Quinine (10 to 100 mumol/L) reduced the compound action potential input-output function in a parallel fashion rather than selectively affecting the low-intensity compound action potential. Quinine (100 mumol/L) reduced cochlear microphonics and summating potential. Neither quinine (100 mumol/L) nor salicylate (5 mmol/L) affected endocochlear potential. These results suggest that salicylate-induced hearing loss is not caused by either antagonism of the hair cell transmitter or cyclooxygenase inhibition, nor is it caused by the same mechanism that causes quinine-induced hearing loss.

Acetates↗
PubMed1998

Fenamates protect neurons against ischemic and excitotoxic injury in chick embryo retina.

Three fenamates (flufenamate, meclofenamate and mefenamate) were examined for their protective effect on neurons under ischemic (glucose/oxygen deprivation) or excitotoxic conditions, using the isolated retina of chick embryo as a model. Retinal damage was evaluated by histology and lactate dehydrogenase assay. Whole-cell recording was used to examine the direct effect of the fenamates on glutamate receptor-mediated currents. The fenamates protected the retina against the ischemic or excitotoxic insult. Part of the neuroprotection by the fenamates derived from inhibition of N-methyl-D-aspartate receptor-mediated currents. However, kainate receptor-mediated currents were not blocked by the fenamates, which nonetheless reduced kainate receptor-mediated retinal damage. Our results raise the possibility that fenamates may serve as lead structures in the development of novel therapeutic agents against brain ischemia.

Animals↗
PubMed1984

Prostaglandin synthetase inhibitors in the treatment of primary dysmenorrhea. Outcome trials reviewed.

Clinical trials of prostaglandin synthetase inhibitors (PGSIs) prescribed for the treatment of primary dysmenorrhea were reviewed as to pain relief effectiveness, frequency and nature of side effects, and methodological adequacy. The review investigated 51 PGSI trials for a total of 1,649 women and 682 menstrual cycles and found that, over all, 72% of dysmenorrheic women reported significant pain relief to PGSI, 18% reported minimal or no pain relief, and 15% showed placebo response. Comparisons among the fenamatic compounds, ibuprofen, indomethacin, and naproxen showed the fenamates to be more effective in providing pain relief. PGSI-associated side effects were minimal for all PGSIs with the exception of indomethacin. Results were evaluated with respect to several methodological problems. Conclusions were drawn that despite these shortcomings, PGSIs are undoubtedly effective and safe for the majority of women with primary dysmenorrhea.

Clinical Trials as Topic↗
PubMed2001

Selective inhibition of Cl(-) conductance in toad skin by blockers of Cl(-) channels and transporters.

We compared the effects exerted by two classes of Cl(-) transport inhibitors on a Cl(-)-selective, passive anion transport route across the skin of Bufo viridis, the conductance (G(Cl)) of which can be activated by transepithelial voltage perturbation or high cAMP at short circuit. Inhibitors of antiporters (erythrosine, eosin) or cotransporters (furosemide) reduced voltage-activated G(Cl) with IC(50) of 6 +/- 1, 54 +/- 12, and 607 +/- 125 microM, respectively; they had no effect on the cAMP-induced G(Cl). The voltage for half-maximal activation of G(Cl) (V(50)) increased compared with controls, but effects on the maximal G(Cl) at more positive clamp potentials were small. Cl(-) channel blockers from the diphenylamino-2-carboxylic acid (DPC) family [dichloro-DPC, niflumic acid, flufenamic acid, and 5-nitro-2-(3-phenylpropylamino)benzoic acid] reduced the voltage-activated G(Cl) with IC(50) of 8.3 +/- 1.2, 10.5 +/- 0.6, 16.5 +/- 3.4, and 36.5 +/- 11.4 microM, respectively, and also inhibited the cAMP-induced G(Cl), albeit with slightly larger IC(50). V(50) was not significantly changed compared with controls; the maximal G(Cl) was strongly reduced. We conclude that the pathway for Cl(-) is composed of the conductive pore proper, which is blocked by the derivatives of DPC, and a separate, voltage-sensitive regulator, which is influenced by blockers of cotransporters or antiporters. This influence is partly overcome by increasing the clamp potential and removed by high concentrations of cAMP, which renders the pathway insensitive to voltage.

Angiogenesis Inhibitors↗
PubMed1991

Aspirin-sensitive asthma: significance of the cyclooxygenase-inhibiting and protein-binding properties of analgesic drugs.

The in vitro release of endogenous and exogenous PgF2 alpha from plasma and serum proteins by aspirin and other analgesic drugs has been studied by RIA and equilibrium-dialysis techniques, respectively. Before aspirin addition, the mean plasma level of PgF2 alpha measured by RIA was significantly lower in aspirin-sensitive asthma (ASA) patients (11.3 +/- 6.5 pg/ml; n = 8) than in aspirin-tolerant asthma (ATA) patients (25.0 +/- 11.4 pg/ml; n = 21). After aspirin addition (50 micrograms/ml) the mean PgF2 alpha level detected in plasma by RIA was higher in ASA patients (97.6 +/- 5.5 pg/ml) than in ATA patients (66.9 +/- 4.5). The binding of [3H]PgF2 alpha to serum protein was significantly inhibited by NSAIDs but not by paracetamol (0.2-1.0 mM). These results implicate PgF2 alpha and the protein-binding property of analgesic drugs in the pathogenesis of aspirin-sensitive asthma.

Acetaminophen↗
PubMed1996

Fenamates potentiate the alpha 1-adrenoceptor-activated nonselective cation channels in rabbit portal vein smooth muscle.

The agonistic action of fenamates on the alpha 1-adrenoceptor-activated cationic current (Icat) in rabbit portal vein smooth muscle was investigated with the whole-cell patch clamp technique. At -50 mV, the fenamates (100-500 microM) increased Icat dose-dependently, up to several fold. This increase was not accompanied by changes in the reversal potential and strongly inhibited by 500 microM Cd2+ or 10 mM procaine. The enhancing effect of fenamates was also observed on the cationic current activated by intracellularly applied GTP gamma S. These results suggest that fenamates may be useful as a new class of activator for receptor-operated cation channels in smooth muscle.

Adrenergic alpha-Agonists↗
PubMed1979

Prostaglandin synthetase inhibitors and dysmenorrhea. A survey and personal clinical experience.

A survey of earlier published studies on treatment of dysmenorrhea with prostaglandin synthetase inhibitors is given and personal clinical experiences are presented. The time when treatment should start in relation to the onset of bleeding is also discussed. A survey of studies published in English and Scandinavian literature yielded 532 patients. Pain relief was experienced in 64 to 100 per cent of the patients in these studies. The incidence of side-effects has generally been low but in a few studies a high incidence was reported. In the current study 34 patients with prinary dysmenorrhea completed the douule-blind, placebo controlled study on naproxen. The patients were treated for two cycles, 16 with naproxen and 18 with placebo. The mean relief score indicated a "slight to good" pain relief in the naproxen group and "no alleviation" in the placebo group. The difference is statistically significant (p = 0.003). Supplementary medication was much more used in the placebo group compared to the naproxen group (p = 0.01). In the placebo group no change whatsoever was demonstrated in alleviation of interference with every-day life, whereas there was a statistically significant improvement in the naproxen group. No major side-effect was registered. Thus none of the subjects withdrew from the study.

Adolescent↗