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Results for “Flufenamic Acid”

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At least 721 records · Page 40Linked to original sources
PubMed1994

PVP-containing solutions for analysis of divalent cation-dependent NMDA responses in Xenopus oocytes.

The electrophysiological analysis of Ca(2+)-conducting ion channels in Xenopus oocytes is difficult due to secondary intracellular effects induced by Ca2+. In the presence of polyvinylpyrrolidone (PVP) membrane currents can be recorded in nominally divalent cation-free solutions. The Ca(2+)-permeable recombinant NMDA receptors of the NR1/NR2A subtype were used as assay system and the results show that PVP has no effect on NMDA receptor-induced currents. Ca2+ and Ba2+ depress NMDA-induced currents at submillimolar concentrations probably by interfering with the Na+/K+ flux. This block is fully reversible as also observed for Mg2+ but shows in contrast no pronounced voltage dependence. PVP-containing solutions may be useful for the analysis of divalent cation-dependent ion channels.

Animals↗
PubMed1985

High-performance liquid chromatographic assay of antiinflammatory drugs incorporated in gel ointments. Separation and stability testing.

High-performance liquid chromatographic determinations of gabexate mesilate (FOY), prostaglandin E1 (PGE1), PGE1-alpha-cyclodextrin (PGE1-CD), prednisolone (PD) and butyl flufenamate (BF) incorporated in gel ointment were investigated. The gel ointment is composed of a carboxy vinyl polymer (1.3%, w/w) and a large amount of an aqueous organic solvent. A methanol extraction system offered simultaneous advantages of the removal of the polymer and the recovery of active ingredients from the gel phase. The recoveries of the drugs were 100%. The stabilities of PGE1, PGE1-CD, FOY, PD and BF incorporated in gel ointment, stored at 5, 25 and 40 degrees C for up to 90 days, were investigated.

Alprostadil↗
PubMed1985

The fibrinolytic action of flufenamate and its influence on plasminogen binding to fibrin.

The effects of the synthetic fibrinolytic agent flufenamate were investigated in a purified system made up of bovine fibrin and human plasminogen. The lysis of the fibrin clots was observed after a 12-hour incubation for flufenamate concentrations ranging from 0.25 to 3 mM. Below 0.25 mM and above 3 mM, no lysis occurred, even after a longer incubation. An increase in plasminogen adsorption on the fibrin clot was also observed in the presence of flufenamate. The amount of plasminogen bound was estimated using 125I labelled Glu-plasminogen or Lys-plasminogen, in the presence of a protease inhibitor to avoid the fibrinolysis induced at lytic concentrations of flufenamate. Maximum binding was observed with both types of plasminogen at a flufenamate concentration of 2.5 mM. The binding, relatively fast at the start of incubation, slowed down progressively, but a real plateau was not reached, even after a 6-day incubation. Plasminogen binding was not saturable, suggesting a non-specific binding type. Although Lys-plasminogen binding was always greater than that of Glu-plasminogen, the effect of flufenamate was more pronounced on Glu-plasminogen binding.

Animals↗
PubMed1979

Prostaglandin synthetase inhibitors antagonize the depressant effects of ethanol.

Several studies indicate that ethanol may depress the central nervous system by altering neurotransmitter release. Evidence obtained from the peripheral nervous system suggests that prostaglandins act as negative feedback inhibitors of transmitter release. If a similar process occurs in the brain, then perhaps ethanol affects transmitter release via a mechanism involving prostaglandins. Prostaglandin synthetase inhibitors were administered to adult HS/Ibg male mice prior to intraperitoneal injection of a hypnotic dose of either ethanol, propanol, or t-butanol. A significant decrease in the length of alcohol sleep time was found: in the ethanol study, this was coupled with a significant increase in waking blood alcohol levels. These results indicate that inhibition of prostaglandin synthesis alters CNS sensitivity to the depressant effects of alcohol. When the same inhibitors were administered prior to other sedative hypnotics, i.e., pentobarbital and chloral hydrate, no effect was found. This suggests that prostaglandins may be specifically involved in the biochemical mechanism of alcohol depression.

Acetaminophen↗
PubMed1988

Cyclic AMP indirectly mediates the extracellular Ca2+-independent release of LH.

This study was undertaken to determine whether cyclic AMP mediates the extracellular Ca2+-independent component of luteinizing hormone (LH) release. Gonadotropin releasing hormone (GnRH) increased cAMP production in female pituitaries incubated in Ca2+-free medium containing 3-isobutyl-1-methylxanthine (IBMX), but was ineffective in male pituitaries. The increases in female pituitaries were inhibited by flufenamate (flu). GnRH-stimulated LH secretion from male pituitaries was completely inhibited in Ca2+-free medium, whereas only a partial inhibition was obtained from female pituitaries, a response prevented by cycloheximide. Infusions of flu completely inhibited the extracellular Ca2+-independent release of LH, while dibutyryl cAMP (dbcAMP) partially restored this component of LH secretion. The dbcAMP-restored response was dependent upon protein synthesis. These results suggest that (i) the extracellular Ca2+-independent component of LH release is indirectly mediated by cAMP through the stimulation of de novo protein synthesis, and (ii) extracellular Ca2+ is required for the activation of adenylate cyclase in male but not in female gonadotrophs.

Animals↗
PubMed1995

Adenosine 3',5'-cyclic monophosphate and the self-priming effect of gonadotrophin-releasing hormone.

An in vitro perifusion system was used to ascertain the role of cAMP in the genesis of the self-priming effect of gonadotrophin-releasing hormone (GnRH) in rat pituitaries. Ten-minute pulses of 20 nmol/l GnRH administered 150 min apart resulted in the manifestation of the self-priming effect, an effect which was inhibited by 5 mumol/l cycloheximide. Forskolin (1 mumol/l) which does not stimulate luteinizing hormone (LH) secretion or affect the initial LH response to GnRH significantly potentiated the second response through protein synthesis-dependent mechanisms. Additionally, an initial 10-min pulse of forskolin alone was sufficient to prime the pituitary to a subsequent pulse of GnRH 150 min later. Interestingly, similar amounts of LH were secreted in response to forskolin + GnRH or GnRH administered 150 min after forskolin. Flufenamate, an inhibitor of GnRH-stimulated increases in cAMP production prevented the manifestation of the self-priming effect of GnRH. Forskolin which bypasses the inhibitory effects of flufenamate on cAMP production reversed the flufenamate-induced inhibition of the self-priming effect of GnRH through protein synthesis-dependent processes. These results suggest that cAMP does not mediate the LH response to an initial exposure of GnRH, but does play a pivotal role in the genesis of the self-priming effect of GnRH through the stimulation of de novo protein synthesis. Once the newly synthesized proteins are available, the nucleotide is not required for the manifestation of the phenomenon.

Animals↗
PubMed1995

Action of diphenylamine carboxylate derivatives, a family of non-steroidal anti-inflammatory drugs, on [Ca2+]i and Ca(2+)-activated channels in neurons.

Ca(2+)-activated channels, including Ca(2+)-activated non-selective (CAN) channels and Ca(2+)-activated Cl- channels play important roles in regulating the electrical activity of neurons. No blockers of neuronal CAN channels have been previously reported. We used 2-electrode voltage clamping to measure membrane currents and fura-2 fluorescence imaging to measure [Ca2+]i in molluscan neurons. We show that the diphenylamine carboxylate derivative flufenamate (FFA), but not mefenamate or the parent compound, cause a transient increase in ICAN and a slow outward current, and a maintained increase in [Ca2+]i. We interpret this as a FFA-dependent release of Ca2+ from intracellular stores and Ca2+ influx, [Ca2+]i-dependent activation of the CAN and slow outward currents, and slow FFA-dependent channel block.

Animals↗
PubMed2004

Differential contribution of pacemaker properties to the generation of respiratory rhythms during normoxia and hypoxia.

Pacemaker neurons have been described in most neural networks. However, whether such neurons are essential for generating an activity pattern in a given preparation remains mostly unknown. Here, we show that in the mammalian respiratory network two types of pacemaker neurons exist. Differential blockade of these neurons indicates that their relative contribution to respiratory rhythm generation changes during the transition from normoxia to hypoxia. During hypoxia, blockade of neurons with sodium-dependent bursting properties abolishes respiratory rhythm generation, while in normoxia respiratory rhythm generation only ceases upon pharmacological blockade of neurons with heterogeneous bursting properties. We propose that respiratory rhythm generation in normoxia depends on a heterogeneous population of pacemaker neurons, while during hypoxia the respiratory rhythm is driven by only one type of pacemaker.

Action Potentials↗