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PubMed1992

Longterm drug therapy for rheumatoid arthritis in seven rheumatology private practices: I. Nonsteroidal antiinflammatory drugs.

The probability of continuation of a particular nonsteroidal antiinflammatory drug (NSAID) over 5 years was estimated for 1,775 courses taken by 532 patients with rheumatoid arthritis treated in 7 rheumatology private practices. Similar results were seen for 15 different NSAID--48% of courses were continued at 12 months, 36% at 24 months, and 20% at 60 months. Only acetylated salicylates, other than plain aspirin, were continued significantly longer than any of the other NSAID. The probability of continuation of plain aspirin was similar to other NSAID, including nonacetylated salicylates and nonsalicylate NSAID. The first NSAID taken by an individual patient was continued only marginally longer than the 4th NSAID taken by the same patient. While most NSAID courses were not continued for long periods, 20% were continued for longer than 5 years, suggesting effective longterm results in this minority of courses.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1992

Comparison of signal transduction mechanisms of alpha-2C and alpha-1A adrenergic receptor-stimulated prostaglandin synthesis.

Prostaglandin (PG) synthesis elicited by adrenergic transmitter in the vascular smooth muscle cells (VSMC) of rabbit aorta is primarily mediated through activation of alpha-2C and alpha-1A adrenergic receptors (ARs). We have now investigated and compared the signal transduction mechanisms involved in alpha-2C and alpha-1A AR-stimulated prostacyclin (PGI2) production, measured as 6-keto-PGF1 alpha, in vascular smooth muscle cells. Norepinephrine, methoxamine (an alpha-1 AR agonist) and UK-14304 (an alpha-2 AR agonist) enhanced 6-keto-PGF1 alpha production. UK-14304 and norepinephrine (in the presence of propranolol), but not methoxamine, reduced basal adenosine 2':3'-cyclic monophosphate (cyclic AMP) as well as forskolin- and isoproterenol-stimulated cyclic AMP accumulation. Forskolin and isoproterenol did not alter basal 6-keto-PGF1 alpha production and alpha AR agonist-induced 6-keto-PGF1 alpha production. Alpha-2C and alpha-1A AR-stimulated 6-keto-PGF1 alpha production was independent of cyclic AMP levels in vascular smooth muscle cells. Both alpha-2C and alpha-1A AR-stimulated 6-keto-PGF1 alpha production required extracellular Ca++. Pertussis toxin prevented inhibition of cyclic AMP accumulation and reduced 6-keto-PGF1 alpha production in response to AR agonists. Guanosine 5'-O-(3-thiotriphosphate) potentiated 6-keto-PGF1 alpha production induced by norepinephrine and UK-14304 but not by methoxamine, whereas at a higher Mg++ concentration (4 mM), guanosine 5'-O-(3-thiotriphosphate) potentiated 6-keto-PGF1 alpha production by all three agonists. In contrast, the effect of UK-14304 on cyclic AMP was prevented in the presence of 4 mM Mg++. These data suggest that the pertussis toxin-sensitive G protein(s) mediated the stimulation of PG synthesis by alpha-1A and alpha-2C AR activation and the decrease in cyclic AMP accumulation by alpha-2C AR activation.

6-Ketoprostaglandin F1 alpha↗
PubMedDate not supplied

Role of prostaglandin E2 (PGE2) in the growth hormone releasing hormone action on growth hormone, insulin and C-peptide in normal men.

Fourteen healthy men were placed in two treatment groups. 1. Seven men received growth releasing hormone (1 microgram/kg BW) intravenously during either saline or prostaglandin E2 (10 micrograms/min) infusion which were started 60 minutes before testing. Growth hormone response to growth releasing hormone was greater during prostaglandin E2 infusion compared to the control study. These data suggest that exogenous prostaglandin E2 positively modulates growth hormone response to growth releasing hormone. In the second group consisting also of 7 men a GRH test was performed before and after 3 days administration of meclofenamate. Meclofenamate significantly reduced plasma levels of stable metabolites of prostaglandin E2 as well as the growth hormone to growth releasing hormone, suggesting that the GRH effect on GH was at least partly under prostaglandin E2 control. GRH significantly reduced serum insulin in the two treatment groups. PGE2 infusion or meclofenamate did not change insulin response to GRH. Serum C-peptide and blood glucose did not change after GRH injection during saline or PGE2 infusions.

Adult↗
PubMed1992

Cyclooxygenase products are not involved in the protection against myocardial infarction afforded by preconditioning in rabbit. Cyclooxygenase pathway's involvement in preconditioning.

The mechanism whereby preconditioning with a transient period of ischemia renders the heart resistant to infarction from a subsequent ischemic insult is unknown. The purpose of this study was to determine whether cyclooxygenase pathways are involved in preconditioning's protection. Two inhibitors of that pathway, meclofenamate (MEC) and aspirin (ASP), were test in an in situ and a blood perfused isolated heart model, respectively. Preconditioning was achieved with 5 minute ischemia and 10 minutes reperfusion. All in situ hearts underwent 30 minute ischemia followed by 180 minute reperfusion, while the isolated hearts experienced 45 minute ischemia plus 120 minute reperfusion. Infarct size was measured with TTC stain. In the in situ model, 39.9% +/- 4.2% of the ischemic zone was infarcted in control hearts but only 8.8% +/- 2.2% in preconditioning hearts. Pretreatment with MEC (5 mg/Kg) caused no alteration of infarct size in either non preconditioned (34.3% +/- 8.3%) or preconditioned hearts (6.7% +/- 3.3%). In isolated hearts, 45 minute ischemia caused 31.0% +/- 5.9% of the ischemic zone to be infarcted in control hearts and only 5.4% +/- 2.2% in preconditioned hearts. Pretreatment with ASP (1 mg/Kg) failed to affect infarct size in either non preconditioned (35.7% +/- 3.7%) or preconditioned hearts (10.2% +/- 1.9%). The data indicate that cyclooxygenase pathways are not involved in the preconditioning's protection.

Analysis of Variance↗
PubMed1992

Double blind randomized controlled trial of sodium meclofenamate (Meclomen) and diclofenac sodium (Voltaren): post validation reapplication of the WOMAC Osteoarthritis Index.

Following several years of development and validation, we applied the WOMAC Osteoarthritis Index as the principal outcome measure in a double blind randomized parallel trial of Meclomen (100 mg po tid) and Voltaren (25 mg po tid). Statistically significant improvements in clinical status were noted in both treatment groups. At the doses studied, between drug differences favoring Meclomen were observed in pain and stiffness, no difference being noted in physical function. No significant between drug difference was noted in tolerability at these same doses. Our study also demonstrated that the relative efficiency of WOMAC was similar to that of the Lequesne and Doyle indices. Finally, we defined the standard deviation necessary to calculate sample size for future studies using the WOMAC index, both for studies based on static scores and those based on change scores.

Adult↗
PubMed1975

A vascular permeability factor in lymphocyte culture supernants from patients with nephrotic syndrome. II. Pharmacological and physicochemical properties.

Pharmacological properties of the "Skin Reactive Factor" demonstrated in nephrotic patients are similar to guinea-pig Skin Reactive Factor. This biological activity is not antagonized by anti-histaminic and anti-serotonin drugs. It is inhibited by meclofenamate and pyridinolcanbamate. It is enhanced by diethyldithiocarbamate and normal human serum. According to this results it could be an activator of the kinin system. Biochemical studies indicate that it is a pepsin destroyed protein, unaffected by Rnase and Dnase. Its electrophoretic mobility is that of an albumin or an alpha1 globulin.

Blood Proteins↗
PubMed1991

Attenuation of azosemide's action in the loop of Henle of rat kidney by nonsteroidal anti-inflammatory drugs.

The purpose of the present study, which was performed in anaesthetized rats, was to clarify whether the nonsteroidal anti-inflammatory drugs (NSAIDs) indomethacin and meclofenamate interact with the diuretic action of the new loop diuretic azosemide (Luret, CAS-27589-33-9). Since azosemide's diuretic action shows a lower onset and a more prolonged duration as compared to classical loop diuretics it was also tested whether azosemide's tubular action is mediated by an active metabolite. The results demonstrate that azosemide, when infused directly into the lumen of superficial loops of Henle, dose-dependently diminished the loops sodium and chloride reabsorption. A half-maximum effect was observed at an azosemide concentration of 3 x 10(-6) mol/l. These results clearly prove that the diuretic effect of azosemide is exerted by the drug itself and does not require metabolism to an active metabolite. Luminal application of the drug also dose-dependently increased early distal sodium and chloride concentrations, indicating that the drug's tubular action is located in the thick ascending limb of Henle's loop. Indomethacin and meclofenamate blunted the diuretic, natriuretic and chloruretic response to azosemide, and microperfusion experiments on single loops of Henle revealed an attenuation by NSAIDs of azosemide's inhibitory action on the loops sodium and chloride reabsorption. The quantitative extent of this interaction was nearly identical to that observed previously for the NSAID-furosemide interaction.

Animals↗
PubMed1991

Evidence for enhanced inhibitory modulation by cyclooxygenase products of noradrenergic neurotransmission in the mesenteric vasculature of young spontaneously hypertensive rats.

The effects of cyclooxygenase inhibition by indomethacin and meclofenamate on pre- and postjunctional aspects of noradrenergic neurotransmission were determined in mesenteric vascular preparations from 4- to 6-week-old spontaneously hypertensive rats (SHRs) and normotensive Wistar-Kyoto rats (WKYs). Perfusion pressure responses to periarterial nerve stimulation and to exogenous norepinephrine (NE) were significantly greater in SHR than in WKY preparations, whereas fractional NE overflow was equivalent between the two strains. Indomethacin and meclofenamate enhanced perfusion pressure responses to periarterial nerve stimulation in both strains. Fractional NE overflow was significantly enhanced by indomethacin but only at 14 Hz in SHR preparations, whereas it was unaffected in WKY preparations. The combination of indomethacin and cocaine resulted in a significant enhancement of perfusion pressure responses to periarterial nerve stimulation in both strains that was significantly greater than that produced by either drug alone. This effect was significantly greater in SHR than in WKY preparations. This combination also resulted in a significant enhancement of responses to exogenous NE in both strains. Fractional NE overflow was significantly increased in SHR preparations in the presence of the combination of cocaine and indomethacin, whereas it remained unaltered in WKY preparations. These findings suggest that a cyclooxygenase product exerts both pre- and postjunctional inhibitory effects on vascular noradrenergic neurotransmission that differ in these two strains of rats. The prejunctional inhibitory effect of this cyclooxygenase product was observed only in SHR preparations and was especially evident in the presence of cocaine.

Animals↗
PubMed1991

Pill-esophagitis caused by nonsteroidal antiinflammatory drugs.

A case of meclofenamate-induced pill-esophagitis is reported, and the relevant literature is reviewed. The role of posture, amount of fluid chaser, esophageal obstruction or dysmotility, drug formulation, physical and chemical properties of the drug, and concomitant ingestion of alcohol, as well as the diagnosis and management of such cases, are discussed.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1991

Effects of meclofenamate on natural killer cell activity.

The effect of meclofenamate on natural killer cell activity was studied in a four hour 51Cr release assay. Meclofenamate, a nonsteroidal anti-inflammatory drug, had no effect on natural killer cell activity when added to the mixture of target (K562) and effector (peripheral blood mononuclear) cells either at the beginning of the reaction or when effector cells were pretreated with meclofenamate for 12-24 hours. However, a significant increase (p less than 0.0005) in the natural killer cell activity was seen when target cells were pretreated with meclofenamate for 12-24 hours prior to their mixing with effector cells. This increase in natural killer cell activity was observed consistently when target cells were taken from different donors.

Cytotoxicity Tests, Immunologic↗
PubMed1990

Analysis of cardiovascular and pulmonary responses to endothelin-1 and endothelin-3 in the anesthetized cat.

Cardiovascular and pulmonary responses to endothelin (ET)-1, ET-3 and neuropeptide Y (NPY) were investigated in the anesthetized cat. ET-1, 0.1 to 1 nmol/kg i.v., decreased or elicited biphasic changes in arterial pressure (AP), whereas ET-3, in the same doses, decreased AP. Both ETs increased cardiac output (CO) and, at the highest doses, a secondary decrease in CO was observed. NPY, 0.3 to 3 nmol/kg i.v., increased AP and at the highest dose decreased CO. All three peptides had inconsistent effects on right ventricular contractile force and increased central venous pressure. ET-1 at lower doses increased heart rate (HR) and, at 1 nmol/kg, caused a biphasic change. ET-3 increased HR, whereas NPY decreased HR. Systemic vascular resistance (SVR) was increased by NPY and decreased by ET-3, whereas ET-1 elicited biphasic changes. ET-1 and ET-3 increased pulmonary arterial pressure, left atrial pressure and caused biphasic changes in pulmonary vascular resistance (PVR). NPY had no significant effect on PAP or PVR. When pulmonary blood flow was maintained constant, ET-1 and ET-3 had only pulmonary vasoconstrictor activity, whereas NPY and the ET analog had no significant effect. The increase in SVR in response to NPY, the decrease in response to ET-3 or the biphasic change in response to ET-1 were not modified by meclofenamate, hexamethonium or propranolol. Increases in HR in response to ET-1 and ET-3 were reduced by the beta receptor and ganglionic blocking agents.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

The dual action of meclofenamate on the contractile response to PGF2 alpha in the guinea-pig trachea.

Indomethacin and meclofenamate (1 mug/ml) enhance contractile action of PGF2 alpha (5-20 mug) in guinea-pig tracheas superfused with Tyrode solution (5 ml/min). Unlike indomethacin, meclofenamate at a concentration of 10 mug/ml antagonizes contractions of guinea-pig tracheas produced by PGF2 alpha (5-20 mug), while the contractile action of histamine (0-5-2-0 mug) is enhanced. It is concluded that low concentrations of meclofenamate (1 mug/ml) inhibit prostaglandin biosynthesis in tracheal smooth muscles and therefore contractile action of exogenous PGF2 alpha is enhanced, while meclofenamate at a high concentration (10 mug/ml) blocks the receptor sites for PGF2 alpha.

Animals↗
PubMed1987

Parasite-accessory cell interactions in murine leishmaniasis. II. Leishmania donovani suppresses macrophage expression of class I and class II major histocompatibility complex gene products.

In the present study, we examined the modulation of MHC class II and class I gene products on BALB/c macrophages infected with the obligate intracellular protozoan Leishmania donovani. Our findings indicated that this organism suppressed macrophage expression of both classes of MHC antigens. These effects varied somewhat, depending on whether cells were in the basal state or were stimulated with interferon-gamma. Thus, class II density on interferon-gamma-treated infected macrophages was suppressed by as much as 90%, relative to lymphokine-stimulated control cells. Induction of H-2K and H-2D by lymphokine treatment of infected macrophages was also markedly reduced. In the basal (non-lymphokine-treated) state, infected cells also showed reduced expression of H-2K and H-2D, but not I-A or I-E. The latter result was related to minimal levels of class II molecules on normal, in vitro cultured macrophages. Suppression of MHC gene products correlated with both the duration and intensity of leishmania infection and could not be overcome by increasing doses of interferon-gamma. Culture of cells under conditions of cyclooxygenase inhibition completely abolished elevated synthesis of prostaglandin E2 by infected macrophages and augmented their responsiveness to lymphokine induction of class II antigens by 60 to 80%. These results indicate that L. donovani is capable of subverting a critical macrophage accessory function required for the induction of T lymphocyte immunity. This mechanism could account, at least in part, for defective parasite-specific cell-mediated immunity seen during infections with this protozoan.

Animals↗
PubMed1989

Adenosine does not mediate the pulmonary vasodilator response of adenosine 5'-triphosphate in the feline pulmonary vascular bed.

Adenosine and ATP produce dose- and tone-dependent responses in the feline pulmonary vascular bed. That is, at baseline (low) pulmonary vascular tone adenosine and ATP produce vasoconstrictor responses and at elevated pulmonary vascular tone adenosine and ATP produce vasodilator responses. The mechanism mediating the vasodilator responses to adenosine and ATP was investigated in the intact-chest cat under conditions of controlled pulmonary blood flow and left atrial pressure. When lobar vascular resistance was raised with U46619, intralobar injections of adenosine and ATP caused dose-related decreases in lobar arterial pressure. The pulmonary vasodilator responses to ATP and adenosine were not altered by atropine, propranolol, meclofenamate or cimetidine indicating that these responses were not mediated by the release of vasodilator prostaglandins or to activation of beta adrenergic, muscarinic or histamine (H2) receptors. The decreases in lobar arterial pressure in response to adenosine were reduced significantly by BWA1433U, an adenosine (P1) receptor antagonist. BWA1433U induced a parallel shift of the adenosine dose-response curve to the right; however, it had no significant inhibitory effect on the decrease in lobar arterial pressure in response to ATP. The P1 receptor antagonist in doses of 10 and 30 mg/kg i.v. had no significant effect on the vasodilator response to nitroglycerin. The present data suggest that vasodilator responses to adenosine in the feline pulmonary vascular bed are mediated by adenosine (P1) receptors, whereas responses to ATP are mediated by a different mechanism that does not involve release of a vasodilator prostaglandin.

Adenosine↗