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PubMed1987

The analgesic and antiinflammatory activity and pharmacologic properties of bromfenac.

Bromfenac sodium (2-amino-3-(4-bromobenzoyl)benzeneacetic acid sodium salt sesquihydrate, AHR-10282B) is a potent long-acting, peripheral, analgesic compound possessing antiinflammatory, antipyretic, and prostaglandin synthetase-inhibiting properties. In the acetylcholine abdominal constriction assay in mice, bromfenac (bromfenac sodium) by the oral route at pretreatment times of 10, 20 and 300 min was respectively 3.7, 6.5 and 2.9 times more potent than zomepirac and 3.4, 6.6., and 44.2 times more potent than suprofen. In dogs bromfenac when given orally was 5.8 times more potent than zomepirac in blocking the nociceptive response to bradykinin. Naloxone did not alter the analgesic properties of bromfenac in mice; and after repeated administration, tolerance to analgesia did not develop. Bromfenac, given orally, was more potent than indometacin in suppressing acute (7.5-20 times) and chronic (3.8 times) inflammation. The gastric and intestinal toxicity potencies of bromfenac, given orally, were comparable with and 1.8 times more potent than indometacin, respectively. Bromfenac was 6.1 to 32.8 times more potent than indometacin in inhibiting the formation of prostaglandin E2 and F2 alpha from microsomes of bovine seminal vesicles, rabbit uteri, and rabbit renal medullae; but it did not block the direct action of prostaglandin E1 (abdominal constriction) and prostaglandin F2 alpha (contraction of the uterus). Bromfenac produced no unwanted central nervous system, cardiovascular, or autonomic effects.

Acetylcholine↗
PubMed1987

A test for analgesics: incoordination in writhing mice.

Acetic acid administered to mice resulted in post-writhing incoordination and a subsequent fall in the rota-rod test. This fall from rota-rod induced by 3% acetic acid was dose-dependently protected by the non-narcotic analgesics. While suprofen was found to be the most potent (ED50 = 15.29 mg/kg), aspirin was found to be the least potent (ED50 = 81.54 mg/kg). The model appears to be more sensitive than the conventional methods for testing non-narcotic analgesics.

Acetates↗
PubMed1983

Acetic acid and phenylquinone writhing test: a critical study in mice.

Studies were planned to establish the dose-effect relationship with both acetic acid and phenylquinone and to find out suitable concentrations for these two chemicals for pre- and post screening. The LD50 of acetic acid and phenylquinone were found to be 3.16% and 0.23%, respectively. Based on the studies conducted, the prescreening and postscreening concentrations of 0.5% is recommended for acetic acid, while for phenylquinone, prescreening concentration of 0.005% and postscreening concentration of 0.02% is advocated. Using this criterion in the acetic acid writhing test, analgin was the most potent analgesic while aspirin was the least. However, suprofen was most potent and paracetamol least among analgesics employed against phenylquinone induced writhing.

Acetates↗
PubMed1982

Effect of prostaglandin synthetase inhibitors on mammary blood flow during experimentally induced mastitis in lactating goats.

Mammary blood flow (MBF) was recorded chronically in lactating goats by means of an electromagnetic flow probe. Experimental mastitis was induced by intramammary injection of E. coli lipopolysaccharides. Control mastitis experiments were accompanied by a significant increase in MBF characterized by 2 conspicuous peaks, by fever, increased heart rate, swelling, heat and pain of the gland, and increased chloride in milk. The non-steroidal anti-inflammatory drugs suprofen, indomethacine and flurbiprofen were potent antipyretics during mastitis but had only little effect on the biphasic MBF pattern. Indomethacine induced a strong and long lasting vasoconstriction in the udder. MBF peak I was quantitatively unaffected although flurbiprofen was able to delay its appearance. All drugs partially suppressed MBF peak II, this being most significantly with flurbiprofen. None of them prevented either swelling of the gland or high milk chloride but all inhibited pain in the gland. MBF peak II may be partially induced by the decrement stage of fever. Locally formed prostaglandins play little or no role in the genesis of MBF peak I but may be involved in MBF peak II.

Animals↗
PubMed1980

Endotoxin-induced inhibition of gastric emptying rate in the rat. The effect of repeated administration and the influence of some antipyretic agents.

Intravenous injection of endotoxin from E. coli O (111)B(4) caused inhibition of gastric emptying rate in conscious Wistar rats. Tolerance induced by repetitive daily intraperitoneal administration of the endotoxin, resulted in a complete abolition of this effect. Insulin, administered subcutaneously, stimulated gastric emptying rate. Pretreatment with this drug opposed the endotoxin-induced inhibitory effect completely. Pretreatment with indomethacin only had a partial antagonistic influence, while other drugs such as flurbiprofen, suprofen and novaminsulphonum had no significant effect upon endotoxin-induced inhibition of gastric emptying rate. Previous studies suggested that some effect of endotoxin other than stimulation of the biosynthesis of prostaglandins should be considered. The results of the present study suggest a similar conclusion. The nonsteroidal anti-inflammatory agents used, did not modify the normal course of gastric emptying in the control rats.

Animals↗
PubMed1994

Non-steroidal antiinflammatory agents. Synthesis and enzyme inhibition of 2-[4-(heteroarylmethyl)phenyl] propanoic acids and analogues.

Some 2-[4-(heteroarylmethyl)phenyl]propanoic acids and phenylacetic and benzoic analogues has been synthesized. All above acids were tested for their inhibitory activity on lipoxygenase and cyclooxygenase, in comparison with NDGA and tolmetin. 2-[4-(Thien-2-ylmethyl)phenyl]propanoic acid 2, strictly related with suprofen, was found the most interesting compound, giving rise to a 79% inhibition of the cyclooxygenase activity at 10(-4) M concentration.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1976

Discriminative stimulus properties of analgesic drugs: narcotic versus non-narcotic analgesics.

Using a food-reinforced two-lever operant procedure, rats (n=6) were trained to discriminate fentanyl (1.25 mg/kg, p.o., t-60') from solvent (1 ml/100 g B.W., p.o., t-60'). The administration of another narcotic analgesic (pethidine) produced a dose-related generalization with the standard fentanyl treatment; six non-narcotic analygesics (suprofen, acetylsalicylic acid, indomethacin, phenacetin, phenylbutazone, tolmetin) were found not to do so. It is concluded that the ability of drugs to produce analgesia is not a sufficient condition for the drugs to produce the narcotic cue as well.

Analgesics↗
PubMed1994

Nonsteroidal anti-inflammatory drugs. Current ophthalmic therapy.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are commonly used in the treatment of ophthalmic inflammatory disease. Currently four topical preparations are available: flurbiprofen and suprofen for the prevention of miosis during surgery; diclofenac for postoperative inflammation following cataract extraction, and ketorolac for the treatment of itching associated with seasonal allergic conjunctivitis. Caution should be exercised, however, as topical and systemic adverse effects may occur including stinging, photophobia, gastric sensitivity, and increased bleeding time. The mechanism of action of NSAIDs is discussed, complications associated with use, and the current and future roles of therapy.

Administration, Oral↗
PubMed1976

Modification of venous stasis thrombosis in the rat by platelet-active drugs and by heparin.

In rats, stasis thrombosis of a renal vein was produced by the occlusion of a vascular segment after induction of systemic hypercoagulability by i.v. injection of ellagic acid. Prostaglandin E1, at doses which reduced platelet retention by glass beads (6 mug/min/300 g i.v.) only slightly reduced the thrombus size. The platelet release inhibitors suprofen and indomethacin, at doses which prolonged tail bleeding time in rats (50 mg/kg i.v.) had no effect on the thrombus size. Heparin (10 and 20 U/kg i.v.) produced a marked, dose-related reduction of venous thrombosis. The platelet-active compound VK774, at the dose levels of 50 to 10 mg/kg i.v., also reduced the thrombus size to about half that of controls. Lower doses (5, 2.5 mg/kg i.v.) had a progressively weaker effect. Binding to ellagic acid or induction of coagulation changes by VK774 are proposed as possible mechanisms of action. It is concluded that, in comparison with the contribution of plasma coagulation, the participation of the aspects of platelet function we measured in the development of venous stasis thrombosis is comparatively small.

Animals↗
PubMed1998

Electron transfer processes in the reactivity of nonsteroidal anti-inflammatory drugs in the ground and excited states.

The nonsteroidal anti-inflammatory drugs (NSAID), naproxen, sulindac and indomethacin, were shown to donate electrons to nitro blue tetrazolium (NBT) when irradiated with UV light in deoxygenated aqueous buffer solution (pH 7.4, 30 degrees C). The reaction was monitored spectrophotometrically by the appearance of the diformazan reduction product from NBT. The electron transfer process facilitates the decomposition of the drugs. Naproxen in the presence of NBT is photodegraded principally to the alcohol (2-[1-hydroxyethyl]-6-methoxynaphthalene) at a rate approximately 20-fold faster than when irradiated alone in deoxygenated conditions. The photoproduct from naproxen also participates in the electron transfer to NBT but at a much slower rate than naproxen. Irradiation of sulindac or indomethacin in the presence of NBT caused the slow photoreduction of NBT to diformazan. In the absence of NBT, indomethacin and sulindac are essentially unreactive when irradiated in aqueous solution. The ability of a number of NSAID to act as electron donors in their ground state was studied by observing their oxidation by potassium peroxodisulfate in pH 7.0 phosphate buffer at 50 degrees C. The HPLC analysis of the drug remaining showed that the 2-arylpropionic acid NSAID (naproxen, ibuprofen, ketoprofen and suprofen) reacted at a rate equivalent to the thermal decomposition of peroxodisulfate. The major products were the same as detected in the photooxidation of these drugs, resulting from decarboxylation and oxygen addition but also included a dimeric compound. On the other hand, the NSAID that do not contain the propionic acid substituent all reacted more slowly with peroxodisulfate, enabling specific reaction rate constants to be evaluated.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1984

Cystoid macular edema in pseudophakia.

Cystoid macular edema after cataract surgery, with or without intraocular lens implantation, has been reported to develop in more than 50% of patients as detected by fluorescein angiography. It is associated with reduced visual acuity in up to 8% of cases. Analysis of ongoing clinical trials at the Wilmer Institute indicates that clinically significant cystoid macular edema develops in a lower percentage of cases (2% total incidence and 0.3% persistent cystoid macular edema) if the intraocular lens implantation was uncomplicated. The factors associated with cystoid macular edema and the importance of considering clinically significant rather than just fluorescein-proven cystoid macular edema are discussed. Results of intraocular lens studies reported to the Federal Drug Administration are updated, and results of an ongoing study of prostaglandin inhibitors at the Wilmer Institute are reported.

Aged↗
PubMed1982

Platelet-mediated vascular contractions: inhibition of the serotonergic component by ketanserin.

In vitro stimulation of washed rat platelets (2.5 X 10(10)/1) with thrombin (0.002 U/1) as well as their activation on de-endothelialized vascular preparations, produced a strong contraction of isolated rat caudal arteries. Pharmacodissection and specific measurements of various mediators (5-hydroxytryptamine, thromboxane B2, ATP) showed the platelet-mediated contraction to be mainly mediated by 5-hydroxytryptamine, either by its direct effect or through amplification of prostaglandin-effects at the level of the vessel or the platelets. Platelet-mediated vasospastic episodes were effectively reduced by ketanserin, a selective 5-HT2 receptor antagonist.

Adenosine Diphosphate↗
PubMed1985

Platelet-mediated vascular permeability in the rat: a predominant role for 5-hydroxytryptamine.

The intradermal injection in rat skin of washed, thrombin-activated platelets produces an increase in vascular permeability, the intensity of which increments with the platelet concentration. Pretreatment of the recipient animals with serotonergic antagonists, including the specific 5-HT2 receptor blocker ketanserin, potently inhibits the platelet-mediated and the 5-HT-induced vascular defect. Amine depletion of platelets or skin tissues with reserpine reduces the response to platelets. Platelet prostanoid and lipoxygenase derivatives play no major role in the vascular response to platelet. The permeability increase induced by exogenous 5-HT and by activated platelets is reduced by alpha 1-adrenergic stimulation with noradrenaline or phenylephrine and by beta 2-stimulation with terbutaline or isoprenaline, and is potentiated by adenosine; this points to a modulation of permeability by blood flow changes and to a direct beta-adrenergic effect at the endothelial cell membrane. This study demonstrates a predominant role for 5-HT in the platelet-mediated vascular permeability increase in a sensitive species like the rat.

Animals↗
PubMed2006

Nonaqueous capillary electrophoretic behavior of 2-aryl propionic acids in the presence of an achiral ionic liquid. A chemometric approach.

Ionic liquids (ILs) appear really attractive as electrolyte additives in nonaqueous capillary electrophoresis (NACE). These salts may offer new possibilities of interactions to modulate analyte effective mobilities. The presence of 1-n-butyl-3-methylimidazolium bis(trifluoromethanesulfonyl)imide (BMIM NTf2) in acetonitrile/alcohol background electrolytes (BGEs) was investigated in this work. The aim of this study was to elucidate the influence of the IL concentration on the electrophoretic behavior of four arylpropionic acids and to identify the interactions between the analytes and the IL cation. The influence on mobility of the IL concentration, the nature and the proportion of the organic solvents, and the concentration of the ionic components of the BGE was first studied by a univariate approach. A four-factor D-optimal experimental design was then applied to provide a deeper insight into analyte interaction with IL cation present both free in BGE and adsorbed onto the capillary wall.

Carbazoles↗
PubMed2004

In vitro effects of risperidone and 9-hydroxy-risperidone on human platelet function, plasma coagulation, and fibrinolysis.

BACKGROUND: Thrombotic events have been reported with the use of antipsychotic compounds, although the incidence, predisposing factors, and biological mechanisms associated with these events in psychiatric patients are subject to debate. OBJECTIVE: The in vitro actions of risperidone and its active metabolite 9-hydroxy-risperidone (9-OH-risperidone) on human platelet function, plasma coagulation, and fibrinolysis were examined to explore whether hematologic effects might be a mechanism for thrombotic events with these compounds. METHODS: Blood was donated by healthy white male subjects who were free of medications (particularly acetylsalicylic acid and nonsteroidal anti-inflammatory compounds). Platelet shape change and adhesion/aggregation reactions to risperidone and 9-OH-risperidone induced by adenosine diphosphate (ADP), collagen, epinephrine, and 5-hydroxytryptamine (5-HT) were tested in human platelet-rich plasma. Arachidonic acid metabolism was assessed in human platelets and rat aortic rings. Plasma coagulation was tested in human platelet-poor plasma. Fibrinolysis was measured in human whole blood. RESULTS: The 12 study subjects ranged in age from 20 to 40 years (median age 30 years). At concentrations of 1 x 10(-5) mol/L (approximately 4180 ng/mL), neither risperidone nor 9-OH-risperidone induced platelet shape change or aggregation, amplified reactions to ADP, or modified platelet adhesion/aggregation induced by collagen or ADP, but they did attenuate epinephrine-induced platelet aggregation (-50% in the case of 9-OH-risperidone; P < 0.05) and 5-HT-induced platelet aggregation (drug concentrations yielding 50% inhibition of 5-HT-induced platelet aggregation, 0.5 and 0.2 ng/mL, respectively). Cyclooxygenase, thromboxane A2 synthase, 12-lipoxygenase, prostacyclin synthase, plasma coagulation, and fibrinolysis were unaffected. CONCLUSIONS: Risperidone and 9-OH-risperidone reduced epinephrine- and 5-HT-induced human platelet aggregation but did not significantly alter other measures of platelet function, plasma coagulation, or fibrinolysis in vitro.

Adult↗
PubMed1985

Pharmacologic therapy of aphakic and pseudophakic cystoid macular edema. 1985 update.

Major advances in the pharmacologic therapy of aphakic cystoid macular edema (ACME) have not occurred since 1982. Topical nonsteroidal anti-inflammatory agents are still not commercially available for ocular therapy. Topical indomethacin remains the one agent which has been proven to be of prophylactic value for angiographic aphakic cystoid macular edema although other non-steroidal agents may also work. The therapeutic value of these compounds for established ACME remains uncertain. No prospective randomized prophylactic or therapeutic trials of either topical or systemic corticosteroids have been performed.

Administration, Topical↗
PubMed1998

Regulating the cancer-inducing potential of non-steroidal anti-inflammatory drugs: some lessons from the 1970s and 1980s.

This article systematically examines government regulation of medicines in the U.K. and the U.S. with specific reference to carcinogenic risk assessment. By taking four non-steroidal anti-inflammatory drugs (NSAIDs) as case studies, it is argued that there have been inconsistencies between regulatory practice and the scientific standards supposed to have been upheld by drug regulatory agencies. Moreover, those inconsistencies are shown to form a trend over time which suggests an erosion and neglect of regulatory rigour during the 1980s. This takes the form of awarding the benefit of the many scientific doubts in carcinogenicity testing to manufacturers rather than to patients.

Animals↗