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At least 793 records · Page 44Linked to original sources
PubMed1997

Subacute and chronic oral toxicity of lornoxicam in cynomolgus monkeys.

Lornoxicam is a novel non-steroidal anti-inflammatory compound in the same chemical class as piroxicam and tenoxicam, with potent anti-inflammatory, antipyretic and analgesic activity. As part of the preclinical safety programme, its toxicity was evaluated in a dose-range-finding and 52-wk toxicity study in cynomolgus monkeys. In the dose-range-finding study, five groups of monkeys (two per sex per group) were dosed orally by gavage for 6 wk with 0, 0.25, 0.5, 1.0 or 2.0 mg lornoxicam/kg/day. Drug-related toxicity was observed in the 1.0 and 2.0 mg/kg/day dose groups only. This included mortality, diarrhoea, prostration, decreased body weight gain and food consumption, faecal occult blood, anaemia, leucocytosis, hypoalbuminaemia, gastrointestinal erosions and ulcerations. On the basis of these results, four groups of monkeys (six per sex per group) were given the compound orally by nasogastric intubation at dose levels of 0, 0.125, 0.25 or 0.5 mg/kg/day for 52 wk. The high-dose level was increased to 0.6 mg/kg/day from wk 39 to wk 52. Treatment was followed by a 4-wk recovery period for two animals per sex per group. Histologically, drug-related changes seen were gastrointestinal erosions, ulcerations and inflammation in males and females at 0.5/0.6 mg/kg/day. Treatment-related clinicopathological findings included decreased haematocrit and hypoproteinaemia (group 0.5/0.6 mg/kg/day males), and hypoalbuminaemia (group 0.5/0.6 mg/kg/day males and females). None of these changes were present after the recovery period, thus indicating reversibility. Plasma concentration of lornoxicam measured 2 hr after dosing increased in a dose proportional manner. The estimated area under the curve (AUC) at steady state increased in a dose-proportional manner and at 0.25 mg/kg was three- to fivefold higher than the human AUC following a 16 mg dose (8 mg b.i.d.). The no-observed-effect level in the chronic toxicity study was 0.25 mg/kg/day.

Administration, Oral↗
PubMed2000

Studies on the anti-inflammatory and related pharmacological properties of the aqueous extract of Bridelia ferruginea stem bark.

The anti-inflammatory profile of the aqueous extract of Bridelia ferruginea stem bark was investigated using both in vivo and in vitro models. The extract exhibited strong topical anti-inflammatory effect shown as inhibition of croton oil-induced ear oedema in mice, and reduced hind-paw swelling and growth retardation in the adjuvant-induced arthritis model in rats, following oral administration at 10, 20, 40 or 80 mg/kg. The extract (10-80 mg/kg, p.o.) caused an inhibition of increase in vascular permeability in both cyclophosphamide-induced haemorrhagic cystitis and acetic acid-induced vascular permeability in rats and mice, respectively. B. ferruginea produced stabilization of erythrocytes exposed to heat and stress-induced lysis. Antipyretic and analgesic properties of the extract were also observed.

Acetic Acid↗
PubMed1998

Effects of lysine clonixinate on cyclooxygenase I and II in rat lung and stomach preparations.

Lysine clonixinate (LC) is a drug of antiinflammatory antipyretic and analgesic activity that produces minor digestive side-effects. This fact induced us to think that LC is possibly a weak COX-1 inhibitor. In order to investigate our hypothesis we inhibited cyclooxygenase activity with LC or indomethacin (INDO) in rat lung and stomach obtained from rats treated with lipopolysacharide (LPS) and control rats. Rat lung preparations incubated with 14C-arachidonic acid synthesise mainly PGE2. LC at 2.5 and 4.1 x 10(-5) M does not modify the basal production of PGE2 (probably COX-1) but at 6.8 x 10(-5) M significantly inhibited PGE2 production (approximately 48.5% inhibition, P<0.001). On the other hand, INDO at 10(-6) inhibited the basal production of PGE2 by around 73%. In LPS-treated rats, the production of PGE2 was significantly higher than in the lungs of control rats, probably due to the induction of COX-2. The addition of LC at 2.7 and 4.1 x 10(-5) M recovered the control values of PGE2 inhibiting, probably only from COX-2 activity. LC at higher concentrations (6.8 x 10(-5) M) and INDO 10(-6) M inhibited PGE2 formed by COX-2 and also partly by COX-1 activity.

6-Ketoprostaglandin F1 alpha↗
PubMed1998

Mutagenicity assay in Salmonella and in vivo sister chromatid exchange in bone marrow cells of mice for four pyrazolone derivatives.

Phenylbutazone (PB), oxyphenbutazone (OPB), antipyrine (AP) and dipyrone (DP) are four important pyrazolone derivatives mainly used as anti-inflammatory, antipyretic and analgesic drugs. At present these are the most widely used pyrazolone derivatives throughout the world. The widespread use of these drugs are of great concern for human health problems. In the present study these four drugs were tested in mutagenicity assays in Salmonella strains TA97a, TA98, TA100 and TA102 using a plate incorporation assay both with and without S-9 mix and for in vivo sister chromatid exchanges (SCE) in bone marrow cells of mice. The first three drugs were negative in all the tester strains but dipyrone showed a weak mutagenic activity at higher concentrations in all four strains both with and without metabolic activation. In the in vivo SCE assay in male mice, all four drugs showed a statistically significant increase in SCE in bone marrow cells when compared with control.

Animals↗
PubMed2002

Determination of diclofenac in rat bile and its interaction with cyclosporin A using on-line microdialysis coupled to liquid chromatography.

Diclofenac is a potent inhibitor of prostaglandin synthesis, as well as an established antipyretic and analgesic agent. To determine diclofenac in rat bile and investigate its hepatobiliary excretion, a procedure using rapid and sensitive high-performance liquid chromatography coupled to microdialysis sampling system was developed. A shunt linear microdialysis probe was inserted into the common bile duct between the liver and the duodenum for continuous sampling of the drug from bile fluids following intravenous administration of diclofenac (1 mg/kg). Separation and quantitation of diclofenac in the bile dialysates were achieved using a microbore reversed-phase C18 column (150x1.0 mm I.D.; particle size 5 microm) maintained at ambient temperature. Samples were eluted with a mobile phase containing 100 mM sodium dihydrogenphosphate (pH 3.1)-acetonitrile (30:70, v/v), and the flow-rate of the mobile phase was 0.05 ml/min. The UV detector wavelength was set at 280 nm. The concentration-response relationship from the present method indicated linearity (r2>0.995) over a concentration range of 5-5000 ng/ml for diclofenac. Intra-assay and inter-assay precision and accuracy of diclofenac fell well within the predefined limits of acceptability (< or = 15%). The diclofenac in rat bile appeared to have a slow elimination phase, with a peak concentration at 20 min following diclofenac administration. The results demonstrated that diclofenac might be secreted into bile in unconjugated form by a canalicular bile acid transporter, and then go through hepatobiliary excretion. These results may provide good clinical evidence showing the value of diclofenac for the treatment of biliary colic. The elimination half-life of diclofenac in the biliary elimination was prolonged by treatment with cyclosporin A, indicating that the drug-drug interaction might affect the hepatobiliary excretion of diclofenac.

Animals↗
PubMed2000

NO-naproxen modulates inflammation, nociception and downregulates T cell response in rat Freund's adjuvant arthritis.

1. Anti-inflammatory non steroidal drugs releasing NO (NO-NSAIDs) are a new class of anti-inflammatory drugs to which has been added an NO-releasing moiety. These compounds have been shown to retain the anti-inflammatory, analgesic and antipyretic activity of the parent compound but to be devoid of gastrointestinal (GI) toxicity. 2. Freund's adjuvant (FA) arthritis was induced in rats by a single intraplantar injection into the right hindpaw of 100 microl of mycobacterium butirricum (6 mg ml(-1)). The effect of equimolar doses of naproxen (1, 3 and 10 mg kg(-1)) and NO-naproxen (1.5, 4.5 and 16 mg kg(-1)) was evaluated using two dosage regimen protocols: (i) preventive, starting oral administration of the drugs at the time of induction of arthritis and for the following 21 days (day 1 - 21); (ii) therapeutic, starting oral administration of the drugs 7 days after adjuvant injection and for the following 14 days (day 7 - 21). 3. Hindpaw swelling (days 3, 7, 11, 14, 17, 21) and nociception (days 15 and 21) were measured. On day 22 rats were sacrificed, draining lymph nodes were removed and T cells isolated. In vitro proliferation of T cells following stimulation with concanavalin A (0.5 - 5 microg ml(-1)) was measured using a tritiated thymidine incorporation assay. IL-2 receptor expression on T cells was measured by FACS analysis. 4. Naproxen and NO-naproxen showed similar activity in reducing oedema formation in the non-injected (controlateral) hindpaw. Both drugs showed anti-nociceptive effect. NO-naproxen was anti-nociceptive at a dose of 4.5 mg kg(-1) while naproxen showed the same extent of inhibition only at a dose of 10 mg kg(-1). 5. T cells were isolated and characterized by FACS analysis. Stimulation of isolated T cells with concanavallin A in vitro caused a significant increase in thymidine uptake. NO-naproxen at a dose of 4.5 mg kg(-1) inhibited T cell proliferation to the same extent as 10 mg kg(-1) of naproxen. 6. Inhibition of T cell proliferation was well correlated with reduced IL-2 receptor expression on T cells. In addition, NO-naproxen reduced both IL-1beta and TNFalpha plasma levels whilst naproxen reduced IL-1beta levels only. 7. In conclusion, both naproxen and NO-naproxen reduce inflammation and nociception associated with arthritis. In addition NO-naproxen interferes to a larger extent with cellular mechanism involved in T cell activation in rat adjuvant arthritis indicating that introduction of the NO moiety in the naproxen structure increases the effect at the level of the immune system.

Animals↗
PubMed2003

Effects of acetaminophen on constitutive and inducible prostanoid biosynthesis in human blood cells.

1. Acetaminophen, an analgesic and antipyretic drug with weak antiinflammatory properties, has been suggested to act as a tissue-selective inhibitor of prostaglandin H synthases (PGHSs) (e.g. COX-1 and COX-2) through its reducing activity, that is influenced by the different cellular levels of peroxides. 2. We have studied the effects of acetaminophen on inducible and constitutive prostanoid biosynthesis in monocytes and platelets in vitro. To discriminate between the inhibitory effect of the drug on PGHS-isozymes vs PGE-synthases (PGESs), parallel measurements of PGE(2) and thromboxane (TX) B(2) were carried out. Since antioxidant enzymes and cofactors, present in plasma, may affect acetaminophen-dependent inhibition of prostanoids, comparative experiments in whole blood vs isolated monocytes were performed. 3. Acetaminophen inhibited LPS-induced whole blood PGE(2) and TXB(2) production, in a concentration-dependent fashion [IC(50) microM (95% confidence intervals): 44 (27-70) and 94 (79-112), respectively]. Therapeutic plasma concentrations (100 and 300 microM) of the drug more profoundly reduced PGE(2) than TXB(2) (71 +/- 3 vs 54 +/- 4 and 95 +/- 0.8 vs 78 +/- 2%, respectively, mean +/- s.e.mean, n = 6, P < 0.01). 4. Differently, in isolated monocytes stimulated with LPS, both PGE(2) and TXB(2) production was maximally reduced by only 60%. 5 At 100 and 300 microM, the drug caused a similar and incomplete inhibition of platelet PGE(2) and TXB(2) production during whole blood clotting (45 +/- 4 vs 54 +/- 4 and 75 +/- 2 vs 75 +/- 1%, respectively, mean +/- s.e.mean, n = 4). 6 In conclusion, therapeutic concentrations of acetaminophen caused an incomplete inhibition of platelet COX-1 and monocyte COX-2 but in the presence of plasma, the drug almost completely suppressed inducible PGE(2) biosynthesis through its inhibitory effects on both COX-2 and inducible PGES.

Acetaminophen↗
PubMed2005

Preclinical pharmacology of lumiracoxib: a novel selective inhibitor of cyclooxygenase-2.

1. This manuscript presents the preclinical profile of lumiracoxib, a novel cyclooxygenase-2 (COX-2) selective inhibitor. 2. Lumiracoxib inhibited purified COX-1 and COX-2 with K(i) values of 3 and 0.06 microM, respectively. In cellular assays, lumiracoxib had an IC(50) of 0.14 microM in COX-2-expressing dermal fibroblasts, but caused no inhibition of COX-1 at concentrations up to 30 microM (HEK 293 cells transfected with human COX-1). 3. In a human whole blood assay, IC(50) values for lumiracoxib were 0.13 microM for COX-2 and 67 microM for COX-1 (COX-1/COX-2 selectivity ratio 515). 4. Lumiracoxib was rapidly absorbed following oral administration in rats with peak plasma levels being reached between 0.5 and 1 h. 5. Ex vivo, lumiracoxib inhibited COX-1-derived thromboxane B(2) (TxB(2)) generation with an ID(50) of 33 mg kg(-1), whereas COX-2-derived production of prostaglandin E(2) (PGE(2)) in the lipopolysaccharide-stimulated rat air pouch was inhibited with an ID(50) value of 0.24 mg kg(-1). 6. Efficacy of lumiracoxib in rat models of hyperalgesia, oedema, pyresis and arthritis was dose-dependent and similar to diclofenac. However, consistent with its low COX-1 inhibitory activity, lumiracoxib at a dose of 100 mg kg(-1) orally caused no ulcers and was significantly less ulcerogenic than diclofenac (P<0.05). 7. Lumiracoxib is a highly selective COX-2 inhibitor with anti-inflammatory, analgesic and antipyretic activities comparable with diclofenac, the reference NSAID, but with much improved gastrointestinal safety.

Animals↗
PubMed1997

Plasma concentrations after rectal administration of acetaminophen in preterm neonates.

Acetaminophen is frequently administered to infants and children for its antipyretic and analgesic properties. Oral administration is the route of choice in daily practice. In some circumstances this is impractical. Rectal administration of acetaminophen is an alternative route. This study measures plasma concentrations following rectal administration of acetaminophen 20 mg.kg-1 (10% Infants' Tylenol Drops, McNeil Consumer Product Co., diluted with an equal volume of sterile water) in five preterm neonates. Serial arterial blood samples were obtained at 0, 15, 30, 60, 120, and 240 min. Pharmacokinetic parameters were (mean +/- SD): Cmax (maximum plasma concentration) of 8.38 +/- 3.92 micrograms.ml-1 and Tmax (time to reach maximum plasma concentration) of 78.0 +/- 40.2 min. Our results show that 20 mg.kg-1 of acetaminophen rectally results in low plasma levels in preterm neonates.

Acetaminophen↗
PubMed2003

Trends in primary health care consumption by the elderly.

Trends in primary health care consumption were monitored in the elderly (60 or more years of age). Respondents (5162) were picked by random mechanical selection. They were monitored for a complex of characteristics composed of frequency of visits to a GP office, frequency of procedures performed at the GP office, drug prescriptions, frequency (and type) of procedures performed at specialists' offices, and hospitalization. The study was conducted in 1982, 1992, 1993 and 1996. Results were statistically analysed. There was a statistically significant increase in the consumption of primary health care by the elderly: GP office visits rose from 80 % to 98.8 %, and there was a quantitative change in procedure types. There was also a marked increase in drug prescription: from 77 % receiving prescriptions in 1982 to 97 % in 1996. The highest consumption was of cardiotonics, analgesics and antipyretics, which corresponds to an increasing prevalence of chronic diseases and multimorbidity. The results of our studies underline the important role of primary care physicians in the care of the elderly, who represent 80 % of the clientele of their offices in our country.

Aged↗
PubMed2001

Causes of Alzheimer's disease: paracetamol (acetaminophen) today? Amphetamines tomorrow?

Phenacetin was implicated as a causative factor in Alzheimer's disease (AD) in 1971. Although the chief metabolite, paracetamol, was earlier identified as responsible for its analgesic and antipyretic properties, a link with senile plaque formation does not appear to have been previously suspected. In common with paracetamol, so-called recreational drugs (RDs) likewise stimulate free radical activity, and might therefore pose a similar danger in terms of causing AD later in life. The case for regarding the brain as an even more delicate and vulnerable structure than currently believed, at risk especially from substances untested in man but of proven neurotoxicity in rodents and non-human primates, needs to be taken more seriously than at present.

Acetaminophen↗
PubMed1994

Nematicidal activities of two phytoalexins from Taverniera abyssinica.

The traditional analgesic and antipyretic Ethiopian drug "Dingetegna" is made of dried root material of Taverniera abyssinica A. Rich (Leguminosae). In a screening for nematicidal natural products, "Dingetegna" extracts showed strong nematicidal activities towards C. elegans. In the following, medicarpin and 4-hydroxymedicarpin were isolated as nematicidal constituents from the extracts. In a microwell plate assay for nematicidal activity, both compounds exhibited an LD50 of 25 micrograms/ml towards C. elegans. Beside these nematicidal effects, weak cytotoxic and antimicrobial activities were observed. In addition, both compounds inhibited oxygen consumption of axenically grown C. elegans, L 1210 cells, and filamentous fungi. Respiration in sensitive bacteria was not affected. In L 1210 cells, the incorporation of precursors into macromolecules was affected in the presence of glucose, indicating that inhibition of respiration is not the only target site of the compounds.

Animals↗
PubMed2001

Principles of appropriate antibiotic use for acute pharyngitis in adults: background.

The following principles of appropriate antibiotic use for adults with acute pharyngitis apply to immunocompetent adults without complicated comorbid conditions, such as chronic lung or heart disease, and history of rheumatic fever. They do not apply during known outbreaks of group A streptococcus. 1. Group A beta-hemolytic streptococcus (GABHS) is the causal agent in approximately 10% of adult cases of pharyngitis. The large majority of adults with acute pharyngitis have a self-limited illness, for which supportive care only is needed. 2. Antibiotic treatment of adult pharyngitis benefits only those patients with GABHS infection. All patients with pharyngitis should be offered appropriate doses of analgesics and antipyretics, as well as other supportive care. 3. Limit antibiotic prescriptions to patients who are most likely to have GABHS infection. Clinically screen all adult patients with pharyngitis for the presence of the four Centor criteria: history of fever, tonsillar exudates, no cough, and tender anterior cervical lymphadenopathy (lymphadenitis). Do not test or treat patients with none or only one of these criteria, since these patients are unlikely to have GABHS infection. For patients with two or more criteria the following strategies are appropriate: (a) Test patients with two, three, or four criteria by using a rapid antigen test, and limit antibiotic therapy to patients with positive test results; (b) test patients with two or three criteria by using a rapid antigen test, and limit antibiotic therapy to patients with positive test results or patients with four criteria; or (c) do not use any diagnostic tests, and limit antibiotic therapy to patients with three or four criteria. 4. Throat cultures are not recommended for the routine primary evaluation of adults with pharyngitis or for confirmation of negative results on rapid antigen tests when the test sensitivity exceeds 80%. Throat cultures may be indicated as part of investigations of outbreaks of GABHS disease, for monitoring the development and spread of antibiotic resistance, or when such pathogens as gonococcus are being considered. 5. The preferred antibiotic for treatment of acute GABHS pharyngitis is penicillin, or erythromycin in a penicillin-allergic patient.

Acute Disease↗
PubMed2002

Determinants of the cellular specificity of acetaminophen as an inhibitor of prostaglandin H(2) synthases.

Acetaminophen has antipyretic and analgesic properties yet differs from the nonsteroidal antiinflammatory drugs and inhibitors of prostaglandin H synthase (PGHS)-2 by exhibiting little effect on platelets or inflammation. We find parallel selectivity at a cellular level; acetaminophen inhibits PGHS activity with an IC(50) of 4.3 microM in interleukin (IL)-1 alpha-stimulated human umbilical vein endothelial cells, in contrast with an IC(50) of 1,870 microM for the platelet, with 2 microM arachidonic acid as substrate. This difference is not caused by isoform selectivity, because acetaminophen inhibits purified ovine PGHS-1 and murine recombinant PGHS-2 equally. We explored the hypothesis that this difference in cellular responsiveness results from antagonism of the reductant action of acetaminophen on the PGHSs by cellular peroxides. Increasing the peroxide product of the PGHS-cyclooxygenase, prostaglandin G(2) (PGG(2)), by elevating the concentration of either enzyme or substrate reverses the inhibitory action of acetaminophen, as does the addition of PGG(2) itself. 12-Hydroperoxyeicosatetraenoic acid (0.3 microM), a major product of the platelet, completely reverses the action of acetaminophen on PGHS-1. Inhibition of PGHS activity by acetaminophen in human umbilical vein endothelial cells is abrogated by t-butyl hydroperoxide. Together these findings support the hypothesis that the clinical action of acetaminophen is mediated by inhibition of PGHS activity, and that hydroperoxide concentration contributes to its cellular selectivity.

6-Ketoprostaglandin F1 alpha↗
PubMed1979

Aspirin-like drugs interfere with arachidonate metabolism by inhibition of the 12-hydroperoxy-5,8,10,14-eicosatetraenoic acid peroxidase activity of the lipoxygenase pathway.

Aspirin, indomethacin, and sodium salicylate are anti-inflammatory, analgesic, and antipyretic. Whereas aspirin and indomethacin inhibit prostaglandin synthetase (cyclo-oxygenase; 8,11,14-eicosatrienoate, hydrogen-donor: oxygen oxidoreductase, EC 1.14.99.1), salicylate does not. However, all three drugs affect the metabolism of arachidonate via the lipoxygenase pathway by inhibiting the conversion of 12-hydroperoxy- to 12-hydroxy-5,8,10,14-eicosatetraenoic acid.

Arachidonic Acids↗
PubMed2004

Dipyrone overdose.

BACKGROUND: Dipyrone is a pyrazolone derivative used as an analgesic and antipyretic. Agranulocytosis, dipyrone's most serious and potentially fatal adverse effect, has led to its withdrawal in several countries. However, agranulocytosis is subject to geographical variability, ratio with at risks ranging from 0.8-23.7. In many countries dipyrone is still widely used in adults and children and even as an over-the-counter (OTC) preparation. Information on the effects of dipyrone overdose is scanty. OBJECTIVE: To determine the demographic and clinical characteristics of dipyrone overdose. METHODS: Retrospective review of prospectively collected poison center data on acute exposure to dipyrone over a three-year period. The data were subjected to descriptive analysis. Mann-Whitney test and Chi-square analysis were performed where relevant. RESULTS: A total of 243 records met the inclusion and exclusion criteria. Median age was 17y (4m-83y), median amount 5 g (250 mg-45 g), and median time to consultation was 2 h (5 min-48 h). Toxic events (49) occurred in 39 (16%) patients; 57% of these were gastrointestinal and all were mild. Time to consultation was longer in the symptomatic patients (4 h vs. 1.5 h, respectively, p=0.001) and in children (8 h vs. 3.5 h in adults). Suicidal patients ingested significantly larger amounts (8 g vs. 3.7 g, respectively, p=0.001), as did patients with gastrointestinal symptomatology (7.5 g vs. 5 g in asymptomatics, p=0.001). No agranulocytosis was reported. DISCUSSION: Dipyrone overdose is associated with mild, mainly gastrointestinal toxicity; this was noted at a median dose of 7.5 g. Early gastrointestinal decontamination may have prevented toxicity. The suggested treatment includes gastrointestinal decontamination (if <1 h since ingestion) and supportive measures.

Adolescent↗
PubMed2000

Mechanism of action of acetaminophen: is there a cyclooxygenase 3?

Acetaminophen, also known as paracetamol, is a nonsteroidal anti-inflammatory drug with potent antipyretic and analgesic actions but with very weak anti-inflammatory activity. When administered to humans, it reduces levels of prostaglandin metabolites in urine but does not reduce synthesis of prostaglandins by blood platelets or by the stomach mucosa. Because acetaminophen is a weak inhibitor in vitro of both cyclooxygenase (COX)-1 and COX-2, the possibility exists that it inhibits a so far unidentified form of COX, perhaps COX-3. In animal studies, COX enzymes in homogenates of different tissues vary in sensitivity to the inhibitory action of acetaminophen. This may be evidence that there are >2 isoforms of the enzyme. Recently, a variant of COX-2 induced with high concentrations of nonsteroidal anti-inflammatory drugs was shown to be highly sensitive to inhibition by acetaminophen. Therefore COX-3 may be a product of the same gene that encodes COX-2, but have different molecular characteristics.

Acetaminophen↗
PubMed1977

Efficacy and tolerance of Flunixin (SCH 14714) in the treatment of postoperative pain, with observations on the methodology of postoperative pain studies.

A new anti-inflammatory, antipyretic and analgesic drug 2(2'-methyl-3'-trifluoromethylanilino)-nicotinic acid (Flunixin, Sch 14714) was compared with aspirin and a placebo in a double-blind study of pain after four different types of operation. Sch 14714 proved to be superior to the two other drugs after herniorraphy and venous surgery of the leg. The frequency of adverse effects after this drug was, at most. 1.2% which did not differ from the side-effect rates of aspirin or placebo. The second and third days after operation yielded a very high rate of optimal pain relief scores resulting in poor discrimination. Thus cross-over studies seem to be superfluous in the study of pain-relieving drugs in the period following surgery. The patients' rather low demand of analgesic drugs indicated that more stringent enrollment criteria should be adhered to. It was also shown that radical venous surgery constituted a good model for pain studies.

Aniline Compounds↗