[Non-narcotic analgesics (antipyretic analgesics, codeine, propoxyphene)].
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Acetaminophen↗
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Further studies on self-administration of antipyretic analgesics and combination of antipyretic analgesics with codeine in rhesus monkeys.
The possible reinforcing effect of acetylsalicylic acid (ASA) was studied in a group of rhesus monkeys that had no history of self-administration of drugs. Rates of lever pressing were compared under conditions in which each lever-pressing response resulted in an infusion of saline, an infusion of saline plus delivery of a food pellet or an infusion of ASA (0.4, 1.0, 2.5 OR 5.0 MG/KG /infusion). Responding was engendered and maintained by the delivery of food pellets but not by infusions of saline alone nor by ASA; however, responding was subsequently engendered and maintained in these monkeys by codeine (0.05 mg/kg/infusion). In another group of monkeys that had been trained to respond under a 10-response fixed-ratio schedule of i.v. infusions of codeine, the possible reinforcing effects of aminophenazone, phenylbutazone and of combinations of each of these drugs with codeine were studied. Aminophenazone and phenylbutazone (0.4-5.0 mg/kg/infusion) did not maintain responding previously engendered by codeine. Mixtures of aminophenazone and phenylbutazone with codeine decreased the number of codeine self-administrations. Thus, codeine intake was reduced when aminophenazone and phenylbutazone were added to codeine in the solution to be self-administered. These experiments suggest that antipyretic analgesics are not effective in reinforcing behavior in the rhesus monkey.
Aminopyrine↗
Antipyretic analgesic drugs as models for studies of drug disposition in old age.
Alterations in drug metabolizing capacity associated with the aging process can be elucidated using analgesic-antipyretic agents as model compounds. Antipyrine serves to profile drug oxidizing capacity. Drug oxidation is significantly impaired in old age, but age-related changes are far greater in men than in women. Acetaminophen analogously serves to profile conjugating capacity, which is minimally influenced by age both in men and in women. Changes in the capacity to biotransform these model compounds are reasonably well predictive of parallel changes in the same person's ability to metabolize other drugs transformed by the same pathway.
Acetaminophen↗
Pharmacological study of ulcerogenic action of antipyretic analgesic agents and their interaction with sodium salicylate.
The present work was undertaken to study and compare the gastric ulcerogenic action of analgesic antipyretic agents in guinea pigs. Their interaction with sodium salicylate was also studied. It was observed that aspirin, both microfined and ordinary, phenylbutazone, indomethacin and sodium salicylate were highly ulcerogenic in guinea pigs, while paracetamol and ibuprofen did not exhibit this action. It was also observed that sodium salicylate did not modify the ulcerogenic action of aspirin (both ordinary and microfined), phenylbutazone, ibuprofen and paracetamol but antagonized significantly the ulcerogenic action of indomethacin.
Animals↗
Prostaglandins and the mode of action of antipyretic analgesic drugs.
Antipyretic analgesics account for more than 95 percent of the analgesic market. The most important agents of this group--salicylates, aniline derivatives such as acetaminophen, and nonacidic pyrazolones--have been used for almost 100 years. Nevertheless, their therapeutic mechanisms and the molecular causes of the most important side effects remain unclear. Several common theories are discussed and challenged.
Animals↗
Renal effects of antipyretic analgesics.
Most antipyretic analgesics can cause acute nephrotoxic effects, including acute tubular necrosis, acute interstitial nephritis, glomerular toxicity, and functional changes, such as "salicyl edema," following large doses of sodium salicylate. Most functional changes are related to acute suppression of prostaglandin synthesis, "the acute prostaglandin-effect," and have been primarily noted with the use of indomethacin. The association between prolonged and excessive consumption of compound analgesics and the development of renal disease and renal failure, characterized by renal papillary necrosis, is now well established. Studies in several countries have shown that the incidence of analgesic nephropathy as an indication for dialysis and transplantation corresponds to the per capita consumption of phenacetin in compound analgesics. Analgesic nephropathy, which is part of a wider clinical syndrome, the analgesic syndrome, is uncommon following the use of single analgesics. Analgesic nephropathy and the analgesic syndrome are discussed in detail, including the development of uroepithelial tumors.
Animals↗
[Nephropathies due to analgesics consumption of antipyretic analgesics in France].
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Acetaminophen↗
[Study on the antipyretic, analgesic effects of qingkailing freeze-dried powder for injection and its antipyretic mechanism].
OBJECTIVE: To investigate the antipyretic, analgesic effects of Qingkailing Freeze-Dried Powder for Injection (QI) and its mechanism of the antipyretic effect. METHODS: The rabbit model of 2, 4-dinitrophenol-induced fever and the rat model of endotoxin-induced fever were established and the body temperatures were observed. Radioimmunoassay was adopted to detect the levels of IL-1beta and cAMP in the hypothalamus of rats. The analgesic effects were tested by hot-plate and writhing reaction method. RESULTS: QI showed marked antipyretic effects on the 2,4-dinitrophenol-induced fever and the endotoxin-induced fever. At the same time, QI remarkably decreased the contents of IL-beta and cAMP in the hypothalamus. QI also remarkably reduced the frequency of acetic acid-induced writhing and delaied the time of licking rear feet. CONCLUSION: QI has antipyretic, analgesic effects. Its mechanism of the antipyretic effects on rats may be inhibiting the production of IL-1beta and accordingly decreasing cAMP in the hypothalamus.
2,4-Dinitrophenol↗
Survey on the utilization of antipyretic analgesic and anti-inflammatory drugs.
OBJECTIVE: To evaluate the prescription of antipyretic analgesic and anti-inflammatory drugs by the medical staff of Nanfang Hospital. METHODS: Drug utilization index (DUI) was used to analyze the prescriptions of antipyretic analgesic and anti-inflammatory drugs to out-patients in the fourth quarter of 2001. RESULTS AND CONCLUSION: In 71.4% of the prescriptions, the DUI ranged from 0.9 to 1.1, indicating basically justified utilization of antipyretic analgesic and anti-inflammatory drugs in Nanfang Hospital though with occasional abuses of somiton tablets. We urge more careful application of these drugs and their compound preparations, especially in infant patients.
Analgesics↗
Separation of five antipyretic analgesics by micellar electrokinetic capillary chromatography.
The derivatives of antipyrine and phenylbutazone are important antipyretic analgesics commonly used in clinical medicine. Although high performance liquid chromatography has been the conventional method used for the analysis of these drugs, in recent years capillary electrophoresis was validated to be a useful method in the analysis of antipyretic analgesics. However, there has been no report on the separation of antipyrine (AP), 4-aminoantipyrine (4-AAP), aminopyrine (APY), dipyrone (DIP) and phenylbutazone (PHE) in the literature. In this paper, a micellar electrokinetic capillary chromatographic (MECC) separation method was described for the five antipyretic analgesics.
Aminopyrine↗
In vitro studies on drug--antibiotic interactions I: analgesics, antipyretics, antimalarials, and tranquilizers.
The antimicrobial effects of some analgesics, antipyretics, antimalarials, and tranquilizers were determined. The phenothiazines were the most active group. The effect of the chosen drugs when combined with a selected number of antibiotics was studied on Staphylococcus aureus and Escherichia coli to determine the type of interaction. Most analgesics, antipyretics, and antimalarials showed either no effect or a synergistic action. However, some exhibited antagonistic effects. All tested tranquilizers were synergistic. Preliminary studies, using electronic absorption spectrometry, indicated that the antagonistic action may be attributed to a physical interaction.
Analgesics↗
FS 205-397: a new antipyretic analgesic with a paracetamol-like profile of activity but lack of acute hepatotoxicity in mice.
FS 205-397 has been designed to mimic or improve the antipyretic/analgesic profile of paracetamol but without inducing hepatic failure. FS 205-397 offers advantages over acetylsalicylic acid since it has caused no gastric lesions in rats and unlike paracetamol it produced no hepatotoxicity in animal models. The antinociceptive potency of FS 205-397 was at least that of acetylsalicylic acid and paracetamol and in some models it was somewhat more potent. FS 205-397 was even active in the hot plate test, a model in which most non-narcotics are inactive. FS 205-397 will offer potent analgesic and antipyretic therapy in man based on an innovative biochemical principle which eliminates the undesirable toxic effects associated with most other non-narcotic analgesics.
Acetaminophen↗
N-trifluoroacetyl derivatives as pharmacological agents. III. Analgesic, antipyretic activities and physicochemical features of some antiinflammatory trifluoroacetanilides.
Further pharmacological (antipyretic and analgesic activities) and physicochemical (pka and relative lipophilicity) studies are reported on some trifluoroacetanilides which have preliminary revealed promising activities in the animal models of acute and chronic inflammation, in analogy with the known antiinflammatory trifluoromethanesulfonanilides.
Acetanilides↗
Analgesic-antipyretic drugs as inhibitors of kallikrein.
The production of kallidin from guinea-pig and ox serum kallidinogen by the action of guinea-pig serum-kallikrein or human salivary kallikrein was inhibited by various analgesic-antipyretic drugs. This effect was obtained in vitro with concentrations of inhibitors which do not inhibit the smooth-muscle-stimulating action of the various polypeptides, but similar to the concentrations needed in vivo to obtain an anti-inflammatory action. The vasodepressor action of intravenously administered human salivary kallikrein in the anaesthetized dog was very markedly inhibited by the intravenous administration of doses of various analgesic-antipyretic drugs which only partially antagonized the responses to kallidin and bradykinin and which left the vasodepressor responses to histamine, acetylcholine and 5-hydroxytryptamine unaffected. In rabbits the accumulation of protein-bound dye at the site of intradermal injection of human salivary kallikrein and guinea-pig serum-kallikrein, but not of bradykinin and kallidin, was inhibited very markedly by the systemic administration of various analgesic-antipyretic drugs.
Acetylcholine↗
Evaluation of analgesic, antipyretic activity and toxicity study of Bryonia laciniosa in mice and rats.
Analgesic, antipyretic activity and toxicity study of the leaves of Bryonia laciniosa Linn. (Family: Cucurbitaceae) was evaluated in the standard animal models. The methanol extract of Bryonia laciniosa (MEBL) was evaluated by hot plate and acetic acid-induced writhing methods to assess analgesic activity. The antipyretic activity of the extract was also evaluated by normal body temperature and yeast-induced hyperpyrexia. The extract showed significant analgesic and antipyretic activity. The MEBL was further evaluated for toxicity at the doses of 125 and 250 mg/kg administered orally for 14 days in rats. At the end of experiments, the blood, liver function and kidney metabolism were observed. The hematological profile and different biochemical parameters such as SGOT, SGPT and ALP were estimated. The present study revealed that MEBL exhibited significant analgesic and antipyretic activity in the tested experimental animal models. The toxicity study indicates that the extract is not toxic at the tested doses.
Alanine Transaminase↗
Spinal cord effects of antipyretic analgesics.
Tissue damage results in the release of inflammatory mediators, including prostaglandins, which sensitive fine nerve endings in the periphery to mechanical and thermal changes. Sensitisation of these nerve endings, or nociceptors, contributes to the phenomenon of hyperalgesia, which routinely accompanies tissue damage. It has been shown that the acidic antipyretic analgesics reduce or down-regulate the enhanced nociceptor sensitivity in damaged tissue, an effect probably attributable to inhibition of prostaglandin synthesis. Recent studies suggest that these drugs may have an additional mechanism of action in the spinal cord or higher centres. When enantiomers of flurbiprofen were used in the rat, it was shown that S- and R-flurbiprofen exert differential antinociceptive effects. The R-enantiomer, which is practically devoid of peripheral cyclo-oxygenase inhibitory activity in vitro, showed comparable analgesic potency to the S-enantiomer, which does inhibit cyclo-oxygenase activity, in experimental models of nociception. It is possible that the antinociceptive action of the R-enantiomer is related to a reduction in prostaglandin synthesis in the CNS rather than at the site of tissue damage, although other mechanisms may also contribute to its antinociceptive action. In contrast to earlier indications, it would appear that a significant part of the antinociceptive action of the antipyretic analgesics is exerted in the spinal cord. The observed accumulation of acidic antipyretic analgesics in inflamed tissue may account for the superior anti-inflammatory activity of these latter compounds.
Analgesics, Non-Narcotic↗
[Study of the risk of analgesic-antipyretic drugs in children].
Poisonings by analgesic-antipyretic drugs in childhood in our country need specific prevention measures because of their incidence and clinical severity. We analysed the clinical-epidemiologic data of 114 cases of poisonings in children under 16 years of age and the results of a questionnaire answered by 507 adults to identify risks factors. The most of these poisonings happened at home; the esposition was accidental in younger children, even if it often depended from therapeutic mishaps; it was more frequently voluntary at the age of 10. Disinformation on risks and lack of appropriate store in the house are the main factors. The prevention therefore must be based either on the education and the use of safe child resistant containers, besides other passive preventive measures.
Accident Prevention↗
Antipyretic analgesics inhibit prostaglandin release from astrocytes and macrophages similarly.
The effect of acid and non-acid antipyretic analgesics on prostaglandin (PG) release from cultured mouse astrocytes and peritoneal macrophages was investigated in order to test the hypothesis that the non-acid compounds are more potent inhibitors of PG formation in brain than in peripheral tissues. Stimulation of the cells by the divalent cation ionophore A 23187 (10(-6) mol/l) induced PG release from astrocytes and macrophages (mainly PGD2 and PGE2, respectively). This PG release was inhibited by acetylsalicylic acid (10(-5) - 10(-6) mol/l) and indomethacin (10(-6) - 10(-9) mol/l) but also by high concentrations (10(-3) - 10(-5) mol/l) of the non-acid compounds 4-methyl-aminophenazone, the main active metabolite of dipyrone (metamizol), and acetaminophen (paracetamol). No difference was found in the inhibitory potency of the drugs in astrocytes and macrophages, suggesting that a specific sensitivity of brain cells toward non-acid antipyretic analgesics does not contribute to their analgesic effect.
Animals↗