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PubMed1999

Acetylsalicylic acid inhibits meningeal nociception in rat.

Although acetylsalicylic acid (ASA) is one of the most commonly administered drugs in the treatment of acute headaches, the sites of its action and the mechanisms of its therapeutic efficacy are still unclear. In this study using extracellular recording we examined the effects of ASA on spontaneous and mechanically evoked activities of neurons within the medullary dorsal horn with input from the parietal dura mater in rat. Their dural receptive fields were identified by von Frey filaments and found to be mainly located at the medial meningeal artery. All units showed spontaneous activity and had convergent input from the face. Neuronal activities were recorded before and after intravenously applied ASA (30 mg/kg) in 13 and saline in four units. Systemic application of ASA inhibited spontaneous and mechanically evoked activity within 15 min after application. Additionally, neuronal activities were recorded before, during and after topical application of ASA (1 mg/ml) onto the parietal dura mater in 5 units. Topically applied ASA inhibited the mechanically evoked activity, whereas the spontaneous activity remained unchanged. It is concluded, that there are different effects of systemic and topical ASA on trigeminal neuronal activity, which may be due to both central and peripheral mechanisms.

Administration, Topical↗
PubMed1992

Direct O-acetylation of N-hydroxy arylamines by acetylsalicylic acid to form carcinogen-DNA adducts.

Acetylsalicylic acid (aspirin) has been shown to acetylate a number of drugs and biological macromolecules. Since enzymatic O-acetylation of N-hydroxy arylamines is regarded as an important activation step for DNA adduct formation, we initially examined the ability of aspirin to serve as an acetyl donor for this reaction, using rabbit liver cytosol. Instead, a direct non-enzymatic reaction was observed. Arylamine-DNA binding was enhanced from 3- to 25-fold at pH 7 by addition of aspirin to reactions containing the N-hydroxy derivatives of 2-aminofluorene (AF), 4-aminobiphenyl, 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline and 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine, but not for 2-amino-3-methylimidazo[4,5-f]quinoline or 2-amino-6-methyldipyrido[1,2-a:3',2'-d]imidazole. Further studies with N-hydroxy-AF showed that reaction rates were first order with respect to both aspirin (0.1-10 mM) and N-hydroxy-AF (0.01-0.1 mM) concentrations. In contrast, aspirin had no effect on reactions conducted at pH 5 where N-hydroxy-AF is known to undergo protonation and react with DNA to form high levels of N-(deoxyguanosin-8-yl)-AF. N-Acetylation of AF by aspirin under these conditions was also negligible. However, the formation of the adduct from N-hydroxy-AF occurred at high yield (64-82%) at pH 7 with either DNA or 2'-deoxyguanosine. HPLC analyses showed only an aspirin-dependent loss of N-hydroxy-AF and concomitant adduct formation, with no detectable formation of solvolysis products. This indicated that the reaction proceeds to a significant extent only upon addition of the nucleophile, and suggests the formation of an O-tetrahedral intermediate that is in equilibrium with both the N-hydroxy derivative and the reactive N-acetoxy arylamine. Thus, the apparent O-acetylation of certain N-hydroxy arylamines selectively by aspirin offers a convenient route for the synthesis of arylamine-DNA adducts. The potential biological significance of this reaction in vivo is also discussed.

Acetylation↗
PubMed1994

Prevention by acetylsalicylic acid of liver cirrhosis and carcinogenesis as well as generations of 8-hydroxydeoxyguanosine and thiobarbituric acid-reactive substances caused by a choline-deficient, L-amino acid-defined diet in rats.

Effects of acetylsalicylic acid (ASA) (aspirin) on the pathogenesis of fatty liver, cirrhosis and hepatocarcinogenesis caused by a choline-deficient L-amino acid-defined (CDAA) diet were examined in male Fischer 344 rats fed a CDAA diet supplemented with 0, 0.1, 0.2, 0.4 or 0.8% ASA for 30 weeks. ASA at concentrations of > 0.2% prevented the development of both cirrhosis and preneoplastic and neoplastic nodules, but without any directly associated prevention of fatty changes. ASA also prevented hepatocyte proliferation and the generation of thiobarbituric acid-reactive substances and 8-hydroxydeoxyguanosine caused by feeding the CDAA diet, analyzed, respectively, after 1, 12 and 12 weeks. The results clearly indicate that the anti-inflammatory drug ASA, which is not a lipotropic factor, can prevent the pathogenesis of cirrhosis and hepatocarcinogenesis caused by a CDAA diet, which is possibly partly associated with the prevention of reactive oxygen species production.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed1970

Acetylsalicylic acid: no chromosome damage in human leukocytes.

Acetylsalicylic acid was added to cultures of human leukocytes at several time periods over a wide range of concentrations (0.1 to 300.0 micrograms per milliliter). Leukocytes were also cultured from human volunteers during the ingestion of two 300-milligram tablets four times daily (2400 milligrams per day) over a 1-month period. No significant increase in chromosome aberrations was detected in vitro or in vivo.

Aspirin↗
PubMedDate not supplied

Examination of parameters determining particle size distribution: acetylsalicylic acid microcapsules.

A method of preparation of acetylsalicylic acid microcapsules has been elaborated. The active ingredient was made suitable for microencapsulation by recrystallization before phase separation coating. Experiments were performed on the basis of factorial design, and parameters which influence the particle size and particle size distribution of microcapsules were characterized quantitatively.

Aspirin↗
PubMed2006

[Resistance to acetylsalicylic acid and clopidogrel: current status].

Resistance to acetylsalicylic acid (ASA) or clopidogrel is understood from the clinical point of view as failure of the drugs to prevent recurrent vascular occlusions. Non-response to ASA and clopidogrel is defined from the laboratory aspect as an inability to cause in vitro detectable platelet function inhibition. It would be beneficial to monitor non-response to ASA or clopidogrel with platelet function methods, which detect the specific effect of these drugs, and thus prevent clinical events caused by failure of therapy. Non-response to ASA and clopidogrel are detected with different platelet function methods, which are not always clinically standardized and are assessing only the global platelet function and not the specific drug effect. Although various studies reporting 5 to 59% non-response for both drugs, support a clinical relevance of ASA and clopidogrel non-response, well-designed clinical prospective trials are required to identify patients with antiplatelet drug resistance. Furthermore, mechanisms explaining this phenomenon of drug resistance are still unknown.

Aspirin↗
PubMed1980

Activity ratio between antiprostacyclin and antiaggregating effects of acetylsalicylic acid, indometacin and ditazole.

The effects of acetylsalicylic acid (ASA) indometacin and ditazole on prostacyclin production from rabbit aortic rings were studied in comparison to their inhibiting activity on platelet aggregation. The result were expressed as the ratio between the drug dose inhibiting by 50% prostacycline production and the minimum oral antiaggregating dose. The following ratios were found: 2.4 for ASA, 7.3 for indometacin and 20.4 for ditazole.

Animals↗
PubMed1983

[Comparative studies on the in vitro dissolution and bioavailability of various acetylsalicylic acid preparations].

For five different brands of acetylsalicylic acid (ASA) preparations the in vitro/in vivo data were determined and tested for comparability. The in vitro dissolution rates were determined by two different methods (Paddle, rotating basket) whereas the in vivo data were obtained from 15 volunteers in a 5-fold cross-over trial. The markedly worse in vitro dissolution (rotating basket) of one preparation is in contrast to the in vivo data which showed bioequivalency of all five preparations. It is doubled that in vitro measurements alone reveal sufficient informations for any predictions of the in vivo characteristics (e.g. bioavailability) of a preparation. It was possible to determine separately ASA and salicylic acid using a highly selective HPLC-method developed by us.

Adult↗
PubMed1995

[Thrombocyte function of healthy probands taking 50 mg of acetylsalicylic acid per day].

The antithrombotic effect of acetylsalicylic acid (ASS) is attributed in part to its inhibitory action on platelet cyclooxygenase and, thereby, thromboxane A2 (TXA2) formation. The therapeutic goal of low-dose ASS regimens was the development of a preparation showing a high inhibitory capacity on platelet TXA2 generation whilst leaving vascular prostaglandin I2 (PGI2) synthesis unaffected, thereby minimizing side effects. The effect of a new acid-resistant preparation of 50 mg ASS (Thrombo-ASS 50 mg) on plasma levels of ASS, salicylate, TXB2, 11-dehydro-thromboxane B2, serum thromboxane B2 and malonyl dialdehyde, the conversion of exogenous 14C-arachidonic acid to TXB2 and hydroxy-5,8,10-heptadecatrienoic acid (HHT), as well as on the urinary metabolites 2,3-dinor-6-oxo-PGF1 alpha and 2,3-dinor TXB2, were compared in a crossover trial to those of a marketed preparation (Aspirin 100 mg) in healthy volunteers after a single dose and repeated administration of ASS. While platelet activity was inhibited by both the test and the reference substance to a comparable extent, vascular PGI2 production (as determined by urinary 2,3-dinor-6-oxo-PGF1 alpha excretion) was less affected by the test substance. These findings confirm the claim that a dosage of 50 mg ASS administered daily as an enteric coated or uncoated tablet is sufficient to almost completely block platelet cyclooxygenase, while the respective vascular enzyme is only minimally affected.

Adult↗
PubMed1994

[Circadian aspects of acetylsalicylic acid induced injury and protective effect of ranitidine on the the upper gastrointestinal tract].

Circadian Aspects of Acetylsalicylic Acid Induced Injury and Protective Effect of Ranitidine on the Upper Gastrointestinal Tract. In a randomised parallel double-blind study the gastric and duodenal effects of 300 mg acetylsalicylic acid (ASA, CAS 50-78-2) daily in the presence and absence of 150 mg ranitidine (Zantic, CAS 66357-35-5) daily was evaluated in 32 healthy volunteers undergoing upper gastrointestinal endoscopy. Drugs were taken over a period of 7 days either at 8 a.m. (n = 16) or at 8 p.m. (n = 16). Endoscopic controls were performed at entry and repeated after 7 days of treatment. At entry both groups showed comparable mucosal damages: 8 a.m. group: ASA/placebo 0.8 +/- 0.1 (stomach) and 0.1 +/- 0.1 (duodenum): ASA/ranitidine 1.0 +/- 0.0 (stomach) and 0.07 +/- 0.06 (duodenum). 8 p.m. group: ASA/placebo 0.9 +/- 0.06 (stomach) and 0.1 +/- 0.09 (duodenum). ASA/ranitidine 0.8 +/- 0.08 (stomach) and 0.07 +/- 0.06 (duodenum). After 7 days of treatment the lesions score increased in the ASA/Placebo group in the 8 a.m. group to 9.1 +/- 1.1 (stomach) and 2.7 +/- 1.0 (duodenum), and in the 8 p.m. group to 10.9 +/- 1.1 (stomach) and to 3.9 +/- 0.9 duodenum). The corresponding values in the ASA/ranitidine group were 2.6 +/- 0.8 (stomach) and 0.2 +/- 0.08 (duodenum) (8 a.m.) and 4.8 +/- 0.8 (stomach) and 0.3 +/- 0.1 (duodenum) (8 p.m.). There was no statistical difference between the morning- and the evening dose of ASA. In addition, ranitidine protection was also time-independent.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2006

[Does acetylsalicylic acid have a negative influence on photodynamic therapy?].

BACKGROUND: Non-thermal photodynamic therapy (PDT) is presently being used for the treatment of certain forms of age-related macular degeneration (AMD). This therapy results in selective occlusion of newly growing vessels. Due to this effectiveness of PDT the question came up whether inhibitors of platelet aggregation have an influence on PDT. PATIENTS AND METHODS: Our retrospective study included 60 patients with mainly classic subfoveal choroidal neovascularizations (CNV) due to AMD. All patients were treated by PDT. Thirty patients took acetylsalicylic acid (aspirin) because of their general disease before and during treatment. In the control group none of the patients took acetylsalicylic acid. RESULTS: Best corrected visual acuity and measured dimension of the choroidal neovascularization showed before beginning PDT no statistically significant difference (visual acuity p=0.676; dimension of CNV p=0.678). Also no significant difference existed between visual acuity (p=0.412; p=0.226; p=0.969) and CNV (p=0.871; p=0.245; p=0.323) at the follow-up examination. CONCLUSION: Our study has shown that acetylsalicylic acid does not have any effect on PDT treatment.

Aged↗
PubMed2004

Reversed-phase capillary electrochromatography for the simultaneous determination of acetylsalicylic acid, paracetamol, and caffeine in analgesic tablets.

The separation and simultaneous determination of caffeine, paracetamol, and acetylsalicylic acid in two analgesic tablet formulations was investigated by capillary electrochromatography (CEC). The effect of mobile phase composition on the separation and peak efficiency of the three analytes was studied and evaluated; in particular, the influence of buffer type, buffer pH, and acetonitrile content of the mobile phase was investigated. The analyses were carried out under optimized separation conditions, using a full-packed silica capillary (75 microm ID; 30.0 cm and 21.5 cm total and effective lengths, respectively) with a 5 microm C8 stationary phase. A mixture of 25 mM ammonium formate at pH 3.0 and acetonitrile (30:70 v/v) was used as the mobile phase. UV detection was at 210 nm. Good linearity was found in the range of 50-200, 20-160, and 4-20 microg/mL for acetylsalicylic acid (r2=0.9988), paracetamol (r2=0.9990) and caffeine (r2=0.9990), respectively. Intermediate precision (RSD interday) as low as 0.1-0.8% was found for retention times, while the RSD values for the peak area ratios (Aanalyte/AIS) were in the range of 1.9-2.9%. The optimized CEC method was applied to the analysis of the studied compounds present in commercial tablets.

Acetaminophen↗
PubMed1997

Effects of meloxicam compared to acetylsalicylic acid in human articular chondrocytes.

Meloxicam is a new nonsteroidal anti-inflammatory drug (NSAID) derived from enolic acid, which has displayed potent anti-inflammatory properties in animal studies combined with low gastrointestinal toxicity. Other NSAIDs have been shown, in vitro, to have a variety of effects on cartilage repair processes in diseased articular cartilage. The aim of this study was to ascertain the effects of meloxicam on some of these processes using in vitro models. Acetylsalicylic acid, a NSAID whose characteristics have been previously elucidated in the models, was used as an active comparator. The effects of meloxicam were different from those of acetylsalicylic acid on chondrocyte clusters. At pharmacologically active concentrations, meloxicam was a potent inhibitor of prostaglandin-E2 production. However, all chondroformative processes were unaffected by meloxicam as indicated by a lack of effect on DNA synthesis and on type-II collagen and proteoglycan levels in chondrocyte culture medium and clusters, while acetylsalicylic acid decreased proteoglycan production and cell proliferation. Consequently, these in vitro findings suggest that meloxicam does not adversely affect the reparative processes active within the cartilage matrix of a diseased joint. This study represents a sound basis for future studies to establish the effects of meloxicam on osteoarthritis disease progression.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1983

Combined ulcerogenic effect of ethanol and acetylsalicylic acid on the gastric mucosa of the rat.

The effect on rat gastric mucosa of ethanol and acetylsalicylic acid given at two doses singly or in combination were studied by administering the drugs into the stomach. 40% ethanol alone caused many ulcerations after 5 h, and the effect was even more marked with simultaneous administration of acetylsalicylic acid (ASA). 10% ethanol and 50 mg ASA/kg b. wt. were tolerated well. The mucosal lesions consisted of coagulation necrosis and hemorrhages, with a disappearance of histamine and serotonin from the mucosal mast cells in and around the lesion.

Animals↗
PubMed2002

Quantitative determination of acetylsalicylic acid and acetaminophen in tablets by FT-Raman spectroscopy.

A procedure for quantitative determination of acetylsalicylic acid and acetaminophen in pharmaceuticals by PLS (partial least squares) and PCR (principal component regression) treatment of FT (Fourier transform)-Raman spectroscopic data is proposed. The proposed method was tested on powdered samples. Three chemometric models were built: the first, for samples consisting of an active substance diluted by lactose, starch and talc; the second, in which a simple inorganic salt was applied as an internal standard and additions were not taken into account; and the third, in which a model was constructed for a commercial pharmaceutical, where all constituents of the tablet were known. By utilising selected spectral ranges and by changing the chemometric conditions it is possible to carry out fast and precise analysis of the active component content in medicines on the basis of the simplified chemometric models. The proposed method was tested on five commercial tablets. The results were compared with data obtained by intensity ratio and pharmacopoeial methods. To appraise the quality of the models, the relative standard error of predictions (RSEPs) were calculated for calibration and prediction data sets. These were 0.7-2.0% and 0.8-2.3%, respectively, for the different PLS models. Application of these models to the Raman spectra of commercial tablets containing acetylsalicylic acid gave RSEP values of 1.3-2.0% and a mean accuracy of 1.2-1.7% with a standard deviation of 0.6-1.2%.

Acetaminophen↗
PubMed2006

Effects of acetylsalicylic acid and acetic acid solutions in VX2 carcinoma cells: in vitro analysis.

PURPOSE: To analyze, in vitro, the effects of acetylsalicylic acid (aspirin) and acetic acid solutions on VX2 carcinoma cells in suspension and to examine the correlation between these effects and neoplastic cell death. METHODS: The VX2 tumor cells (10(7) cells/ml) were incubated in solutions containing differing concentrations (2.5% and 5%) of either acetylsalicylic acid or acetic acid, or in saline solution (controls). Every five minutes, cell viability was tested (using the trypan blue test) and analyzed under light microscopy. RESULTS: Tumor cell viability (in %) decreased progressively and, by 30 minutes, neoplastic cell death had occurred in all solutions. CONCLUSION: Based on this experimental model and the methodology employed, we conclude that these solutions cause neoplastic cell death in vitro.

Acetic Acid↗
PubMed2005

[Antithrombotic therapy after myocardial infarction: arguments for the use of acetylsalicylic acid and coumarin derivatives].

Patients who survived myocardial infarction and who are being treated with the current optimal therapy (antithrombotics, statins and beta-blockers), have a 10-20% chance of death, re-infarction and stroke within in the first year. A possible explanation for this could be an increased activation and generation ofthrombin for at least 6 months following the cardiovascular event preceding preventative therapy. Acetylsalicylic acid and clopidogrel do not affect activation by thrombin of the platelet aggregation and the clotting cascade. The additional use of cumarin derivatives could therefore reduce the chance of recurring thrombotic events, and subsequently improve prognosis. Since the nineteen-nineties several randomised trials have been conducted to study the clinical relevance ofcumarin derivatives both with and without acetylsalicylic acid, in patients who had had a myocardial infarction. The conclusions of these studies were not unambiguous. If the international normalized ratio (INR) was kept > 2 for a long period, by means of frequent check-ups and effective dosage adjustment, the chance of death, recurrent myocardial infarction or stroke was 30-50% lower than when acetylsalicylic acid only was used. The risk of bleeding was raised by 2-4 times, but there were no life-threatening episodes of bleeding. In view of the recent development of anticoagulant agents, for which monitoring seems to be becoming unnecessary, identification of patients who would benefit most from a combined antithrombotic strategy is warranted.

Anticoagulants↗
PubMed1989

Acute damage of gastroduodenal mucosa by acetylsalicylic acid: no prolonged protection by antacids.

Twenty healthy volunteers participated in a double-blind, crossover study to evaluate endoscopically whether low-dose antacids have any prolonged and pH-independent protective capacity against gastroduodenal mucosal damage induced by acetylsalicylic acid. Antacid or placebo one tablet q.d.s. was given for 1.5 days. Acetylsalicylic acid (1.5 g) was administered 3 h after the last dose of antacid/placebo, and gastroscopy was performed 1 h thereafter. Thirteen of 20 subjects showed a decrease in total damage with antacids as compared with placebo, but the difference did not reach statistical significance. Thus, protection by antacids against acetylsalicylic acid-induced gastric mucosal lesions could not be documented at a time when intragastric pH presumably had returned to normal.

Adult↗