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PubMed1991

[Pharmacokinetic interactions between alcohol and acetylsalicylic acid].

Twelve healthy test subjects ingested 0.75 g alcohol/kg body weight in 500 ml carbon dioxide-free mineral water and 1,000 mg powdered acetylsalicylic acid (on average, 13.1 mg/kg body weight) on an empty stomach at 9 a.m. to test the interaction between alcohol and acetylsalicylic acid. Whereas acetylsalicylic acid does not have any effect on the kinetics of alcohol, alcohol effects the metabolism of acetylsalicylic acid. However, an additional restriction of psychophysical performance was not observed.

Adolescent↗

PubMed1979

Dosage of salicylates for children with juvenile rheumatoid arthritis. A prospective clinical trial with three different preparations of acetylsalicylic acid.

41 children with juvenile rheumatoid arthritis (JRA) and 6 with postinfectious arthropathies, aged 3--15 years, were treated with acetylsalicylic acid for 14 days during which time the patients were hospitalized. Three different acetylsalicylic acid preparations were used: a microencapsulated form, an enteric-coated form and standard acetylsalicylic acid tablets. Serum salicylate concentrations were measured by Trinder's photometric method. With doses of 90--120 mg/kg/day symptoms of salicylism appeared in about 50% of the cases. Daily doses of 2 g/m2 (not exceeding 70 mg/kg) proved relatively safe in this study, whereas symptoms and signs of intoxication appeared at doses exceeding 3 g/m2/day. In this respect there were no significant differences between the three acetylsalicylic acid preparations used. The results of this study also suggest that the serum salicylate concentrations should not exceed 2000 mumol/l (about 27 mg/100 ml). The symptoms of salicylism correlated closely with serum salicylate levels, which, in turn, correlated well with the dosage in g/m2. Elevation of serum aspartate aminotransferase was noted in 1/3 of the cases. All of these had a dose exceeding 2 g/m2, and the frequency of elevated enzyme activities increased with increasing dosage. In the group receiving enteric coated form of acetylsalicylic acid, there were fewer positive benzidine tests (12%) than in the two other groups (22--28%).

Adolescent↗

PubMed1983

Comparative study on the effects of acetylsalicylic acid, indomethacin and paracetamol on metabolites of arachidonic acid in plasma, serum and urine in man.

The effects of acetylsalicylic acid, indomethacin and paracetamol on the plasma and serum levels and the urinary excretion of arachidonic acid metabolites in man were demonstrated. The inhibition of prostaglandin synthesis was reflected better in the urinary excretions than in the plasma levels of arachidonic acid metabolites. A clear-cut reduction by acetylsalicylic acid and indomethacin in serum T X B2 can be reached within 24 h. Paracetamol had no uniform influence on the prostaglandins studied. The values returned to the initial level in seven days after indomethacin and in two weeks after acetylsalicylic acid treatment. In some cases a rebound overshoot in prostaglandin concentrations was observed after the discontinuation of the treatment.

Acetaminophen↗

PubMed1988

Sulfation in vitro of mucus glycoprotein by submandibular salivary gland: effects of prostaglandin and acetylsalicylic acid.

Enzymatic sulfation of mucus glycoprotein by rat submandibular salivary gland and the effect of prostaglandin and acetylsalicylic acid on this process were investigated in vitro. The sulfotransferase enzyme which catalyzes the transfer of sulfate ester group from 3'-phosphoadenosine-5'-phosphosulfate to submandibular gland mucus glycoprotein has been located in the detergent extracts of Golgi-rich membrane fraction of the gland. Optimum enzyme activity was obtained at pH 6.8 with 0.5% Triton X-100, 25 mM NaF and 4 mM MgCl2, using the desulfated glycoprotein. The enzyme was also capable of sulfation of the intact mucus glycoprotein, but the acceptor capacity of such glycoprotein was 68% lower. The apparent Km of the submandibular gland sulfotransferase for salivary mucus glycoprotein was 11.1 microM. The 35S-labeled glycoprotein product of the enzyme reaction gave in CsCl density gradient a 35S-labeled peak which coincided with that of the glycoprotein. This glycoprotein upon reductive beta-elimination yielded several acidic 35S-labeled oligosaccharide alditols which accounted for 75% of the 35S-labeled glycoprotein label. Based on the analytical data, the two most abundant oligosaccharides were identified as sulfated tri- and pentasaccharides. The submandibular gland sulfotransferase activity was stimulated by 16,16-dimethyl prostaglandin E2 and inhibited by acetylsalicylic acid. The rate of enhancement of the glycoprotein sulfation was proportional to the concentration of prostaglandin up to 2.10(-5) M, at which point a 31% increase in sulfation was attained. The inhibition of the glycoprotein sulfation by acetylsalicylic acid was proportional to the drug concentration up to 2.5.10(-4) M at which concentration a 48% reduction in the sulfotransferase activity occurred. The apparent Ki value for sulfation of salivary mucus glycoprotein in presence of acetylsalicylic acid was 58.9 microM. The results suggest that prostaglandins may play a role in salivary mucin sulfation and that this process is sensitive to such nonsteroidal anti-inflammatory agents as acetylsalicylic acid.

16,16-Dimethylprostaglandin E2↗

PubMed1996

Dietary (n-3) and (n-6) polyunsaturates and acetylsalicylic acid alter ex vivo PGE2 biosynthesis, tissue IGF-I levels, and bone morphometry in chicks.

This study examined the effects of dietary (n-6) and (n-3) polyunsaturated fatty acids (PUFA) and acetylsalicylic acid (ASA) on bone ash content, morphometry, fatty acid composition, ex vivo PGE2 biosynthesis, tissue IGF-I concentration, and serum alkaline phosphatase (ALPase) activity in chicks. Newly hatched chicks were fed a semipurified diet containing soybean oil (S) or menhaden oil / safflower oil (M) at 90 g/kg. At 4 days of age, chicks were divided into four equal treatment groups receiving 0 mg [symbol: see text] or 500 mg [symbol: see text] of ASA/kg of diet: S[symbol: see text]ASA, M[symbol: see text]ASA, S[symbol: see text]ASA, and M[symbol: see text]ASA. Lipid and ASA treatments did not affect bone length, bone ash, or bone mineral content in chicks. Chicks fed M had increased fractional labeled trabecular surface and tissue level bone formation rates, independent of ASA treatment, compared with those given S. A significant fat x ASA interaction effect was found for trabecular bone volume, thickness, separation, and number. Chicks fed S had higher 20:4(n-6) but lower 20:5(n-3) concentrations in liver and bone compared with those given M. Ex vivo PGE2 biosynthesis was higher in liver homogenates and bone organ cultures of chicks fed S compared with the values for those given M at 17 days. ASA treatment decreased ex vivo PGE2 production in liver homogenates and bone organ cultures of chicks, independent of the dietary lipids. Chicks fed ASA had a lower concentration of IGF-I in tibiotarsal bone compared with those not given ASA at 19 days. Serum ALPase activity was higher in chicks given M compared with those fed S, but the values were reversed with ASA feeding. This study demonstrated that both dietary fat and ASA modulated bone PGE2 biosynthesis, and that (n-3) PUFA and fat x ASA interactions altered bone morphometry.

Alkaline Phosphatase↗

PubMed2004

Life-history traits of standard and autochthonous cladocerans: II. Acute and chronic effects of acetylsalicylic acid metabolites.

Metabolic products are often more toxic than their pharmacological parent compounds. Therefore, the acute and chronic effects of the main metabolites--salicylic acid (SAL), gentisic acid (GEN), and o-hydroxyhippuric acid (HDP)--of acetylsalicylic acid (ASA), the active ingredient in Aspirin and many other pharmaceuticals, were assessed using standard (Daphnia magna) and autochthonous (Daphnia longispina) cladocerans. The sequence of decreasing levels of acute and chronic toxicity of ASA metabolites to daphnids was GEN > SAL > HDP. HDP did not present acute toxicity, but chronic exposures enabled the production of abnormal neonates and, in particular, egg abortion. Thus, reproduction was the end point most susceptible to HDP. On the other hand, SAL and GEN induced changes in the normal patterns of reproduction and growth of both species. In general, D. longispina was more sensitive than was D. magna, although the population growth of the autochthonous species was superior under SAL exposures than that of the standard test species. Although the concentrations that were determined to have a toxic effect were above the levels detected in aquatic environmental samples, exposure to low levels of pharmacologically active substances for a duration longer than the test period may induce changes in nontarget organisms.

Animals↗

PubMed2004

[Acetylsalicylic acid for the primary prevention of cardiovascular disease in diabetic patients].

Large-scale trials have shown that primary prevention using acetylsalicylic acid is useful in all patients with a cardiovascular risk exceeding 1.5% annually. In these patients the benefits of prevention outweigh the risks of bleeding. Almost all patients with diabetes mellitus are at high risk of developing cardiovascular disease. Additionally, most diabetics have other cardiovascular risks besides diabetes, providing further argument for prevention with acetylsalicylic acid. Only very few prospective trials have confirmed that acetylsalicylic acid treatment in patients with diabetes mellitus reduces their risk of cardiovascular disease and myocardial infarction. Treatment with acetylsalicylic acid should be considered in all patients with diabetes, especially in view of their decreased survival after a cardiovascular event, myocardial infarction in particular. If acetylsalicylic acid is contra-indicated treatment with clopidogrel is an alternative.

Aspirin↗

PubMed1980

Arachidonic acid-induced malondialdehyde formation in rat platelets. Kinetic aspects and inhibition by acetylsalicylic acid and indomethacin.

Malondialdehyde (MDA) is a stable product of arachidonic acid metabolism, catalyzed by the enzyme cyclo-oxygenase. The experimental conditions for measuring the kinetic of MDA formation in rat platelet-rich plasma were defined. In platelets stimulated with arachidonic acid MDA formation was almost linear for a limited period of time (between 0 and 2 min) and was concentration-dependent with saturation kinetics. The hyperbolic curves obtained were recast in a linear plot (according to transformation S/V versus S) and straight lines fitting all experimental points were obtained. The apparent Km value of arachidonic acid was 0.49 +/- 0.09 mM and Vmax 1.44 +/- 0.06 nmoles MDA/1.4 x 10(9) platelets/min. The apparent type of inhibition and the relative potency of acetylsalicylic acid and indomethacin on MDA formation were also investigated. Inhibition by both drugs was concentration-dependent, and was much stronger when either drug was preincubated with platelets for 10 min than for 1 min. Analysis of the data by Dixon plots (1/V versus inhibitor concentrations) revealed an apparently competitive type of inhibition. It is suggested that both acetylsalicylic acid and indomethacin inhibit cyclo-oxygenase in platelet-rich plasma by a similar mechanism, not involving covalent binding of either drug to the enzyme.

Animals↗

PubMed1993

Increased susceptibility to metal catalysed oxidation of diabetic lens beta L crystallin: possible protection by dietary supplementation with acetylsalicylic acid.

The effect of dietary supplementation with acetylsalicylic acid on the increased modification, and susceptibility to modification, of lens crystallins from the streptozocin diabetic rat, has been determined. This was done by the measurement of characteristic markers of protein post-translational oxidative modification and glycation, in beta L crystallins purified from the lenses of control, diabetic and acetylsalicylic acid-supplemented diabetic animals, with no further manipulations, and again following the application of an in vitro graded oxidative insult. Crystallins prepared from the diabetic, in comparison with control animals, exhibited a higher level of bityrosine- and AGEP-like fluorescence as well as a loss of tryptophan fluorescence and sulphydryl groups. Exposure to an oxidative insult (in the form of CuSO4 and ascorbate) increased all parameters in beta L crystallins, irrespective of their source. However, the effects were most pronounced in the diabetic in which the effects of oxidative stress were always greater than the control crystallin. Dietary supplementation of the diabetic group with acetylsalicylic acid (100 mg kg-1 body weight day-1) had a marked effect in decreasing the level of modification induced in diabetic crystallins, by in vitro metal catalysed oxidative stress, lowering the levels of AGEP- and bityrosine-like fluorescence and carbonyl group formation. Increasing the oxidative stress by addition of increasing concentrations of H2O2, induced stress proportional increases in the indicators of protein modification in all beta L crystallins, irrespective of source. The increase in damage in relation to H2O2 concentration was greater in those crystallins from diabetic animals, revealing a greater susceptibility to such oxidative stress.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMedDate not supplied

Acetylsalicylic acid reduces viral shedding induced by thermal stress.

PURPOSE: To investigate the effect of acetylsalicylic acid on ocular shedding of herpes simplex virus type 1 (HSV-1). MATERIALS AND METHODS: Mice that were latent for the McKrae strain of HSV-1 were treated with acetylsalicylic acid, a nonspecific inhibitor of cyclooxygenases, either prophylactically or at the time of heat stress-induced viral reactivation. The effect of the drug on viral shedding in the tear film, infectious virus in the cornea and trigeminal ganglion, and viral DNA in the cornea and trigeminal ganglion was determined. RESULTS: Acetylsalicylic acid inhibited heat stress-induced shedding of virus in the tears and reduced the numbers of corneal and trigeminal ganglion homogenates containing virus. Intraperitoneal therapeutic and oral prophylactic plus therapeutic treatments were similar in their ability to inhibit reactivation. CONCLUSIONS: The results indicate that a cyclooxygenase inhibitor such as acetylsalicylic acid can reduce recurrent viral infection in mice. These findings may implicate prostaglandins as agents in the viral reactivation process and suggest that therapy to suppress viral reactivation using nontoxic inhibitors of prostaglandin synthesis may be effective in humans.

Administration, Oral↗

PubMed1993

Impact of treatment with acetylsalicylic acid on the proaggregatory effects of adrenaline in vitro in patients with stable angina pectoris: influence of the anticoagulant.

1. The impact of oral acetylsalicylic acid treatment on the enhancing effect of adrenaline on platelet aggregation in vitro was investigated in patients with stable angina pectoris. In addition, the influence of different anticoagulants (i.e. hirudin and citrate) on platelet aggregation in vitro was compared. 2. Eighty-four patients with stable angina pectoris were studied. Sixteen patients were on acetylsalicylic acid treatment (150-250 mg daily), whereas 68 patients were free from acetylsalicylic acid. Platelet-rich-plasma was prepared from citrate- or hirudin-anticoagulated blood. The EC50 (i.e. the concentration of agonist required to produce half-maximal aggregation) for the ADP-induced extent of aggregation was determined. Thereafter the enhancing effect of adrenaline (10 and 50 nmol/l) on ADP-induced aggregation (at EC50) was investigated. 3. In the patients with angina, acetylsalicylic acid caused the expected effects on ADP-induced platelet responses. Adrenaline significantly enhanced both the extent of aggregation and the initial rate of aggregation (primary aggregation), irrespective of the anticoagulant used. In acetylsalicylic acid-treated patients (citrated platelet-rich plasma) the extent of aggregation was partly inhibited, but no significant effect on the rate of aggregation could be observed. 4. A comparative substudy of the anticoagulants in healthy subjects (n = 8) showed that both the aggregating effect of ADP per se and the enhancing effect of adrenaline on ADP-induced aggregation (at EC50) were less influenced by acetylsalicylic acid when evaluated in hirudinized platelet-rich plasma (i.e. with physiological levels of extracellular calcium) as compared with citrated platelet-rich plasma.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Diphosphate↗

PubMed1999

Subjective gastrointestinal tolerability of acetylsalicylic acid and paracetamol after single dose treatment.

UNLABELLED: A prospective, randomised, double-blind, parallel group, two center, single-dose study was conducted to evaluate and compare the incidence of upper gastrointestinal complaints of acetylsalicylic acid and paracetamol. 600 healthy volunteers received acetylsalicylic acid (2 effervescent tablets of 400 mg), paracetamol (2 effervescent tablets of 500 mg) or placebo (2 effervescent tablets) in three treatment groups. Subjects filled in a questionnaire at 0.5, 1, 2, 3 and 4 h after dosing to evaluate eight upper gastrointestinal symptoms, which were stomach pain, burning sensation, nausea, heartburn, gas, burping, indigestion and upset stomach. The primary study objective was to show equivalence between acetylsalicylic acid and paracetamol. RESULTS: The absolute number of subjects reporting gastrointestinal intolerance were 50 of 200 in the placebo group, 46 of 200 in the paracetamol group and 56 of 201 in the acetylsalicylic acid group. The statistical test showed equivalence between both active substances. CONCLUSION: The rate of gastrointestinal intolerance following a single dose of two effervescent tablets of acetylsalicylic acid is equivalent to that of paracetamol and not different from gastrointestinal intolerance of placebo.

Acetaminophen↗

PubMed1999

Low-dose and high-dose acetylsalicylic acid for patients undergoing carotid endarterectomy: a randomised controlled trial. ASA and Carotid Endarterectomy (ACE) Trial Collaborators.

BACKGROUND: Endarterectomy benefits certain patients with carotid stenosis, but benefits are lessened by perioperative surgical risk. Acetylsalicylic acid lowers the risk of stroke in patients who have experienced transient ischaemic attack and stroke. We investigated appropriate doses and the role of acetylsalicylic acid in patients undergoing carotid endarterectomy. METHODS: In a randomised, double-blind, controlled trial, 2849 patients scheduled for endarterectomy were randomly assigned 81 mg (n=709), 325 mg (n=708), 650 mg (n=715), or 1300 mg (n=717) acetylsalicylic acid daily, started before surgery and continued for 3 months. We recorded occurrences of stroke, myocardial infarction, and death. We compared patients on the two higher doses of acetylsalicylic acid with patients on the two lower doses. FINDINGS: Surgery was cancelled in 45 patients, none were lost to follow-up by 30 days, and two were lost by 3 months. The combined rate of stroke, myocardial infarction, and death was lower in the low-dose groups than in the high-dose groups at 30 days (5.4 vs 7.0%, p=0.07) and at 3 months (6.2 vs 8.4%, p=0.03). In an efficacy analysis, which excluded patients taking 650 mg or more acetylsalicylic acid before randomisation, and patients randomised within 1 day of surgery, combined rates were 3.7% and 8.2%, respectively, at 30 days (p=0.002) and 4.2% and 10.0% at 3 months (p=0.0002). INTERPRETATION: The risk of stroke, myocardial infarction, and death within 30 days and 3 months of endarterectomy is lower for patients taking 81 mg or 325 mg acetylsalicylic acid daily than for those taking 650 mg or 1300 mg.

Aged↗

PubMed2001

LC method for the analysis of acetylsalicylic acid, caffeine and codeine phosphate in pharmaceutical preparations.

An accurate, simple, reproducible and sensitive method for the determination of acetylsalicylic acid, caffeine and codeine phosphate has been developed and validated. Acetylsalicylic acid, caffeine and codeine phosphate were separated using a microBondapack C(8) column by isocratic elution with flow rate 1.0 ml/min. The mobile phase composition was 125/125/250/0.5 (v/v) isopropyl alcohol, acetonitrile, water and o-phosphoric acid. The samples were detected at 215 nm using photo-diode array detector. The linear range of detection for acetylsalicylic acid, caffeine and codeine phosphate were between 0.40 and 1000, 0.25 and 250, and 0.48 and 96 microg/ml, respectively. The linearity, range, selectivity, system performance parameters, precision, accuracy, and ruggedness for acetylsalicylic acid, caffeine and codeine phosphate were also shown to have acceptable values.

Analgesics, Opioid↗

PubMedDate not supplied

Urticaria/angioedema-type sensitivity to aspirin and other nonsteroidal anti-inflammatory drugs. Diagnostic value of anamnesis and challenge test with acetylsalicylic acid.

The aim of this study was to determine the value of challenge tests with acetylsalicylic acid in the diagnosis of ASA-induced urticaria. The study was performed in 71 patients with suspected urticaria/angioedema-type sensitivity to ASA. Anamnesis confirmed sensitivity in 67 patients (94.4%) and showed that sensitive patients usually suffered from extensive urticaria (37 patients, i.e 55.5%) after ingestion of ASA. Eight patients (12%) reacted with loss of consciousness and 4 (6.0%) with edema of the larynx. Oral challenge test with acetylsalicylic acid was performed in 53 patients, in 49 (92.4%) of whom it was positive. Threshold doses of acetylsalicylic acid ranged from 40 to 300 mg. In 11 patients, the test was repeated and in 8 it was performed 3 times. It was observed that both the threshold acetylsalicylic acid doses and the time of appearance of sensitivity symptoms were variable. All ASA-sensitive patients reacted to indomethacin in a similar manner as to ASA. Paracetamol, on the other hand, was well tolerated by all 25 evaluated patients with urticaria/angioedema-type sensitivity to ASA.

Acetaminophen↗

PubMed2000

Effects of caffeine and paracetamol alone or in combination with acetylsalicylic acid on prostaglandin E(2) synthesis in rat microglial cells.

Paracetamol has mild analgesic and antipyretic properties and is, along with acetylsalicylic acid, one of the most popular "over the counter" analgesic agents. However, the mechanism underlying its clinical effects is unknown. Another drug whose mechanism of action is unknown is caffeine, which is often used in combination with other analgesics, augmenting their effect. We investigated the inhibitory effect of paracetamol and caffeine on lipopolysaccharide (LPS)-induced cyclooxygenase (COX)- and prostaglandin (PG)E(2)-synthesis in primary rat microglial cells and compared it with the effect of acetylsalicylic acid, salicylic acid, and dipyrone. Furthermore, combinations of these drugs were used to investigate a possible synergistic inhibitory effect on PGE(2)-synthesis. Both paracetamol (IC(50)=7.45 microM) and caffeine (IC(50)=42.5 microM) dose-dependently inhibited microglial PGE(2) synthesis. In combination with acetylsalicylic acid (IC(50)=3.12 microM), both substances augmented the inhibitory effect of acetylsalicylic acid on LPS-induced PGE(2)-synthesis. Whereas paracetamol inhibited only COX enzyme activity, caffeine also inhibited COX-2 protein synthesis. These results are compatible with the view that the clinical activity of paracetamol and caffeine is due to inhibition of COX. Furthermore, these results may help explain the clinical experience of an adjuvant analgesic effect of caffeine and paracetamol when combined with acetylsalicylic acid.

Acetaminophen↗

PubMed1994

Acetylsalicylic acid--inducer of cytochrome P-450 2E1?

Pretreatment of rats with acetylsalicylic acid or sodium salicylate stimulates the metabolism of dichloromethane to carbon monoxide as measured by the carboxyhemoglobin level in blood. Simultaneous administration of dichloromethane and acetylsalicylic acid or sodium salicylate, respectively, was accompanied by reduced carboxyhemoglobin formation. In liver microsomes of rats pretreated with acetylsalicylic acid the p-nitrophenol hydroxylase activity was increased. It is concluded that (i) cytochrome P-450 2E1 is involved in the metabolic conversion of both dichloromethane and salicylic acid, and (ii) salicylic acid may be an inducer of cytochrome P-450 2E1.

Animals↗

PubMed1983

Improved measurement of acetylsalicylic acid esterase in serum.

A fixed-time incubation method for measuring acetylsalicylic acid esterase was improved by using a higher concentration of the substrate, acetylsalicylic acid, and an activator, Ca2+. The enzymatic activity in serum was 25-fold that measured by earlier methods. Inhibition studies showed a pattern similar to that reported for cholinesterase. Use of cholinesterase inhibitor in sample tubes for determination of acetylsalicylic acid and salicylic acid is recommended.

Adult↗