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PubMedDate not supplied

Comparison of two enteric-coated acetylsalicylic acid preparations by monitoring steady-state levels of salicylic acid and its metabolites in plasma and urine.

In a randomized three-way crossover study, 12 healthy male volunteers were given multiple oral doses, i.e. 1.5 g b.i.d. for 7 days, of two different types of enteric-coated acetylsalicylic acid (ASA) preparations, one being a conventional enteric-coated tablet (ET) and the other enteric-coated granules (EG) in a capsule; conventional ASA tablets were used as a reference. Plasma levels and excretion of salicylic acid and some of its metabolites were investigated under steady-state conditions. Plasma salicylic acid (SA) and salicyluric acid (SUA) levels were determined using a liquid chromatographic method. Two separate analyses were done to quantitate the metabolites in urine. SA, SUA, and gentisic acid were each assayed by the method used for plasma. Total salicylate was also determined. There was no significant difference in urinary excretion of total salicylate between the three formulations. A diurnal variation in the excretion of SUA and SA in urine was found. The two enteric-coated formulations provided significantly higher morning plasma concentrations than the conventional aspirin. The AUC was found to be significantly higher for ET than for the other two formulations. EG gave more uniform plasma levels during the studied 12-h intervals and also less inter- and intra-individual variations than ET, indicating that a b.i.d. regimen may be suitable for EG.

Adult↗
PubMed1994

Effect of acetylsalicylic acid and dexamethasone on antibody production in adjuvant arthritis.

The production of antibodies to IgG and type II collagen occurs in a similar fashion in human rheumatoid arthritis and adjuvant arthritis. In this study, the effect of dexamethasone (DXT) and acetylsalicylic acid (ASA) on antibody synthesis was analysed. Daily treatment with DXT (0.3 mg/kg per day p.o.) or with ASA (200 mg/kg per day p.o.) from day 14 to day 56 after arthritis induction inhibited both the synthesis of antibodies to IgG and type II collagen and also the humoral immune response to the mycobacteria that induced the disease. The immunosuppressive response was similar for both drugs: DXT, which is known to suppress the immune response, and ASA, a classical anti-inflammatory agent.

Analysis of Variance↗
PubMed1991

Effects of triflusal and acetylsalicylic acid on microthrombi formation in experimental brain ischemia.

Ischemic cerebral infarcts induce hypercoagulation and microthrombosis, thus leading to vessel occlusion and reduction of local cerebral blood flow. Antiaggregant therapy can reduce the formation of microthrombi. We tested the effect of acetylsalicylic acid (ASA) and triflusal (2-acetoxy-4-tri-fluoromethylbenzonic acid) on the formation of microthrombi after middle cerebral artery (MCA) occlusion. Six groups of rats, each consisting of six animals received either ASA or triflusal at dosages of 12.5, 25 or 50 mg/1,000 g b.wt./day. One control group was sham-operated, in another control group MCA occlusion was performed; both groups received no therapy. The number of microthrombi was counted 7 days after MCA occlusion on paraffin sections. The highest number of microthrombi was found in the group with MCAO and without therapy (mean 28 microthrombi/animal). In treated groups a reduction of the number of microthrombi could be stated. The strongest reduction was achieved in the group treated with 12.5 mg triflusal (mean 5.2). No statistic significant difference in the number of microthrombi was found between the groups treated with 12.5 mg triflusal and 50 mg ASA (mean 8.7) compared to sham-operated control animals (mean 4.3, p greater than 0.05). Treatment with 12.5 mg triflusal was superior to 50 mg ASA in preventing microthrombi formation (p less than 0.05). These results indicate, that in experimental brain ischemia the number of microthrombi can be effectively reduced by application of antiaggregatory drugs.

Animals↗
PubMed1982

Effect of acetylsalicylic acid on symptoms and hydrogen excretion in the disaccharide tolerance test with lactose or lactulose.

Prostaglandins play a role in the pathogenesis of symptoms of food intolerance. An alleviation of lactose intolerance by premedication with the prostaglandin-synthesis inhibitor acetylsalicylic acid (ASA) has been reported. We studied the effect of 900 mg of ASA and of a glucose placebo on disaccharide intolerance symptoms and on breath hydrogen (H2) excretion in 16 healthy adult males 12 of whom were lactose malabsorbers and received 50 g of lactose 30 to 40 min after ASA; the remaining four were lactose absorbers and received 30 g of lactulose. Premedication with ASA had no significant effect on the severity and duration of intolerance symptoms and on the timing of H2 excretion. In contrast, the maximal breath H2 concentration and the total H2 excretion were significantly increased after ASA administration. We conclude that prostaglandins are of minor importance in causing the usually moderate symptoms of disaccharide intolerance. Prostaglandin-synthesis inhibition by ASA may reduce the motility of the colon thereby permitting more colonic gas (derived from unabsorbed carbohydrates) to be absorbed and excreted.

Aspirin↗
PubMed1992

In vitro platelets/endothelial cells interactions in presence of acetylsalicylic acid at various dosages.

Venous endothelium is able to release in vitro substances which modifies platelet aggregation. A vascular fragment incubated in Michaelis buffer (pH 7.30), aliquoted and tested on platelet-rich-plasma partially inhibits the aggregometry parameters. Addition of acetylsalicylic acid (ASA) at ultra low dose (0.1 nM final solution in the incubation tube) presents a reversed effect on this inhibition. To explain this phenomenon, 6-keto-PGF1 alpha and von Willebrand factor were dosed in the incubation media. After determination of an active level of 6-keto-PGF1 alpha (200 pg/100 microliters), 2 series were made: series 1 included the values below 200 pg/100 microliters incubation media, series 2, the values above 200 pg/100 microliters incubation media. When the vascular fragment was incubated as described above, the results of aggregometry ratio for series 1 were: test A (without ASA): 0.84 +/- 0.18, test B1 (with 0.1 nM of ASA): 0.87 +/- 0.13. For series 2, they became: test A: 0.75 +/- 0.27, test B1: 0.93 +/- 0.16. Control was always: 1.00 +/- 0.00. For the same groups, 6-keto-PGF1 alpha values were: for series 1, test A: 81 +/- 57, test B1: 81 +/- 60 pg/100 microliters incubation medium, for series 2, test A: 596 +/- 495, test B1: 383 +/- 263 pg/100 microliters incubation medium. Analyses were also performed with 2 high doses of ASA (B2: 10(5) nM and B3: 10(6) nM final solution) in the same experimental conditions. In these groups, aggregation parameters were decreased (0.86 +/- 0.14 for 10(5) nM, 0.84 +/- 0.15 for 10(6) nM) as well as 6-keto-PGF1 alpha production (189 +/- 199 for 10(5) nM, 152 +/- 182 for 10(6) nM). For these two last ASA treatments, comparison of the results in groups set up according to the sensitive 6-keto-PGF1 alpha value (200 pg/100 microliters solution) showed no modification. So it seems that a certain reactive state, specific of ultra low dose treatment is necessary for the vascular endothelium to be sensitive at such treatment.

6-Ketoprostaglandin F1 alpha↗
PubMed1996

Effect of captopril on prostacyclin and nitric oxide formation in healthy human subjects: interaction with low dose acetylsalicylic acid.

1. Angiotensin converting enzyme inhibitors have been suggested to act in part by potentiating the stimulatory effect of bradykinin on endothelial prostacyclin and/or nitric oxide (NO) formation. This may give rise to interaction with cyclo-oxygenase inhibiting drugs like acetylsalicylic acid, which is most often used in low doses in patients with cardiovascular diseases. 2. We investigated the effects of captopril (2 x 25 mg day-1), or ASA (1 x 100 mg day-1), or the combination of both drugs for 7 days, on blood pressure, prostanoid and NO formation rates in a double-blind, double dummy, randomized crossover study in 13 healthy female subjects. The urinary metabolites of thromboxane A2 (2,3-dinor-TXB2) and prostacyclin (2,3-dinor-6-keto-PGF1 alpha), and PGE2 were measured by gas chromatography/tandem mass spectrometry in urine on days 1, 6 and 7 of each medication. NO formation was assessed using urinary NO3- and cyclic GMP as indicators. 3. Urinary 2,3-dinor-6-keto-PGF1 alpha excretion was not significantly changed by either captopril, ASA, or their combination. Urinary 2,3-dinor-TXB2 excretion was inhibited by > 80% by ASA alone or in combination with captopril (each P < 0.05), but was not affected by captopril alone. Urinary PGE2 excretion was not significantly changed by either of the treatments. Urinary NO3- and cyclic GMP excretion rates were not significantly changed by captopril, ASA, or their combination. 4. Blood pressure was slightly reduced by captopril. ASA had no effect on blood pressure when given alone, nor did it modulate the effect of captopril on blood pressure during co-administration. Angiotensin II/angiotensin I ratio (index of ACE activity) was significantly decreased by captopril alone or in combination with ASA, but was unaffected by ASA alone. 5. Captopril does not stimulate prostacyclin formation in healthy human subjects in a dose sufficient to substantially inhibit ACE activity. Co-administration of ASA significantly inhibits 2,3-dinor-TXB2 excretion, but does not interfere with the blood pressure lowering effect of captopril in healthy human subjects.

Adult↗
PubMed2001

Efficacy and safety of metamizol vs. acetylsalicylic acid in patients with moderate episodic tension-type headache: a randomized, double-blind, placebo- and active-controlled, multicentre study.

We assessed the efficacy and safety of oral single doses of 0.5 and 1 g metamizol vs. 1 g acetylsalicylic acid (ASA) in 417 patients with moderate episodic tension-type headache included in a randomized, double-blind, placebo- and active-controlled, parallel, multicentre trial. Eligibility criteria included 18-65 years of age, history of at least two episodes of tension-type headache per month in the 3 months prior to enrollment, and successful previous pain relief with a non-opioid analgesic. Treatment arms were metamizol 0.5 g (n = 102), metamizol 1 g (n = 108), ASA 1 g (n = 102) and placebo (n = 105). The analgesic efficacy of 0.5 and 1 g metamizol vs. placebo was highly statistically significant (alpha: 0.025; one-sided) for sum of pain intensity differences, maximum pain intensity difference, number of patients with at least 50% pain reduction, time to 50% pain reduction, maximum pain relief and total pain relief. A trend towards an earlier onset of a more profound pain relief of 0.5 and 1 g metamizol over 1 g ASA was noticed. All medications including placebo were almost equally safe and well tolerated.

Adolescent↗
PubMed2006

Randomized controlled trial of acetylsalicylic acid in aneurysmal subarachnoid hemorrhage: the MASH Study.

BACKGROUND AND PURPOSE: A previous systematic review of randomized trials suggested a positive effect of antiplatelet therapy in patients with aneurysmal subarachnoid hemorrhage (SAH). We performed a randomized controlled trial to assess whether acetylsalicylic acid (ASA) reduces the risk of delayed ischemic neurological deficit (DIND) in patients with SAH. METHODS: Criteria for inclusion were aneurysm treatment within 4 days after SAH. Trial medication (14 daily suppositories with 100 mg ASA or placebo) was started within 12 hours after aneurysm treatment. Analysis for the primary outcome event DIND was made according to the "on-treatment" principle and for the secondary outcome measures "poor outcome" and "nonexcellent outcome" according to the "intention-to-treat" principle. RESULTS: Inclusion was stopped after the second interim analysis, when 161 of the planned 200 patients were included, because by then the chances of a positive effect were negligible. At the final analysis, ASA did not reduce the risk of DIND (hazard ratio, 1.83; 95% CI, 0.85 to 3.9). The relative risk reduction for poor outcome was 21% (relative risk, 0.79; 95% CI, 0.38 to 1.6). CONCLUSIONS: ASA given after aneurysm treatment does not appreciably reduce the occurrence of DIND.

Aneurysm, Ruptured↗
PubMed1997

Salicylate levels in rat stomach tissues after administration of aspalatone and acetylsalicylic acid in relation to their ulcerogenicity.

To study the mechanism for the low ulcerogenicity of the antithrombotic agent aspalatone ([3-[2-methyl-4-pyronyl)]-2-acetyloxybenzoate, CAS 147249-33-0), the metabolism and disposition of aspalatone were compared with those of acetylsalicylic acid (ASA) in the gut wall in relation to the salicylate level in the stomach tissues following oral administration in pyrolus-ligated rats. Both aspalatone and ASA were essentially stable in gastric juice and were absorbed in stomach unchanged. In glandular portion of the stomach, salicylate level found at 10 min post-dose in aspalatone (80 mg/kg)-and in ASA (50 mg/kg)-treated group was 67 +/- 43 nmol/g tissue and 2000 +/- 250 nmol/g tissue, respectively. In non-glandular (rumen) tissue, salicylate was not detected in the aspalatone group, whereas it reached a concentration of up to 1100 +/- 130 nmol/g tissue in the ASA group. As a result of the relative stability of the ester bond connecting the salicylic acid and maltol groups towards hydrolysis in the stomach and entrapment of ASA due to ion trapping, a lower salicylate level was observed in the stomach after oral aspalatone administration, and this may, at least in part, be the underlying mechanism for the low ulcerogenicity of aspalatone.

Animals↗
PubMed1979

[Clinical-experimental studies on the inhibition of thrombocyte function with acetylsalicylic acid and with indobufen].

The mode of action of two inhibitors of platelet function is reported. At low doses both substances inhibit platelet aggregation, at higher doses they inhibit the availability of platelet factor 3 and liberation of platelet factor 4. Acetylsalicylic acid, however, possesses a long-lasting effect produced by irreversible acetylation of platelet membrane. This was demonstrated in a series of clinico-experimental studies in which 14C-labelled ASA was used. Indobufen was found to cause transitory changes of platelet function. It is easily washed out from platelets and binds loosely to cytosol proteins of platelets, as shown in studies with 14-C-labelled indobufen. In contrast to ASA, it exerts an effect on platelets lasting for a few hours only.

Aspirin↗
PubMed1987

Effects of acetylsalicylic acid on intramuscular bone matrix implants and composite grafts in rats.

Antigen-extracted, autolyzed, demineralized bone matrix and bone matrix combined with isogeneic bone marrow (i.e., a composite graft) were placed in the musculature of young male rats. The influence of acetylsalicylic acid (ASA) on the osteogenic potential of these bone-inducing materials was studied during an 18-day period. ASA (150 mg/kg/12 h) was used to obtain anti-inflammatory serum levels comparable with those in humans. Resorption of the implanted matrix and new formation of bone were quantified using collagen- and mineral-tracing radioisotopes and collagen and calcium analyses. The matrix implants showed a slow tissue turnover and produced only small amounts of new bone, with no significant differences between ASA-treated and control rats. However, during the last 24 h of the study the ASA-treated implants had a significantly hampered rate of new bone formation. The tissue turnover and new bone yield, as well as the rate of new bone formation, increased in the control composite grafts but not in the ASA-treated composite grafts. Thus, the results indicate an inhibitory effect of ASA on the bone-forming capacity of bone marrow.

Animals↗
PubMed1982

Effect of acetylsalicylic acid on renal function in systemic lupus erythematosus.

Glomerular filtration rate (GFR; 51Cr-EDTA clearance), serum creatinine concentration and urinary excretion of prostaglandins were measured in 8 patients with systemic lupus erythematosus (SLE) before and after 2 weeks of treatment with acetylsalicylic acid (ASA). ASA 65 mg/kg or up to 4 g/daily was given as a sustained release preparation. The serum salicylate concentration ranged from 0.3 to 1.6 mmol/l. Serum creatinine after 1 and 2 weeks and GFR after 2 weeks of ASA treatment showed no significant changes. There was a clearcut decrease in urinary excretion of prostaglandins PGE2 and PGF2 alpha, by 44% and 50%, respectively. It is concluded that therapeutic doses of ASA do not cause deterioration of GFR in patients with SLE and normal or moderately reduced renal function.

Adult↗
PubMed1995

Amelioration of radiation nephropathy by acetylsalicylic acid.

This investigation was carried out to assess the amelioration by two antithrombotic drugs of radiation nephropathy in mice. Mouse kidneys were given split-dose irradiation to total doses between 17 and 22 Gy. A first group of animals was given acetylsalicylic acid (ASA) in drinking water, a second received daltroban, a thromboxane A2/prostaglandin H2 receptor antagonist, and a third received normal tap water, serving as a control. Both antithrombotic drugs were started 1 week prior to the irradiation and were given throughout the whole follow-up period. Renal function was assessed every 4 weeks from 18 weeks after the start of irradiation onwards by measuring the [51Cr] EDTA retention and haematocrit. The dose of ASA (600 mg/kg/day) caused an inhibition of thromboxane A2 and prostacyclin biosynthesis to 19 +/- 10 (mean +/- SEM) and 85 +/- 22%, respectively, as assessed by the excretion of their urinary metabolites. A significant sparing effect on the renal function after irradiation was observed in the ASA-treated animals. Using the latency time to reach 4% residual plasma activity of [51Cr] EDTA, a dose-modifying factor of 1.19 was calculated. No effect was seen with daltroban (10 mg/kg/day). Histopathological analysis of the kidneys at 12 months after irradiation demonstrated a substantially lower level of damage in the ASA-treated mice compared with daltroban-treated and radiation-only animals. These data indicate that long-term treatment with ASA is effective in reducing renal functional impairment after irradiation.

6-Ketoprostaglandin F1 alpha↗
PubMed1991

Persistent inhibition of platelet function during long-term treatment with 75 mg acetylsalicylic acid daily in men with unstable coronary artery disease.

One-hundred-and-ninety-three men with unstable coronary artery disease (CAD) (i.e. unstable angina or a non-Q wave myocardial infarction) were randomized in a double-blind fashion to acetylsalicylic acid (ASA) 75 mg daily (n = 100) or placebo (n = 93) within 72 h of admission to the Coronary Care Unit. Platelet function was evaluated as ex vivo aggregation toward collagen and ADP before and after 5 days, 1, 12, 18 and 24 months of treatment. ASA decreased aggregation by collagen 1 mg l-1 from 81.3 +/- 1.7% before to 34.0 +/- 1.7% after 1 month (P less than 0.001), while no change was observed in the placebo group. Aggregation by ADP 1 microM after 1 month was 42.1 +/- 1.1% and 51.0 +/- 2.0% in the ASA and placebo groups respectively (P less than 0.001). The platelet inhibition by ASA was maintained during 24 months. All ASA patients had reduced aggregation during treatment. A cumulative dose of 300 mg (4 doses of 75 mg) was not enough for maximal inhibition at the second aggregation test. Thus, ASA 75 mg daily causes platelet inhibition in all patients without attenuation during long-term treatment. If low dose ASA is started in unstable coronary artery disease a loading dose exceeding 300 mg is suggested.

Adult↗
PubMed1989

Intestinal permeability and antigen absorption in rheumatoid arthritis. Effects of acetylsalicylic acid and sodium chromoglycate.

Intestinal permeability was measured using cow's milk beta-lactoglobulin absorption (BLG) as a permeability marker in 14 patients with active and inactive rheumatoid arthritis (RA) under three different conditions: after a washout period, after treatment with acetylsalicylic acid (ASA) associated with disodium chromoglycate (DSCG), and with ASA only. No intolerance to cow's milk was present and serum IgE levels were in the normal range in 12 of 14 patients. IgG anti-IgE were present in 7 of 13 patients tested. When off treatment the intestinal permeability to BLG in RA patients was not increased as compared to controls, but we found a significative difference between active and inactive RA. ASA administration strongly increased BLG absorption, not prevented by DSCG pretreatment. In normal controls treated with a single dose of ASA we obtained similar results. Our results suggest that prolonged treatment with nonsteroidal anti-inflammatory drugs induces an increase of food antigen absorption, apparently not related to anaphylaxis mediator release, with possible clinical effects.

Adult↗
PubMed2002

Characterization of physical state of mannitol after freeze-drying: effect of acetylsalicylic acid as a second crystalline cosolute.

Freeze-drying of mixed solutes is a preparative technique widely used in the pharmaceutical industry. The presence of an amorphous form or changes in the crystalline form can affect solid state stability. In this work, acetylsalicylic acid (AAS) was chosen as a model drug, and was mixed with mannitol, a commonly used bulking agent in formulation of tablets. Variations in the final freeze-dried crystalline forms were found after changing the ratios of the two co-solutes. Samples were analysed by powder X-ray diffractometry and differential scanning calorimetry. A major amorphous form and a minor crystalline delta-mannitol form were produced during the mannitol freeze-drying process. The crystal form of mannitol in the two-component system depended on the AAS:mannitol ratio. The AAS was mostly crystalline, regardless of the amount of mannitol present. A major delta-mannitol and a minor amorphous form were obtained when AAS was present in a high percentage (75% w/w). When AAS percentages of 50 and 25% (w/w) were present during the drying process, the mannitol was found in a highly crystalline form.

Amides↗
PubMed1994

Effect of acetylsalicylic acid on inhibition of ex vivo platelet aggregation and secretion by SKF 107260, a novel GPIIb/IIIa receptor antagonist.

SKF 107260 is a potent pentapeptide antagonist of the platelet membrane glycoprotein receptor GP IIb/IIIa. The in vitro platelet inhibitory effects of SKF 107260, acetylsalicylic acid (ASA), and their combination, on collagen-induced platelet aggregation and secretion (ATP release) were assessed in human whole blood. Additionally, the concentration-response relationships for these inhibitors were compared for males and females in order to explore gender differences in platelet responsiveness. SKF 107260 caused a concentration-dependent inhibition of platelet aggregation which was significant at concentrations > or = 30 nM. ASA also caused a concentration-dependent inhibition of platelet aggregation which was significant at concentrations > or = 1 mg/dl. The addition of ASA 1 mg/dl to increasing concentrations of SKF 107260 resulted in a more pronounced inhibition of platelet aggregation than when either agent was used alone. These data suggest a pharmacologic interaction, especially at SKF 107260 concentrations < or = 30 nM. Since ATP release was significantly inhibited at concentrations > or = 1 nM, platelet secretion appears to be more sensitive than aggregation to inhibition by SKF 107260. These data suggest that platelet secretion in response to collagen is dependent on the aggregation response mediated by GP IIb/IIIa. In conclusion, SKF 107260 is a potent inhibitor of both whole blood platelet aggregation and secretion and these anti-aggregatory effects may be augmented by concomitant ASA administration.

Adenosine Triphosphate↗
PubMed1994

Effects of nocloprost clathrate on absorption of acetylsalicylic acid.

The cytoprotective prostaglandin E2 analog nocloprost clathrate (NOCLO) is tested as a prophylactic for gastrointestinal lesions of NSAID. The effects of 400 micrograms NOCLO versus respective placebos with and without equivalent amounts of beta-cyclodextrin on the pharmacokinetic behavior of acetylsalicylic acid (ASA), given 30 min after NOCLO, were studied in two single-blind, parallel-group trials. The trials were performed in 15 male healthy volunteers (age 21-25 years, body weight 62-94 kg, body height 172-187 cm) with known N-acetylation and debrisoquine type hydroxylation phenotype. ASA, salicylic acid (SA), and salicyluric acid (SU) in plasma and SA and SU in urine were measured by HPLC. NOCLO delayed the absorption of ASA (increased tmax, lower Cmax) significantly in comparison with both placebos. AUC and clearance values were not changed by NOCLO premedication. There were neither differences between the two placebo groups nor between the two groups pretreated with NOCLO with regard to any pharmacokinetic parameter. The changes in drug absorption are caused by the sum of those cytoprotective effects of prostaglandin which are also determinants of drug absorption.

Acetylation↗