Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ACETYLSALICYLIC ACID”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 721 records · Page 40Linked to original sources
PubMed1988

Detection of small inhibitory effects of acetylsalicylic acid (ASA) by platelet impedance aggregometry in whole blood.

Our investigations have demonstrated on 10 volunteers receiving either 500 mg or 100 mg acetylsalicylic acid (ASA) that a low collagen concentration (1 microgram/ml) can best detect the aggregation defect caused by ASA. With the impedance aggregometry the mean inhibition reaches 82% and 52% with 500 mg and 100 mg ASA, respectively. Collagen at higher concentration (3 micrograms/ml) as well as ADP 10 and 25 mumol/l are less sensitive, less than 25% inhibition was recorded. These results suggest that a 1 microgram/ml concentration of collagen is adequate for the control of the ASA effect up to 6 days after intake of 100 mg. Furthermore, the von Willebrand factor (vWF) dependent platelet aggregation induced by 0.6 and 1.0 mg/ml ristocetin was clearly diminished after ASA. Therefore, a ristocetin screening test in whole blood for vWF disorder is possibly distorted when the test is performed within 6 days from ASA administration.

Adult↗
PubMed1991

Effects of acetylsalicylic acid in stroke patients. Evidence of nonresponders in a subpopulation of treated patients.

Platelet reactivity (PR) was tested two and 12 hours after acetylsalicylic acid (ASA) intake in 82 stroke patients, aged 59 +/- 14 years (33 female and 49 male). 10% of these patients showed a pathologically enhanced PR at least two hours after intake of 500 mg ASA (= primary ASA-nonresponder (PNR)). Only 10 hours later, a further 26% of these ASA treated patients exhibited a pathological platelet reactivity (greater than 1.25) (= secondary ASA-nonresponder (SNR)). Single ASA dosages of 500 mg or 200 mg were of identical effectiveness. Additional administration of metoclopramide in combination with 100 mg ASA was more effective as compared to a single dosage of 1000 mg ASA. Those who were SNR at onset of ASA therapy remained SNR as well 28 days later. The change from a normal, ASA corrected PR, to pathological PR values before a period of 12 hours ended seemed a sudden and irreversible event that could only be corrected by the next ASA application.

Aged↗
PubMed1996

Induction of hepatic cytochrome P4502E1 in rats by acetylsalicylic acid or sodium salicylate.

Studies were conducted on the mechanism of the ethanol-inducible cytochrome P450 (cytochrome P4502E1, CYP 2E1) induction by acetylsalicylic acid (ASA) or its metabolite salicylate (SAL). Many exogenous inducers of CYP 2E1 seem to increase CYP 2E1 by post-transcriptional activation without elevation of its mRNA level. Administration of a single high dose of ASA or SAL produces a significant increase in the activity of the hepatic microsomal p-nitrophenol hydroxylase in rats. Pretreatment of ASA-treated rats with a blocker of mRNA transcription, actinomycin D, or a blocker of protein synthesis, cycloheximide, markedly suppressed this enhanced activity of microsomal p-nitrophenol hydroxylase. The CYP 2E1 mRNA levels in livers of control rats and rats treated with ASA or SAL were measured by Northern blot analysis. Significantly elevated CYP 2E1 mRNA levels were measured in livers of treated rats compared with mRNA amounts of the control group. These data suggest that mRNA elevation seems to be characteristic for ASA induction, while other inducing agents show different patterns and mechanisms of activation.

Animals↗
PubMed2005

Emboli rate during and early after carotid endarterectomy after a single preoperative dose of 120 mg acetylsalicylic acid--a prospective double-blind placebo controlled randomised trial.

PURPOSE: To investigate whether a single pre-operative dose of 120 mg acetylsalicylic acid (ASA) decreased either (1) emboli rate, as detected by transcranial Doppler (TCD), during and early after carotid endarterectomy (CEA) and (2) clinical intra- and post-operative signs suggestive of embolism or increased bleeding tendency. DESIGN: Prospective, double-blind placebo controlled trial. PATIENTS AND METHODS: One-hundred consecutive patients were randomised to receive either 120 mg ASA (n = 48) or placebo (n = 49) by suppository on the night before CEA; three patients were excluded. Emboli were counted and expressed as emboli rate (ER). The incidence of bleeding complications was assessed. Surgeons were asked to indicate which patients had received ASA or placebo. RESULTS: There were no significant differences between the ASA and placebo groups in ER in the intraoperative and postoperative periods. ER higher than 0.9 min(-1) was associated with a significantly increased risk of complications (26 vs. 0%, P < 0.01). No extra bleeding complications were observed in the ASA group. Surgeon assessment of whether or not ASA had been administered had a sensitivity of 42% and a specificity of 70%. CONCLUSION: A single pre-operative dose of ASA (120 mg) did not reduce significantly the emboli rate during and after CEA and surgeons could not correctly identify whether or not ASA had been administered.

Aged↗
PubMed2002

Effects of paracetamol and propacetamol on gastric mucosal damage and gastric lipid peroxidation caused by acetylsalicylic acid (ASA) in rats.

We have studied the effect of paracetamol and its pro-drug propacetamol on gastric mucosal damage induced by acetylsalicylic acid (ASA) and its possible relation to changes in gastric lipid peroxidation status in rats. Paracetamol or propacetamol were administered intragastrically 1h before ASA (300 mg kg(-1)) in the following equivalent doses: 62.5, 125.0 and 250.0 mg kg(-1) or 125.0, 250.0 and 500.0 mg kg(-1), respectively. The effects of the tested agents were compared to that of prostaglandin E2 (PGE2) 15, 30 and 60 mg kg(-1). Gastric ulcer formation was estimated morphometrically 4h after ASA administration. Malondialdehyde (MDA), glutathione (reduced, GSH, and oxidized, GSSG) and uric acid (UA) were determined in gastric mucosa and blood plasma and used as biochemical markers of the oxidative status. The results showed that paracetamol (250, 125, 62.5 mg kg(-1)) and propacetamol (500, 250, 125 mg kg(-1)) diminished the area of ASA-induced gastric lesions. The effect of propacetamol was more pronounced than that of paracetamol and similar to that of PGE2. Gastric MDA increased 3-fold in the ASA-group. The tested agents reduced it by a range of 30-70%. In all pretreated groups gastric glutathione and UA levels were found higher than that of control group and lower than that of ASA-group. Paracetamol and propacetamol, as well as PGE2, diminished the lipid peroxidation in plasma to a lesser extent than in gastric mucosa, but maintained elevated levels of the selective plasma antioxidant UA. These results show that the ASA-induced gastric mucosal damage is accompanied by the development of oxidative stress, evidenced by the accumulation of MDA, and concomitant initial activation of cell antioxidant defences. As paracetamol and propacetamol tend to decrease gastric lesions caused by ASA and alter gastric mucosal MDA, glutathione and UA values in a favorable manner, it could be suggested that their effects on the gastric mucosa could be related to interference with oxidative stress development.

Acetaminophen↗
PubMed1980

Acetylation of prostaglandin endoperoxide synthetase with acetylsalicylic acid.

Incubation of purified prostaglandin endoperoxide synthetase from sheep vesicular glands with aspirin results in a covalent binding of the acetyl group of acetylsalicylic acid to the protein. During this acetylation, the cyclooxygenase activity is lost, but not the peroxidase activity. The reaction is completed when almost one acetyl group is bound per polypeptide chain (Mr = 68 000). After proteolysis of [3H]acetyl-protein with pronase, radioactive N-acetylserine was obtained. Originally, however, the hydroxyl group of an internal serine residue in the chain is acetylated. The formation of N-acetylserine can be explained by a rapid O leads to N acetyl shift as soon as the NH2 group of serine is liberated. A radioactive dipeptide was isolated from a thermolysin digest of the [3H]acetyl-enzyme containing phenylalanine and serine, phenylalanine being its N-terminal amino acid. Automatic Edman degradation of native and acetylated enzyme showed that only one polypeptide sequence was present: Ala-Asp-Pro-Gly-Ala-Pro-Ala-Pro-Val-Asn-Pro-X-X-Tyr-. The N-terminal sequence has an apolar character.

Acetylation↗
PubMedDate not supplied

Effect of acetylsalicylic acid on liver plasma membrane Ca2+ ATPase activity.

In the present study, the effects of low- and non-toxic high doses of acetylsalicylic acid (ASA) on liver plasma membrane Ca2+ ATPase activity and also on some membrane lipid components were investigated in rats. ASA was administered to rats by means of a gastric tube at doses of 50 mg/kg and 200 mg/kg, daily, for 30 days. Chronic oral administration of high dose of ASA resulted in significant increases in liver plasma membrane cholesterol and phospholipid levels, whereas the membrane lipids appeared not to be affected by low dose of ASA. Liver plasma membrane Ca2+ ATPase activity was found to be significantly inhibited following high dose of ASA treatment. Low dose of ASA administration caused a slight, but non-significant decrease in enzyme activity. It is concluded that the inhibition of Ca2+ ATPase activity produced by high dose of ASA treatment may be expected to cause Ca2+ accumulation in liver cells, thereby leading to the cell injury.

Animals↗
PubMed1988

[Acetylsalicylic acid pseudoallergy: an anomaly of thrombocyte function?].

After a short historical review, the clinical symptomatology of the pseudoallergic reactions (PAR) after intake of acetylsalicylic acid (ASS) is examined. An intolerance to ASS mostly becomes manifest as bronchial asthma--sometimes up to a status asthmaticus: it is frequently combined with vasomotoric rhinopathia and nasal polyps (so-called "aspirin triad") or as urticaria and angio-edema, seldom as a shock reaction. These symptoms can - in contrast to an allergy--appear at the first intake of the drug. Changes in the arachidonic acid metabolism are of pathogenetic importance, as all substances that inhibit the cyclooxygenase pathway [e.g., most of the nonsteroidal anti-inflammatory drugs (NSAIDs)] are not tolerated by ASS-sensitive patients. Generally, a typical clinical history is sufficient for the diagnosis. Due to the fact that the ASS and NSAID pseudoallergy so far cannot be proved by in vitro methods, oral or inhalative provocation tests are needed when the tolerance situation to the drugs is unknown. However, these tests present high risks. A research group working with Capron (Lille) has recently been able to prove that washed platelets from patients with an analgetic asthma syndrome show an abnormal in vitro response to ASS or NSAID - like indomethacin and fluriprufen - which is characterized by liberation of cytocydal supernatants against parasites, as well as of free O2 radicals, which can be detected by chemiluminescence. Therefore, a platelet anomaly of arachidonic acid metabolism seems to be pathognomonic for ASS asthma. It is not yet known whether or not this is also related to ASS urticaria.(ABSTRACT TRUNCATED AT 250 WORDS)

Arachidonic Acid↗
PubMed1995

[High dosage acetylsalicylic acid administration for prevention of acute cerebral ischemia].

6 studies with a placebo-controlled, double blind, randomized protocol on the effect of acetylsalicylic acid (ASA) in a dosage of higher than 100 mg/day have been published. The preventive effect for TIA was obvious without a significant difference between males and females. The effect on secondary cerebral ischemic attacks after completed infarcts has not been sufficiently proven with the ASA. The preventive effect for cerebral ischemic attacks in normals without preceding strokes or TIA has not been shown.

Aspirin↗
PubMed1984

[Low-dose acetylsalicylic acid (100 mg/day) following aortocoronary bypass operation].

A prospective, randomized, double-blind, placebo-controlled trial was conducted to evaluate the efficacy of Acetylsalicylic Acid (ASS) (100 mg/d, starting 24 h after operation) on vein graft patency. Sixty of 88 patients having undergone surgery entered the study; in 24 of 31 patients in the placebo group and 22 of 29 patients in the ASS-group angiography was performed 4 months postoperatively. There were no significant differences between the groups with respect to age, number of diseased vessels or previous myocardial infarctions. Mean number of grafts per patient was 2,2 (placebo) and 1,8 (ASS) for proximal anastomoses (p less than 0.10) and 3.4 (placebo) and 2.6 (ASS) for distal anastomoses (p less than 0.05). Graft occlusion rate for proximal anastomoses was less in the ASS-group, 10% (4/40), as compared with placebo 32% (17/53) (p less than 0.05). Graft occlusion rate for distal anastomoses was also less in the ASS group, 19% (11/57) as compared to 35% (28/81) in the placebo group (p less than 0.10). All grafts were patent in 16/22 patients in the ASS group but only in 9/24 in the placebo group (p less than 0.05). On designation of patients without postoperative angiograms but cardiovascular events as well as those with at least one graft occluded as "failures", the incidence of the latter was 9/29 in the ASS group and 20/31 in the placebo group (p less than 0.05). Early postoperative bleeding was similar in both groups, no side effects of ASS were observed. In this trial with initiation of low - dose ASS therapy 24 h after operation, antiplatelet therapy reduced the graft occlusion rate significantly.

Aspirin↗
PubMed2004

Acetylsalicylic acid inhibits ATP diphosphohydrolase activity by platelets from adult rats.

BACKGROUND AND METHODS: The in vitro effect of the nonsteroidal anti-inflammatory drug, acetylsalicylic acid (ASA), on the extracellular adenine nucleotide hydrolysis by intact rat blood platelets was studied. RESULTS: Our results demonstrate that aspirin, at final concentrations of 2.0 and 3.0 mM, inhibits ATP extracellular hydrolysis in vitro by approximately 17% and 21%, respectively. Aspirin, at a final concentration of 3.0 mM, also inhibited in vitro extracellular ADP hydrolysis by approximately 41%. The same concentrations of this drug, however, did not alter AMP hydrolysis by intact rat blood platelets under similar assay conditions. The kinetic analysis demonstrated that the inhibition of ADP and ATP hydrolysis by aspirin in rat platelets is of the uncompetitive type. CONCLUSION: In this study, we demonstrated an inhibitory effect of ASA upon E-NTPDase 3 activity of platelets from adult rats and discussed the significance of our findings.

5'-Nucleotidase↗
PubMed1991

Regional effects of indomethacin, acetylsalicylic acid and SC-19220 on the contractility of rabbit renal pelvis (pacemaker regions and pelviureteric junction).

The effects of the cyclooxygenase inhibitors indomethacin and acetylsalicylic acid (ASA) and the prostaglandin (PG) antagonist 1-acetyl-2-[8-chloro-10,11-dihydrodibenz (b,f)(1,4) oxazepine-10-carbonyl]hydrazine (SC-19220) on smooth muscle strips from the rabbit renal pelvis were examined. Circularly oriented tissues were taken from within the renal pelvis and subdivided into the four adjoining regions, from fornix to pelviureteric junction (PUJ). They were set in a tissue bath and isometric tension changes were recorded. Spontaneous contractions were observed and electrical field stimulations evoked twitch-like contractions. The frequency of spontaneous contractions was dependent on the region within the renal pelvis from which they were dissected, gradually decreasing from fornix (3.92/min.) to PUJ (0.43/min.). Indomethacin (10(-5)M) or ASA (10(-4)M) significantly increased the frequencies of spontaneous contractions in all four regions. In the upper three regions (pacemaker regions), both agents significantly decreased the amplitudes of spontaneous and stimulation-induced contractions. In the PUJ region, both agents significantly increased the amplitudes of spontaneous and stimulation-induced contractions. SC-19220 (3 x 10(-5)M) significantly increased the frequencies and decreased amplitudes of spontaneous contractions in all four regions. These results suggest that the PUJ has different contractile characteristics from those of pacemaker regions and that decrease of amplitude by indomethacin or ASA is based on their cyclooxygenase inhibitor property.

Animals↗
PubMed1999

Influence of nutritional status on the pharmacokinetics of acetylsalicylic acid and its metabolites in children with autoimmune disease.

BACKGROUND: It is unknown whether nutritional status associated with autoimmune disease alters the pharmacokinetics of acetylsalicylic acid (ASA) and its metabolites. OBJECTIVE: We studied the effects of the nutritional status of children with autoimmune disease on the disposition of ASA and its metabolites. DESIGN: A prospective, open-label study was performed with 21 children aged 3-15 y who required ASA therapy. Children received 25 mg ASA/kg orally. Blood samples were drawn before and 0.5, 1.0, 2.0, 4.0, 8.0, 12.0, and 24.0 h after ASA administration; urine samples were collected at different intervals. ASA and its metabolites were measured in plasma and urine. Nutritional status was assessed previously. RESULTS: The ASA maximum plasma concentration, area under the curve, and total clearance were significantly lower in underweight children than in normal-weight children. The elimination rate constants of gentisic acid (GA), salicyluric acid (SUA), and salicylic acid (SA) in plasma were slower for underweight children than for normal-weight children. The distribution volume of SUA increased significantly (r = 0.92) when the deficit percentage in weight-for-height increased. Underweight children excreted less GA and SA, but more SUA, than did normal-weight children. CONCLUSIONS: These observations suggest a decrease in the hydrolysis and oxidative reactions of the metabolic pathway of ASA and its metabolites in underweight children. The study illustrates the need for pharmacokinetic data to establish the individual doses of drugs, particularly in conditions that alter nutritional status.

Adolescent↗
PubMed1975

The treatment of rejection. A trial of acetylsalicylic acid, dipyridamole, and heparin.

Serial studies of platelet and fibrinogen survival were performed in 26 nonimmunosuppressed dogs after allogenic renal transplant operations. Treatment with acetylsalicylic acid, dipyridamole, and heparin failed to improve the selective platelet destruction which occurred in untreated animals, and it did not improve postoperative longevity. There was a high incidence of postoperative wound and intrarenal hemorrhage after heparin treatment. These results are consistent with the hypothesis that platelet destruction is a consequence rather than the cause of acute graft rejection, and it is concluded that antithrombotic therapy is not of practical benefit in preventing acute rejection.

Animals↗
PubMed1987

Acetylsalicylic acid inhibits non-immunologic contact urticaria.

To investigate the mechanisms of non-immunologic contact urticaria (NICU), the effects of 1g + 1g of acetylsalicylic acid (ASA) on contact reactions to methyl nicotinate, diethyl fumarate, benzoic acid, cinnamic acid, cinnamic aldehyde and dimethyl sulfoxide were studied in 21 test subjects. Erythema and edema reactions were observed visually, and the changes in the skin blood flow were monitored using laser-Doppler flowmetry. ASA had a significant inhibitory effect on erythema from all 6 agents and also on edema from all substances except dimethyl sulfoxide. The mechanism of the effect may be a result of the inhibitory influence of ASA on prostaglandin bioformation. Thus, to avoid false negative test results, non-steroidal anti-inflammatory drugs should not be used during NICU tests.

Acrolein↗