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At least 631 records · Page 35Linked to original sources
PubMed1987

Protective effect of triflusal and acetylsalicylic acid against arachidonic acid induced cerebrovascular occlusion in anesthetized rats.

Within 60 sec after intracarotid injection of 0.33 mg/kg arachidonic acid, a pronounced attenuation of electrocortical activity, approaching electrocerebral silence, was induced in the ipsilateral hemisphere of anesthetized and heparinized rats. This effect was a consequence of the cerebrovascular occlusion due to platelet aggregates induced by arachidonic acid. This model has been used to evaluate the protective effect of acetylsalicylic acid (ASA) and of triflusal 2 hr after a single oral dose of 50 mg/kg or after 50 mg/kg, for 5 days. Pentylenetetrazol at 10 mg/kg, i.v. exerts a stimulant effect on CNS, and was used as a positive control. ASA and triflusal exhibit a protective effect in about 35% of animals when acutely administered. After chronic treatments (5 days), the effect of triflusal (60% protection) was superior to that of ASA (27% protection) (p less than 0.01).

Animals↗
PubMed1993

Acetylsalicylic acid, at high concentrations, inhibits vascular smooth muscle cell proliferation.

The growth of human smooth muscle cells in culture is inhibited by acetylsalicylic acid (ASA). In comparison to control, the proliferation of cells treated with 270 mg/L lysinmono(acetylsalicylate)/30 mg/L glycine was inhibited by 50-90% under different culture conditions. Cell numbers per well (control vs. treated) were as follows: (a) 470,500 +/- 55,890 vs. 24,750 +/- 4,030 (p < 0.002) after 6 days in the presence of 10% fetal calf serum (FCS), (b) 160,500 +/- 9,920 vs. 74,000 (p < 0.001) after 8 days in the presence of 10% human serum; and (c) 387,000 +/- 29,420 vs. 35,250 +/- 1,110 (p < 0.001) after 8 days in the presence of 5% FCS. Significant inhibition of growth by lysinmono(acetylsalicylate) at 90 mg/L was noted only for cultures grown with 10% FCS. Lower concentrations of this drug were ineffective under all culture conditions. Higher dosages of ASA, which would prevent not only platelet aggregation but also smooth muscle cell growth, may therefore be indicated in therapy of patients who undergo percutaneous transluminal coronary angioplasty (PTCA) or coronary artery transplantation.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1983

Systemic availability of acetylsalicylic acid in normal men and women and its effect on in vitro platelet aggregability.

The systemic availability of acetylsalicylic acid (ASA) after oral ingestion of 1 g in an effervescent formulation was 16.3 +/- 2.0% and 16.9 +/- 3.2% of the ingested dose in normal women and men, respectively. The average plasma half-life of ASA in each sex was also identical at 18.5 +/- 1.4 and 18.1 +/- 1.2 min, respectively. The inhibitory effect of ASA on collagen-induced platelet aggregation in vitro on blood from both sexes was studied. The IC50 was 23.9 +/- 2.9 micrograms/ml in females and 22.5 +/- 2.7 micrograms/ml in males, which did not differ significantly. The inhibition by salicylic acid (SA) of the antiaggregatory effect of ASA was similar in both sexes with increases in IC50 to 33.5 +/- 5.1 micrograms/ml in females (p less than 0.02) and to 29.5 +/- 3.8 micrograms/ml in males (p less than 0.05). It is concluded that the observed sex-difference in the antithrombotic effect of ASA cannot be explained neither by differences between females and males in the pharmacokinetic properties of ASA after oral ingestion, nor by differences in the in vitro effect of ASA on the platelet aggregation induced by collagen.

Adult↗
PubMed1981

Effect of acetylsalicylic acid on iron absorption in the rat.

The in vivo administration of 59Fe to the rat accompanied by acetylsalicylic acid (ASA) enhanced significantly counts in blood, spleen, liver and femur without affecting those of the intestine. The results suggest that ASA augments iron absorption either via an inhibitory action on the synthesis of prostaglandins or by a purely chemical mechanism.

Anesthesia↗
PubMed2006

[Acetylsalicylic acid does not alter the mechanoelectrical transduction of mammalian outer hair cells in vitro].

BACKGROUND: High doses of acetylsalicylic acid (ASS) induce tinnitus and hearing loss. This ototoxic side effect of ASS is characterized by a decrease in spontaneous and evoked otoacoustic emissions. A decrease in otoacoustic emissions is found not only in mammals, but also in non-mammalian ears without electromotile outer hair cells. The molecular mechanism underlying ASS ototoxicity seems to be competitive binding to and a block of the motor molecule prestin. In non-mammalian species, ASS ototoxicity is possibly explained by an effect on the hair bundle. RESULTS: The present data from the outer hair cells of the adult guinea pig cochlea show a reduction in the membrane capacitance by maximally 42%, probably as a result of ASS binding competitively to the motor molecule. However, spontaneous and evoked receptor currents were not modulated by ASS. CONCLUSION: The results suggest an influence of ASS on outer hair cell somatic electromotility, without a concomitant effect on hair-bundle function.

Animals↗
PubMed1979

Influence of acetylsalicylic acid on plasma glucose, insulin, glucagon, and growth hormone levels following tolbutamide stimulation in man.

The effects of acetylsalicylic acid (ASA), a known inhibitor of prostaglandin (PG) synthesis, on plasma glucose, insulin, glucagon and growth hormone (GH) responses to tolbutamide were examined in ten normal volunteers. Treatment with 3.2 g ASA daily for 3 days caused a significant reduction in basal plasma glucose levels (p less than 0.05); by contrast, basal insulin rose from 23 +/- 2 to 31 +/- 2 microU/ml (p less than 0.01). No significant changes in the basal concentrations of glucagon and GH were found after ASA. Insulin response to tolbutamide was significantly augmented after ASA (p less than 0.01) while GH response to hypoglycemia was reduced (p less than 0.05). The pattern of plasma glucose and glucagon was not significantly modified by the treatment. Since ASA seems to have an action opposite to PGE on insulin and GH secretion, it is possible that the ASA may work through inhibition of PG synthesis.

Adult↗
PubMed1982

Effect of acetylsalicylic acid on blood glucose and glucose regulatory hormones in mild diabetes.

In order to investigate the effect of acetylsalicylic acid (ASA) on glucose tolerance and glucose regulatory hormones, ASA was given to 14 diabetic patients for seven days by two different methods. A 50 g oral glucose tolerance test (OGTT) was performed before and after the treatment. Nine of 14 diabetics received a dosage of 1.5 g of ASA three times a day for seven days plus 1.5 g on the eighth day one hr before the test (group I). The other 5 patients had the same dosage of ASA as group I, but were not administered ASA prior to the second OGTT (group II). In group I the ASA treatment improved the glucose tolerance associated with sustained rise of plasma insulin significantly, whereas no significant change in glucose tolerance or plasma insulin was observed in group II compared the pretreatment level. The ASA had no significant effect on plasma glucagon or gastric inhibitory polypeptide in either group I or group II. These results suggest that ASA allievates glucose intolerance in maturity onset diabetics by a direct enhancement of insulin secretion, and, moreover, that it is important to maintain elevated ASA concentrations in their blood.

Adult↗
PubMed1984

Effect of acetylsalicylic acid and of indomethacin on diuresis in man: the role of cyclo-oxygenase inhibition.

The effect of acetylsalicylic acid (ASA, 3 g/day for 3 days) and of indomethacin (IND, 150 mg/day for 3 days) on diuresis and on the excretion of prostaglandin E2 (PGE2) was studied in six healthy, male volunteers. After overnight deprivation the subjects received an oral water load (20 ml/kg) and hourly urine volumes were replaced by an equivalent volume of water by mouth for 4 h. Pretreatment with both ASA and IND induced a comparable suppression (P less than 0.05 to less than 0.001) in the excretion of PGE2, but only IND also reduced (P less than 0.05) diuresis, free water clearance and the excretion of sodium. The excretion of creatinine was uninfluenced by both ASA and IND. These data indicate that a mechanism other than cyclo-oxygenase inhibition is involved in the effect of IND and ASA on diuresis in man.

Adult↗
PubMed1997

Inhibition of the growth of 12V-ras-transformed rat fibroblasts by acetylsalicylic acid correlates with inhibition of NF-kappa B.

Epidemiological studies have demonstrated a correlation between regular aspirin (acetylsalicylic acid; ASA) use and a decreased risk for the development of cancer. We here show that ASA inhibits the growth of 12V-ras-transformed rat fibroblasts in vitro at pharmacological concentrations. This effect appeared to be unrelated to inhibition of cyclooxygenase, since other cyclooxygenase inhibitors did not inhibit cell growth. A number of nuclear transcription factors have been implicated as mediators of transformation. ASA has recently been reported to inhibit the activation of one such factor, NF-kappa B. We found that NF-kappa B binding activity was decreased in ASA-treated 12V-ras-transformed cells. Inhibition of NF-kappa B activation was not due to a general inhibitory effect, since AP-1 binding activity was not affected. We conclude that ASA inhibits the growth of 12V-ras-transformed fibroblasts, possibly via inhibition of NF-kappa B.

Animals↗
PubMed1976

Hypersensitivity to acetylsalicylic acid (ASA) and tartrazine in patients with asthma.

One-hundred and forty asthmatics were tested perorally with acetylsalicylic acid (ASA), and/or with the azo-colour tartrazine; a fall in PEF of more than 20% was accepted as a positive result. About one quarter of the patients displayed a positive reaction to one of the two tested agents. No significant correlation was found between the reactions of these, and the presence of atopy, nasal polyposis, sinusitis, rhinitis, sensitivity to cold air, the age at onset, duration of asthma, or history of sensitivity to alcoholic drinks. The history suggested sensitivity to ingested, possibly coloured, food and drink, in only about one third of the tartrazine-positive cases. The ASA provocation tests were mainly applied to patients with doubtful or negative histories of sensitivity to ASA-containing drugs. The frequency of cross-reactivity between the two tested agents was statistically significant; patients reacting to tartrazine were for the most part, also sensitive to ASA. Tests for sensitivity to analgesics and food additives should be conducted as a routine measure in asthmatics, and sensitive patients should be given information on suitable medication and dietary control.

Adolescent↗
PubMed1985

Acetylsalicylic acid and juvenile rheumatoid Arthritis. Effect of dosage interval on the serum salicylic acid level.

A 2-dose regimen and a 3-dose regimen, both with the same daily dose of acetylsalicylic acid, were compared in 8 patients with juvenile rheumatoid arthritis. The regimens were given according to a cross-over design. The serum salicylic acid levels over 24 hours were studied at the end of each treatment period. As expected somewhat greater fluctuations in the salicylic acid levels were observed with the 2-dose than with the 3-dose regimen. However, therapeutically effective serum levels were observed for most of the 24 hour period with both regimens. It is suggested that a 2-dose regimen has advantage with regard to simplicity and compliance. The pharmacokinetic findings indicate that a 2-dose regimen may be useful in patients with juvenile rheumatoid arthritis.

Adolescent↗
PubMed2001

Effect of acetylsalicylic acid on endogenous I kappa B kinase activity in lung epithelial cells.

The anti-inflammatory effect of acetylsalicylic acid (ASA) has been thought to be secondary to the inhibition of prostaglandin synthesis. Because doses of ASA necessary to treat chronic inflammatory diseases are much higher than those needed to inhibit prostaglandin synthesis, a prostaglandin-independent pathway has been emerging as the new anti-inflammatory mechanism of ASA. Here, we examined the effect of ASA on the interleukin (IL)-1 beta- and tumor necrosis factor (TNF)-alpha-induced proinflammatory cytokine expression and evaluated whether this effect is closely linked to the nuclear factor (NF)-kappa B/I kappa B-alpha pathway. A high dose of ASA blocked IL-1 beta- and TNF-alpha-induced TNF-alpha and IL-8 expression, respectively. ASA inhibited TNF-alpha-induced activation of NF-kappa B by preventing phosphorylation and subsequent degradation of I kappa B-alpha in a prostanoid-independent manner. TNF-alpha-induced activation of I kappa B kinase was also suppressed by ASA pretreatment. These observations suggest that the anti-inflammatory effect of ASA in lung epithelial cells may be due to suppression of I kappa B kinase activity, which thereby inhibits subsequent phosphorylation and degradation of I kappa B-alpha, activation of NF-kappa B, and proinflammatory cytokine expression in lung epithelial cells.

Aspirin↗
PubMed1978

Short-term effect of acetylsalicylic acid analogue on pituitary-thyroid axis and plasma cortisol level in healthy human volunteers.

The effect of acetylsalicylic acid analogue (aloxiprinum; Superpyrin Spofa) administered perorally in a daily dose of 1 g per 10 kg body weight on serum levels of free thyroxine (FT4), total thyroxine (T4), triiodothyronine (T3), cortisol (F) and thyrotrophin (TSH) was studied in healthy human volunteers. In a first experiment the drug was administered for 3 days to 7 subjects, the total daily dose being divided into 4-5 aliquots, while the same total dose was administered within 4 h to another 8 subjects in a second experiment. In both experiments a highly significant increase of FT4 was found during the period of treatment, while the levels of other hormones i.e. (T3, T4, F and TSH) were decreased, in most cases significantly. After the withdrawal of the drug there was not only a return of all levels to the initial value, but in most cases an "overshoot" above this value was detected.

Adult↗
PubMed1977

Effects of different doses of acetylsalicylic acid on renal oxygen consumption.

The aim of the present study was to examine the acute effect of acetylsalicylic acid (ASA) on renal oxygen consumption (Qo2) and renal sodium excretion (UNaV) in anaesthetized dogs. With plasma salicylic acid (SA) concentrations ranging from 200-400 microgram/ml, Qo2 increased 36% (P less than 0.05) in spite of a 16% decrease in renal blood flow. At plasma SA concentrations of 80-200 microgram/ml Qo2 was significantly increased 45 min after the onset of ASA infusion. UNaV decreased from 97.7 to 21. 5 mumol/min (P less than 0.05). Glomerular filtration rate and absolute tubular reabsorption of sodium (RNa) was unchanged. The ratio RNa/Qo2 decreased from 31.0 to 21.3 (P less than 0.05). Renal lactate uptake increased. The results are most consistent with an uncoupling affect of ASA on oxidative phosphorylation in the kidney.

Animals↗
PubMedDate not supplied

Effects of aspirin (acetylsalicylic acid) and Cataflam (potassium diclofenac) on some biochemical parameters in rats.

The effects of graded doses of aspirin (acetylsalicylic acid) and cataflam (potassium diclofenac) on serum aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, 5'Nucleotidase, methaemoglobin, total and conjaged bilirubin were investigated in wistar rats. Results showed a significant increase (P < 0.05) in the levels of alanine animotransferase, aspartate amino transferase, methaemoglobin, total and conjugated bilirubin upon treatment of animals with both drugs. Aspirin significantly decreased (P < 0.05, P < 0.00) the activity of alkaline phsophatase but increased the activity of 5'ucleotidase while cataflam significantly increased the activity of alkaline phosphatase (P < 0.001) and 5'nucletodase (P < 0.05). These effects were however dose dependent and the biochemical implications of these results are discussed.

Alanine Transaminase↗
PubMed2002

[Acetylsalicylic acid in primary prevention of cardiovascular events; literature study].

OBJECTIVE: To evaluate literature data on the use of acetylsalicylic acid (ASA) as a primary prevention measure for cardiovascular events. DESIGN: Literature search. METHOD: Using Medline, all randomised placebo-controlled trials of ASA published between 1985 and 1 May 2001, and which used cardiovascular morbidity and death as outcome measures were identified (search query: 'aspirin' and 'primary prevention'). Using the raw data presented in the source publication on death, fatal and non-fatal myocardial infarctions and cerebrovascular accidents (CVAs), all relative and absolute risk reductions were recalculated with confidence intervals. RESULTS: In healthy middle-aged men, men with an increased cardiovascular risk profile and persons with diabetes mellitus or hypertension, the use of ASA reduces the incidence of myocardial infarction and has a neutral effect on cerebrovascular events. The protective effect of ASA seemed most marked in those persons with an increased risk of manifest atherosclerotic vascular disease. CONCLUSION: Notwithstanding these findings, for each patient it remains essential to weigh up the cardiovascular risk profile against the small increased risk of complications when prescribing ASA.

Aged↗
PubMed1992

In vitro effects of Etodolac and acetylsalicylic acid on human chondrocyte metabolism.

The effects of two nonsteroidal anti-inflammatory drugs (NSAIDs), Etodolac (ETO) and acetylsalicylic acid (ASA), used at pharmacological concentrations, were tested on several metabolic parameters of human chondrocytes cultivated in three-dimensional culture. The results indicated that proteoglycan synthesis was significantly decreased by ASA treatment, whereas Etodolac did not affect this parameter. Neither ASA nor Etodolac modified type-II collagen production. Both NSAIDs were potent inhibitors of PGE2 production, but Etodolac was more efficient at equimolar concentrations. In contrast, collagenolytic activity was unaffected by Etodolac.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1986

[Acute injury to the gastric mucosa by acetylsalicylic acid. A comparative endoscopic study in man with oral prostaglandin analogs, omeprazole and ranitidine].

The deleterious effects of acetylsalicylic acid (ASA) on gastric mucosa have been well documented in experimental and clinical studies. With a direct endoscopic assay system we evaluated in healthy volunteers whether pretreatment with prostaglandin analogues (misoprostol, rioprostil), omeprazole and ranitidine prevented ASA-induced gastric mucosal injuries. Ranitidine (2 X 150 mg/d) in large antisecretory doses almost completely abolished these changes (p less than 0.05). By contrast, misoprostol (4 X 50 micrograms/d and 4 X 200 micrograms/d), rioprostil (3 X 100 micrograms/d), omeprazole (5 mg and 10 mg/d) as well as ranitidine in non-antisecretory doses (2 X 25 mg/d) did not reduce gastric mucosal injury after single-dose ASA administration. The results of this trial indicate that socalled cytoprotective doses of prostaglandins, omeprazole and ranitidine in contrast to animal findings are not effective in preventing acute ASA-induced mucosal damage.

Adult↗