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At least 127 records · Page 7Linked to original sources

PubMed1986

Maternal ingestion of acetylsalicylic acid inhibits fetal and neonatal prostacyclin and thromboxane in humans.

Small doses of maternal acetylsalicylic acid have proved to prevent preeclampsia. To study the mechanism of this action of acetylsalicylic acid, healthy women ingested 100 mg (n = 13) or 500 mg (n = 14) of acetylsalicylic acid during labor at term. The fetal prostacyclin synthesis, as assessed by the production of 6-ketoprostaglandin F1 alpha (a metabolite of prostacyclin) by the umbilical artery, was reduced from 21.3 +/- 1.6 ng/gm/min of dry weight in the controls (n = 25, mean +/- SE) to 7.8 +/- 1.1 ng/ml/min (p less than 0.001) in infants of mothers receiving 500 mg of acetylsalicylic acid, but it was unchanged in infants with mothers receiving 100 mg of acetylsalicylic acid (19.5 +/- 2.3 ng/gm/min). Maternal ingestion of 500 mg of acetylsalicylic acid also was accompanied by reduced (p less than 0.10) urinary excretion of 6-ketoprostaglandin F1 alpha in neonates during the first 3 days of life. The fetal platelet thromboxane A2 synthesis, as assessed by the release of thromboxane B2 (a metabolite of thromboxane A2) during spontaneous clotting of the umbilical blood (63.4 +/- 4.2 pg/10(5) platelets, n = 22), was inhibited in infants born to mothers given 100 mg (14.0 +/- 3.7 pg/10(5) platelets, p less than 0.001) or 500 mg of acetylsalicylic acid (6.1 +/- 3.5 pg/10(5) platelets, p less than 0.001). The thromboxane B2 release by the umbilical artery (1.1 +/- 0.1 ng/gm/min, n = 13) also was decreased in infants of mothers receiving 500 mg of acetylsalicylic acid (0.57 +/- 0.1 ng/gm/min, n = 7, p less than 0.01). Thus a small dose of maternal acetylsalicylic acid (100 mg) inhibits only the fetoplacental thromboxane A2 but leaves prostacyclin production unaffected.

Adult↗

PubMed1981

[On the pharmacokinetics of tiaprofenic acid and its possible interactions with acetylsalicylic acid and aluminum hydroxide (author's transl)].

To clarify the question whether pharmacokinetic properties of tiaprofenic acid (presumable trade name Surgam) can be changed by simultaneous application of aluminum hydroxide or acetylsalicylic acid (ASA) a randomized study of 7 healthy volunteers was carried out. The results show that the bioavailability as well as the pharmacokinetic profile of orally administered tiaprofenic acid is not changed by the mentioned compounds.

Aluminum Hydroxide↗

PubMed1981

[Comparison of the efficacy of diflunisal and acetylsalicylic acid in rheumatoid arthritis (author's transl)].

Diflunisal, a new difluorophenyl derivative of salicylic acid was compared with acetylsalicylic acid in 16 patients with rheumatoid arthritis in a double-blind study during 8 weeks. All patients who had taken Diflunisal and showed a good therapeutic response were treated with Diflunisal over additional 24 weeks. Diflunisal showed a statistically significant better efficacy than acetylsalicylic acid in all subjective and objective parameters. Above all the grip strength improved greatly in the Diflunisal group. In the patients who were included in the following 24 week study with Diflunisal the successful treatment could be continued through the whole study period. Day-pain and morning stiffness showed statistically significant improvement. Side effects appeared during the double-blind study only in the acetylsalicylic acid group. The results of the study showed Diflunisal in an average dosage of 500 to 1000 mg per day to be a useful drug in the treatment of rheumatoid arthritis not least due to the negligible side effects.

Adult↗

PubMed1996

Lack of influence of glycine on the single dose pharmacokinetics of acetylsalicylic acid in man.

Galenic formulations consisting of acetylsalicylic acid and glycine were developed to improve solubility of the drug, even in case of ingestion without intake of water. It was the aim of this study to investigate the potential influence of glycine on pharmacokinetics after single oral administration of 1,000 mg of acetylsalicylic acid. Therefore, a bioequivalence study using a randomized crossover design (reference = without glycine, test = with glycine) in 12 healthy male volunteers (age 22 - 38 (median 26) years, body weight 64 - 83 (median 75) kg) was performed. Pharmacokinetic characteristics (AUC, Cmax, tmax, t1/2, MRT) were taken or calculated on the basis of plasma concentration/time profiles. For both acetylsalicylic acid and salicylic acid the 90% confidence intervals of the ratios of the expected median values (microT and microR) for the primary characteristics AUC and Cmax of the test and reference formulation were included in the equivalence range of 80 - 125%, which in case of multiplicative model is accepted for concluding bioequivalence. Therefore, lack of influence of glycine on the pharmacokinetics of acetylsalicylic acid including its major metabolite salicylic acid was concluded.

Adult↗

PubMed1988

Inhibitory effect of acetylsalicylic acid on platelet function in patients with completed stroke or reversible ischemic neurologic deficit.

The purpose of our study was to investigate the effects of different doses of acetylsalicylic acid on platelet aggregation. Among inpatients of the National Taiwan University Hospital, 236 cases of completed stroke and seven cases of reversible ischemic neurologic deficit that were diagnosed by computed tomography of the brain and that had not ingested acetylsalicylic acid or acetylsalicylic acidlike drugs for greater than 2 weeks before admission were selected for this study. Thromboxane B2 and 6-keto-PGF1 alpha were measured by radioimmunoassay, threshold concentration of adenosine diphosphate was measured by Born's method, and circulating platelet aggregates were measured by the method of Wu and Hoak. Various single doses of acetylsalicylic acid (75, 300, or 600 mg) or 300 mg acetylsalicylic acid every 6 hours for four doses or one dose of 300 mg acetylsalicylic acid with 75 mg dipyridamole significantly suppressed the mean plasma thromboxane B2 concentrations and elevated the mean adenosine diphosphate threshold concentrations. Abnormal plasma thromboxane B2 concentrations, adenosine diphosphate threshold concentrations, or circulating platelet aggregate ratios were significantly normalized after administration of these regimens. The effects were not significantly different among treatment groups. Forty milligrams of acetylsalicylic acid seemed to have less platelet-inhibitory effect. A single dose of 75 mg acetylsalicylic acid significantly inhibited platelet hyperfunction and effectively corrected the abnormal plasma thromboxane B2 concentrations, adenosine diphosphate threshold concentrations, and circulating platelet aggregate ratios. Higher doses did not enhance the inhibitory effect. In addition, this single dose of acetylsalicylic acid did not significantly suppress plasma 6-keto-PGF1 alpha. We conclude that 75 mg acetylsalicylic acid per day is adequate to inhibit platelet hyperfunction.

Adenosine Diphosphate↗

PubMed1992

[The effect of low-dose acetylsalicylic acid on platelet aggregation parameters in vitro].

In order to elucidate whether a single dose of 150 mg acetylsalicylic acid three times a day, provokes significant changes into platelet aggregation, we analyzed a group of 50 patients who underwent coronary revascularization. During 48 hours before surgery, all patients received 100 mg dipyridamole orally every 6 hours and 1 hour after the end of the operation 100 mg dipyridamole via nasogastric tube. Patients were then randomized into three groups to receive 3 times a day a capsule containing: 50 mg acetylsalicylic acid, 50 mg acetylsalicylic acid plus 75 mg dipyridamole or placebo. Before the antiplatelet therapy was started, the day of the operation and 5 days after the onset of the treatment, blood samples were taken to determine platelet aggregation (turbidimetric technique) and the thromboxane A2 liberation. The three groups were comparable for all the studied clinical and angiographic variables. Preoperative dipyridamole did not provoke significant changes in platelet aggregation (acetylsalicylic acid group 86.5 +/- 10% vs 71 +/- 28.8%; acetylsalicylic acid + dipyridamole group 81.5 +/- 7.8% vs 75.3 +/- 22.7%; placebo group 83.7 +/- 8.9% vs 70 +/- 21.5%). After 5 days of treatment with acetylsalicylic acid, both groups under active treatment showed a significant (p less than 0.001) decrease of aggregability (acetylsalicylic acid 12.8 +/- 4.4%; acetylsalicylic acid + dipyridamole 20.5 +/- 17%; placebo 72 +/- 21.5%).(ABSTRACT TRUNCATED AT 250 WORDS)

Aspirin↗

PubMed1976

Effects of various amino acids on gastric lesions induced by acetylsalicylic acid (ASA) and gastric secretion in pylorus-ligated rats.

The simultaneous oral administration of various amino acids such as L-lysine, L-arginine, L-histidine, L-serine and others at 750, 250 or 83.3 mg/kg in pylorus-ligated rats produced a marked prevention of the gastric mucosal damages caused by oral acetylsalicylic acid (ASA) at 100 mg/kg. In regard with L-lysine and L-arginine, it was assumed that these amino acids might inhibit the ASA-induced gastric lesions through neutralization of acid because of the high alkalinity of these amino acids. In addition, the lesser effect of the hydrochoride salts of these amino acids as compared with the free form on ASA-induced gastric lesions was observed. The other effective amino acids markedly prevented the back diffusion of acid in response to ASA, suggesting as one of the possible mechanisms of lesion formation. However, L-cysteine, which exerted insignificant effect on ASA-induced gastric lesions, also prevented the back diffusion of acid even though the Na+ concentration had not returned to the control level.

Amino Acids↗

PubMed1988

[Changes in stomach and duodenal mucosa caused by acetylsalicylic acid therapy].

The ulcerogenic effect of acetylsalicylic acid on the gastric and duodenal mucosa is well known. In a retrospective survey we analysed 1203 gastroscopic investigations from 1980 to 1986. Of these patients 47 were under therapy with acetylsalicylic acid for at least 4 weeks and 39 of them (82.9%) showed pathologic changes of the gastric and duodenal mucosa. The residual 1156 patients received no therapy; among these only 426 patients (36.8%) showed pathologic changes of the gastric and duodenal mucosa. The significant difference in the incidence of peptic lesions of the gastroduodenal mucosa between the two patient groups confirms the existence of an ulcerogenic side effect of acetylsalicylic acid.

Aspirin↗

PubMed1992

Effect of continuous, long-term administrations of acetylsalicylic acid on hematological and hemocoagulation changes in the rat.

Acetylsalicylic acid is currently being widely used either itself or in combination with the other substances for the prevention of thromboembolic events. Its effect is particularly given by the inhibition of the cyclooxygenase enzyme participating in the metabolism of eicosanoids. The recommended doses of acetylsalicylic acid as well as frequency of administrations are very different. The present work is aimed at estimating the effect of the continuous administration of acetylsalicylic acid for 28 days on hematological and hemocoagulation changes in the rat. The experimental results suggest that long-term administrations of acetylsalicylic acid should be used cautiously in human medicine. They signalize the need of long-term, aimed clinical studies of hematological parameters of patients preventively treated with acetylsalicylic acid, also with respect to the producer of this substance. It is also impossible to neglect regular controls of necessary parameters for the estimation of the efficiency of the given therapy in each patient with respect to individual reactions. The dosage should also be adjusted with respect to the age, sex and individual sensitivity of the organism.

Animals↗

PubMed1995

Chronopharmacological study of acetylsalicylic acid in mice.

Influence of dosing time on pharmacological effects and toxicity of acetylsalicylic acid was investigated in ICR male mice under light-dark (12:12) cycle. Significant circadian rhythms (day-night rhythms) were demonstrated for hypothermal and analgesic effects at 1 h after an injection of acetylsalicylic acid (200 mg/kg, i.p.) (P < 0.01, respectively). The rhythmic patterns of acetylsalicylic acid induced analgesia and hypothermia resembled overall the rhythms occurring in the non-drugged state. Injection of acetylsalicylic acid resulted in a parallel increase in latency to hot plate and a parallel decrease in rectal temperature. The relationship between plasma salicylate concentrations and responses was not clear. There was also a significant circadian rhythm in acetylsalicylic acid (850 mg/kg, i.p.) induced toxicity with the highest mortality at 17:00 and the lowest one at 05:00 (P < 0.05). Dosing time dependent kinetics of salicylate seems to be related to the rhythm of toxicity of the drug. The time in circadian stage at which acetylsalicylic acid is administered is essentially important in the actions of acetylsalicylic acid.

Analgesics↗

PubMed2004

Effect of vitamin C-releasing acetylsalicylic acid on gastric mucosal damage before and after Helicobacter pylori eradication therapy.

The interaction between Helicobacter pylori (H. pylori) and nonsteroidal anti-inflammatory drugs (NSAIDs) such as acetylsalicylic acid is still controversial. This study was designed to compare the effect of acetylsalicylic acid and vitamin C-releasing acetylsalicylic acid on the gastric mucosal damage and microbleeding before and after eradication of H. pylori in 10 young healthy volunteers. Acetylsalicylic acid induced significantly more gastric lesions and higher microbleeding than acetylsalicylic acid-vitamin C. After successful H. pylori eradication therapy, acetylsalicylic acid induced significantly higher mucosal lesions and microbleeding than before eradication. In contrast, after acetylsalicylic acid-vitamin C, gastric lesion index was significantly lower and eradication therapy failed to aggravate it. All H. pylori-positive subjects showed significant up-regulation of antioxidant enzyme (superoxide dismutase, catalase, glutathione peroxidase). Plain acetylsalicylic acid stronger than acetylsalicylic acid-vitamin C reduced gastric gene expression of these antioxidant enzymes. H. pylori eradication significantly decreased expression of these enzymes and this was further enhanced by plain acetylsalicylic acid, but not acetylsalicylic acid-vitamin C. Under plain acetylsalicylic acid therapy, the expression of proinflammatory cytokines was increased before and after eradication of H. pylori. We conclude that vitamin C combined with acetylsalicylic acid, unlike plain acetylsalicylic acid without vitamin C, protects gastric mucosa in man probably due the attenuation of oxidative stress and proinflammatory cytokines.

Adolescent↗

PubMed1986

Effect of acetylsalicylic acid on fatty acid omega-hydroxylation in rat liver.

The effect of acetylsalicylic acid on the cytochrome P-450-mediated fatty acid omega-hydroxylation system was assessed in male Sprague-Dawley rats after they were fed a diet containing 1% (w/w) acetylsalicylic acid. A 3-fold increase in the specific activity of laurate omega-hydroxylation was observed in the acetylsalicylic acid fed rats in comparison to control rats. This effect of acetylsalicylic acid was unique as the specific activities of other cytochrome P-450-mediated reactions were not increased. The induction of the laurate omega-hydroxylation system was also manifested in a rapid formation of its dicarboxylic acid derivative, dodecanedioic acid, as the omega-hydroxy derivative was further oxidized by alcohol and aldehyde dehydrogenases. These results suggest the acetylsalicylic acid is similar to other peroxisomal proliferating agents in that it also induces the microsomal fatty acid omega-hydroxylation system and may account for the appearance of unique dicarboxylic acids in Reye's syndrome patients.

Animals↗

PubMed2004

Effects of buffered and plain acetylsalicylic acid formulations with and without ascorbic acid on gastric mucosa in healthy subjects.

BACKGROUND: The most frequently reported adverse events associated with acetylsalicylic acid intake are minor gastrointestinal complaints. Galenic modifications, such as buffered formulations with or without ascorbic acid, may improve the benefit-risk ratio by decreasing the local mucosal side-effects of acetylsalicylic acid. AIM: To assess endoscopically-proven gastrointestinal lesions and the amount of gastric microbleeding of four different buffered and plain acetylsalicylic acid formulations, one containing paracetamol. METHODS: A randomized, four-fold cross-over study was performed in 17 healthy subjects who underwent serial oesophago-gastro-duodenoscopy before and after each course of 4-day dosing. Gastric aspirates were collected for the determination of haemoglobin concentrations to detect microbleeding. RESULTS: Buffered acetylsalicylic acid plus ascorbic acid yielded the lowest Lanza score, the lowest increase in the number of mucosal petechiae and the lowest increase in the amount of gastric microbleeding. Subjects receiving acetylsalicylic acid plus paracetamol plus caffeine showed the highest Lanza score of all treatments, and a considerably greater sum of petechiae in the oesophagus, stomach and duodenum compared with those receiving buffered acetylsalicylic acid plus ascorbic acid. CONCLUSIONS: The trial confirms that buffering of acetylsalicylic acid improves local gastric tolerability. Acetylsalicylic acid in combination with ascorbic acid shows significantly fewer gastric lesions and the lowest increase in gastric microbleeding compared with the other tested formulations.

Adult↗

PubMed1989

Effects of clofibrate and acetylsalicylic acid on hepatic carnitine palmitoyltransferase synthesis.

Clofibrate and acetylsalicylic and have both been reported to increase carnitine palmitoyltransferase (CPT) activity when administered to rats. The purpose of the present study was to determine the mechanism of the increase in CPT activity. Rats (150-200 g) were fed one of the following: chow, chow with 0.5% clofibrate, or chow with 1% acetylsalicylic acid for 2 weeks. At the end of this time, hepatic CPT activity was increased 4-fold over control in the clofibrate group and 3.6-fold over control in the acetylsalicylic acid group. Immunoreactive protein increased 4.0- and 3.6-fold, respectively, over control. Transcription rates of hepatic nuclei were increased 2.8- and 1.9-fold over control in the clofibrate and acetylsalicylic acid groups, and hepatic mRNA levels increased 2.8- and 2.0-fold respectively. These data indicate that increases in CPT activity caused by clofibrate and acetylsalicylic acid administration are due, at least in part, to increased CPT protein, resulting from increased transcription rate and levels of mRNA specific for CPT.

Acyltransferases↗

PubMed1978

Acetylsalicylic acid hydrolase of gastric mucosa.

Acetylsalicylic acid hydrolase activity of rabbit fundic gastric mucosa has been isolated from the soluble 100,000 X g supernate. The enzymatic activity was partially purified by ammonium sulfate precipitation. The Km for acetylsalicylate was 2 mM and pH optimum was 8.6. The activity was insensitive to ionic strength, slightly inhibited by inclusion of 100 mM Cl-, and demonstrated no requirement for Ca2+ or Mg2+. Acetylsalicylic acid esterase was markedly inhibited by sodium cholate and sodium dodecyl sulfate. The enzyme was insensitive to sulfhydryl reagents with the exception of p-chloromercuribenzenesulfonic acid, which markedly inhibited the enzyme. Diisopropyl fluorophosphate (DFP) inhibited enzymatic activity with a Ki of 9 X 10(-9)M. Eserine was also inhibitory with a Ki of 0.25 mM. Inhibition by DFP at low concentration and by eserine at millimolar concentrations suggests that this enzyme is related to the group of aliphatic esterases. Identification of potent inhibitors will enable studies to define the role of this enzyme with the use of experimental preparations in which systemic toxicity can be avoided.

Animals↗

PubMed1978

Uptake by blood components and by subcellular platelet fractions of 1-14C-acetylsalicylic acid.

1-14C-Acetylsalicylic acid was used to study the distribution and the kinetics of the acetyl group in blood components. Tests were carried out in 4 patients in vivo and on four blood samples in vitro. At various intervals after tagging, whole blood, plasma, platelets and platelet fractions were examined. In vitro, relative activity was found to be higher in platelets than in all other blood components. When platelet fractions were examined, the highest specific activity was found in membranes. In vivo, rapid disappearance of activity from circulation was observed. The decrease of activity was slower in platelets than in whole blood and in plasma. The highest specific acitivty was again found in platelet membranes. The half-life of the 14C tag was measured in all components. It was found to be longest in platelet membranes where it corresponded to the half-life of platelets in circulation. From the results obtained, the conclusion was drawn that irreversible acetylation of the platelet membrane must be considered to be one of the main causes of platelet dysfunction induced by acetylsalicylic acid.

Aspirin↗

PubMedDate not supplied

Influence of acetylsalicylic acid and metabolites on DU-145 prostatic cancer cell proliferation.

Conflicting reports have been published on the anti-tumour activities of acetylsalicylic acid in various cancers. Therefore, the effect of acetylsalicylic acid and its major metabolites has been studied on human prostatic carcinoma DU-145 cells. Investigations concentrated on the influence of acetylsalicylic acid, salicylic acid and salicyluric acid, on cell proliferation, DNA- and protein synthesis of DU-145 cells. DNA and protein synthesis determinations were done in vitro by [3H]thymidine and [3H]glycine incorporation, respectively. No effect on cell plating efficiency was observed, however proliferation studies showed that acetylsalicylic acid and salicylic acid inhibited cell growth (10 mM, 100% inhibition). No significant effect on cell proliferation was ascertained with salicyluric acid. Both DNA and protein synthesis were 40% inhibited by 0.1 mM acetylsalicylic acid. This study demonstrates that acetylsalicylic acid exhibits a significant influence on cell growth of prostatic DU-145 cells. These preliminary results may contribute to a better understanding of the anti-tumour capabilities of acetylsalicylic acid.

Aspirin↗

PubMed2006

Synthesis and transdermal properties of acetylsalicylic acid and selected esters.

The primary aim of this study was to determine the transdermal penetration of acetylsalicylic acid and some of its derivatives, to establish a correlation, if any, with selected physicochemical properties and to determine if transdermal application of acetylsalicylic acid and its derivatives will give therapeutic drug concentrations with respect to transdermal flux. Ten derivatives of acetylsalicylic acid were prepared by esterification of acetylsalicyloyl chloride with ten different alcohols. The experimental aqueous solubility, logD and transdermal flux values were determined for acetylsalicylic acid and its derivatives at pH 4.5. In vitro penetration was measured through excised female human abdominal skin in diffusion cells. The experimental aqueous solubility of acetylsalicylic acid (6.56 mg/ml) was higher than that of the synthesised acetylsalicylate derivatives (ranging from 1.76 x 10(-3) to 3.32 mg/ml), and the logD of acetylsalicylic acid (-0.85) was lower than that of its derivatives (ranging from -0.25 to 1.95). There was thus an inverse correlation between the aqueous solubility data and the logD values. The experimental transdermal flux of acetylsalicylic acid (263.83 nmol/cm(2)h) was much higher than that of its derivatives (ranging from 0.12 to 136.02 nmol/cm(2)h).

Anti-Inflammatory Agents, Non-Steroidal↗