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At least 703 records · Page 39Linked to original sources
PubMed1982

[Studies on the pharmacological bases of fetal toxicity of drugs. (I). Relation of fetal toxicity and tissue concentration of acetylsalicylic acid with pyrogen in pregnant rats].

The mechanism for the enhancing effect of pyrogen (lipopolysaccharide, LPS) on the fetal toxicity of acetylsalicylic acid (ASA) was studied in pregnant rats. The lethality of ASA was significantly enhanced by LPS in male rats. The fetal toxicity of ASA including fetal death, resorption, growth retardation, and skeletal anomalies (wavy rib and asymmetry of sternebra) was slightly observed in the dams that received a single dose of ASA (125 to 500 mg/kg, p.o.) on the 15th day of gestation, but it was markedly increased by LPS (20 micrograms/kg, i.v.). The enhancement of the toxicity of ASA by LPS was also observed in the maternal body weight gain until term. The plasma concentrations of ASA and salicylic acid (SA), the major metabolite of ASA, were increased by LPS. The tissue concentrations of SA were also increased in the following order: placenta, brain, fetus, uterus, liver and kidney. The ATP levels of placenta and fetus were not influenced by ASA alone, but markedly decreased by both LPS and ASA.

Abnormalities, Drug-Induced↗
PubMed1998

[Acetylsalicylic acid in therapy of migraine].

The paper reports the results of preventive therapy of 105 patients with migraine without aura by acetylsalicylic acid in doses 1000, 500 and 100 mg (in 3 groups of patients). The data were presented about the efficiency of these schemes of treatment as well as about the predictors and contra-indications for their prescription. Central and peripheral mechanisms of drug's action were considered.

Aspirin↗
PubMedDate not supplied

[Effect of chronic administration of epaden and acetylsalicylic acid on the antithrombotic potential of blood vessel walls in rabbits].

The effect of a new domestic polyunsaturated fatty acid (PUFA) concentrate called epaden on the blood coagulation system was studied in comparison with acetylsalicylic acid (ASA). The antithrombotic potential of the blood vessel wall was determined by release of the inhibitors of thrombocyte aggregation, fibrinolysis activators, and anticoagulants in rabbits under immobilization induced stress conditions. In the control group, the immobilization stress resulted in a decrease of the collagen-induced platelet aggregation, a drop in the fibrinogen level, and an increase in the tissue-type plasminogen activator (t-PA) activity. The administration of ASA and epaden reduced a drop in the fibrinogen level caused by the immobilization stress. Animals receiving epaden showed a decrease in the ADP-induced platelet aggregation and an increase in the t-PA activity in comparison with the levels before modeling stressed conditions. No such effect was observed in the group treated with ASA. It is suggested that the additional antithrombotic effect of epaden observed under the immobilization stress conditions is related to a protective action of this substance on the vessel wall.

Animals↗
PubMed1995

Simultaneous fluorimetric determination of acetylsalicylic acid metabolites in urine by partial least squares multivariate calibration.

A method is described for the simultaneous determination of the main urinary acetylsalicylic acid (aspirin) metabolites, salicyclic, salicyluric and gentisic acids, based on their native fluorescence. The urine was extracted into diethyl ether in acid medium, and back-extracted with glycine/sodium hydroxide buffer solution at pH 9.4. A comparative study of the results found using the excitation, the emission and the combination of the excitation plus the emission spectral data, as analytical signals, was performed. The data set, composed of the excitation plus the emission spectra, was selected as the analytical signal. The optimum wavelengths to record the excitation (lambda(em)=444 nm) and the emission spectra (lambda(ex)=323 nm) were selected to maximize the contribution from gentisic acid, which is the minor urinary metabolite. Partial least squares (PLS-1) multivariate calibration was then applied for the determination. Recovery values from urine samples spiked with salicyclic, salicyluric and gentisic acids varied from 90.1 to 97.6% (mean 93.6%), from 90.0 to 110% (mean 97.9%) and from 89.9 to 104.7% (mean 98.5%), respectively.

Journal Article↗
PubMed1998

Determination of acetylsalicylic acid and salicylic acid in skin and plasma by high-performance liquid chromatography.

This study describes a HPLC method to determine the concentrations of acetylsalicylic acid (ASA) and salicylic acid (SA) in human stratum corneum and in plasma. The stratum corneum layers for ASA/SA analysis were removed from three patients with postherpetic hyperalgesia treated with topical and oral aspirin. Blood samples were also collected from the same patients. Tape strippings were placed in acetonitrile and sonicated for 15 min. After centrifuging, aliquots of the supernatant were injected into the chromatograph. ASA and SA from plasma samples were extracted on Isolute C8 columns. Due to interfering peaks in the tape samples, HPLC conditions were slightly different for tape and plasma samples. ASA and SA were separated on a LiChrospher 100 RP-18 column at 1 ml/min using a water-phosphate buffer (pH 2.5)-acetonitrile mobile phase (35:40:25, v/v/v). A linear response to quantities of ASA from 0.1 to 100 microg/cm2 and of SA from 0.1 to 5 microg/cm2 in tape and to quantities of ASA 0.1 to 2 microg/ml and 1 to 50 microg/ml was obtained and the recovery from tape and plasma samples was over 98%. The method is sensitive (0.1 microg/cm2) and specific enough to allow the determination of the drugs in the skin not only after topical but also after oral administration. A good sensitivity was also obtained in plasma (0.1 microg/ml) allowing study of the kinetics of ASA and SA in plasma after oral administration. Concentrations of ASA after topical administration were 100-200 times higher than after oral administration. Plasma levels of ASA and SA after oral administration were similar to those previously found. No ASA or SA were detected in plasma after topical ASA administration.

Administration, Oral↗
PubMed2004

An in vitro model for the detection of reduced platelet sensitivity to acetylsalicylic acid.

A discovery of 'aspirin resistance' has prompted the search for fast and reliable methods for the monitoring of antiplatelet efficacy of acetylsalicylic acid (ASA). Our aims were: (1) to evaluate the in vitro model-based method for detecting a reduced platelets' sensitivity to ASA using a point-of-care platelet function analyser PFA-100; and (2) to propose a simple method of data analysis that might be successfully employed to discriminate between 'good' and 'poor' responders to aspirin. Whole blood platelets from healthy volunteers were incubated in vitro with 30 microg/ml ASA (the in vitro method under evaluation) or analysed following a 10-day intake of an average 150 mg ASA (Aspirin Protect) daily (the reference ex vivo method). According to polynomial regression analysis of the bimodally distributed data, the donors with lower ('ASA poor responders') or higher platelet sensitivity to ASA ('ASA good responders') were discriminated at 58.6% of platelet function inhibition. Despite the similar proportions of 'ASA poor responders' (44 versus 41% using the ex vivo and in vitro tests, respectively), 30% of discordant classifications point to a rather unsatisfactory convergence between both methods. Due to a considerable discordance between the in vitro and ex vivo tests of ASA efficacy performed with the use of the PFA-100 system, the former cannot be reliably and interchangeably used for the monitoring of aspirin therapy and the selection of an effective therapeutic ASA dose. A novel approach to data analysis of the distribution of platelet inhibition rates facilitates an evaluation of cut-off points required to discriminate between 'poor responders' and 'good responders' to aspirin.

Adult↗
PubMedDate not supplied

Ocular delivery of acetylsalicylic acid by repetitive coulomb-controlled iontophoresis.

To investigate the potential of transscleral coulomb-controlled iontophoresis (CCI) for repetitive delivery of acetylsalicylic acid (ASA) into the eye, a total of 50 rabbits was included in this study. Fourteen animals received serial CCI treatment. Fourteen animals underwent CCI with either ASA or balanced salt solution (BSS) for at least 6 days at 24- and 48-hour intervals. Eighteen animals received a single CCI application, while 18 animals were injected with 15 mg ASA/kg body weight intravenously. HPLC analysis was performed to determine the levels of salicylic acid (SA) in ocular tissues. Apart from clinical follow-up, 2 rabbits in the ASA and BSS groups were examined by electroretinography, and 2 animals were examined histologically. Though high concentrations of SA were measured, no alterations were observed clinically, histologically and electrophysiologically. Repetitive CCI demonstrated its potential as a topical drug delivery system for ASA into the eye. This transscleral delivery of ASA resulted in significant and sustained intraocular concentrations of SA without side effects. Iontophoresis may be advantageous in clinical administration maintaining therapeutic levels of ASA while avoiding adverse effects associated with the systemic administration of nonsteroidal anti-inflammatory drugs.

Animals↗
PubMed1982

Acetylsalicylic acid in combination with dihydroergotamine for preventing thromboembolism.

In a prospective randomized clinical trial involving 150 patients who underwent major abdominal surgery, acetylsalicylic acid (ASA) and dihydroergotamine (DHE) were examined either alone or in combination for their potential to prevent thromboembolism. Combined treatment with ASA and DHE was found to be more effective in preventing the spread of thrombi and their propagation to the femoral veins.

Adult↗
PubMed1991

Effects of different hirudins and combinations of low doses of hirudin, heparin and acetylsalicylic acid in a rat microcirculatory thrombosis model.

Two recombinant hirudins (r-hirudin), natural hirudin and hirudin in combination with heparin or acetylsalicylic acid (ASA) have been studied in a thrombosis model in which rat mesenteric venules of a diameter of 20-30 microns were injured by well-defined argon laser lesions. In the animal model all hirudins showed significant and dose-dependent antithrombotic effects in doses between 0.05 and 0.1 mg/kg after single intravenous and subcutaneous injections. The antithrombotic effect of single (0.2 mg/kg i.v. or 0.1 mg/kg s.c.) injections lasted longer than 4 h (i.v.) or 6 h (s.c.). Hirudin at a dose of 0.1 mg/kg and heparin at doses of 0.05 mg/kg showed a significant antithrombotic effect 2 h after subcutaneous injection. When heparin and hirudin were injected together at this dosage, the effect of the combination was in the same range as that of unfractionated heparin or hirudin alone. An additive antithrombotic effect was observed if a low dose of r-hirudin (0.1 mg/kg) was combined with a moderate dose of ASA (10 mg/kg).

Animals↗
PubMedDate not supplied

No effect of acetylsalicylic acid on B-thromboglobulin and platelet factor 4 plasma levels in patients with transient ischaemic attacks.

We studied the effect of acetylsalicylic acid (ASA) versus placebo on B-thromboglobulin (B-TG) and platelet factor 4 (PF4) plasma levels and ADP-induced platelet aggregation in 25 male patients with transient ischaemic attacks (TIA). The patients were allocated randomly to two groups: 14 patients received oral treatment with ASA 500 mg b.i.d. for 14 days, 11 patients placebo b.i.d. for the same period. B-TG and PF4 plasma levels and ADP-induced platelet aggregation were determined in basal conditions, and two hours, and seven and fourteen days after starting with ASA or placebo. In addition, the same parameters were studied in a group of 20 healthy males of matched age. Basal levels of plasma B-TG and PF4 and the maximal amplitude of ADP-induced platelet aggregation were abnormally high in TIA patients. ASA caused a significant reduction of B-TG plasma levels in TIA patients 2 hours after the first administration, but no effect was observed at the 7th and 14th day of treatment. PF4 plasma levels were unaffected by ASA treatment. It is concluded that ASA, at the dose conventionally used in clinical trials, does not affect the release of two alpha-granule proteins.

Aged↗
PubMed1976

Effects of L-glutamine of acetylsalicylic acid or taurocholic acid-induced gastric lesions and secretory changes in pylorus-ligated rats under normal or stress conditions.

An oral dosing of either acetylsalicylic acid (ASA) or taurocholic acid (TCA) to pylorus-ligated rats subjected to water-immersion stress produced severe damage to the gastric musoca in contrast to the irritation observed in non-stressed ones. The irritative activity of ASA or TCA on gastric mucosa under stress was dose-dependent. Stress itself (23 degrees C, 7 hr) did not induce any appreciable changes in gastric mucosa under stress wasic mucosa of rats. L-glutamine, given together with SAS or TCA, significantly prevented the potentiated development of SAS- or TCA-induced gastric lesions in stressed rats. L-glutamine also prevented in varying degrees the reduction of acid and increment of Na+ ion in gastric juice accumulated in stressed rats in response to ASA or TCA.

Animals↗
PubMed2004

[Platelet function tests for monitoring of acetylsalicylic acid: clinical significance in antiplatelet treatment].

Several studies have demonstrated with the use platelet function tests (PFT) that subgroups of patients under acetylsalicylic acid (ASA) fail to produce the anticipated antiplatelet effect. This phenomenon as well as the clinical failure of ASA to protect patients from thromboembolic complications has been termed ASA resistance (AR) or ASA nonresponsiveness. Several subtypes of AR can be distinguished by PFT. The following PFT were used to characterize AR: optical aggregometry, platelet aggregation in whole blood, platelet function analyzer (PFA-100), platelet reactivity test or platelet aggregate ratio, flow cytometry and thromboxane B(2) generation. All PFT have in common that their widespread clinical use is substantially limited due to complex preanalytic factors, reduced specificity and poor reproducibility. PFT are not interchangeable for monitoring antiplatelet treatment. Three prospective clinical trials revealed a possible relationship between AR and subsequent cardiovascular events. There is a need for a simple and reliable assay for predicting the clinical efficacy of antiplatelet therapy. Recent data demonstrate that none of the currently available assays including the PFA-100 system are capable to accomplish these objectives.

Aspirin↗
PubMed2000

Comparison of three in vitro assays at evaluation of IC50 of acetylsalicylic acid, ferrous sulfate, amitriptyline, methanol, isopropanol and ethylene glycol in human cancer cells HeLa.

Evaluation of the 50% inhibitory concentration (IC50) of acetylsalicylic acid, ferrous sulfate, amitriptyline, methanol, isopropanol and ethylene glycol was done on human cancer cells cultured in in vitro conditions. Three different in vitro assays were used in this study: the plating efficiency test, the microprotein test and the neutral red uptake test. Obtained results were evaluated by statistical methods. All used methods seem to be useful for screening a cytotoxic potential of the tested chemicals. The knowledge of cytotoxic effects of frequently used chemicals on mammalian cells is important not only for necessary in vitro genotoxicity and carcinogenicity studies but also for assessing the toxicity of chemicals to find out possible hazards to the human health. Results presented in this paper underline the usefulness of the wider methodological approach for the comparison of the different endpoints as well as a necessity for selection of a battery of in vitro cytotoxicity tests allowing to estimate the possible harmful effects of xenobiotics.

2-Propanol↗
PubMed1988

Influence of acetylsalicylic acid and BM 13177 on blood pressure and efficacy of antihypertensive drugs in spontaneously hypertensive rats.

The effects of the cyclooxygenase inhibitor acetylsalicylic acid (ASA) and of the TXA2 receptor antagonist BM 13177 on blood pressure and on the efficiency of antihypertensive drugs were investigated in spontaneously hypertensive rats (SHR). ASA and BM 13177 applicated once caused a significant, but short-lasting decrease in blood pressure in SHR. In contrast, repeated application of ASA (3 x 100 mg/kg) caused a slight, but significant increase in blood pressure. Pretreatment with BM 13177 (60 mg/kg i.v.) did not influence the antihypertensive effect of the drugs clonidine, propranolol and dihydralazine. Pretreatment of SHR with ASA intensified significantly the effect of these drugs on blood pressure, independent of their mode of action, and on heart rate (dihydralazine). The formation of TXB2 in the aorta thoracica in ASA pretreated SHR 20 min after drug application, was more strongly inhibited than was the formation of PGI2. Therefore the TXA2/PGI2 balance shifted in favor of the latter. However, in normotensive rats, ASA was without any effect on blood pressure and on the antihypertensive efficacy of the drugs. In conclusion it could be suggested that prostanoids are involved in the short term as well as in the long term regulation of the blood pressure and in the blood pressure lowering activity of drugs at least in a hypertensive state.

Animals↗
PubMed1986

In vitro teratogenicity of acetylsalicylic acid on rat embryos: studies with various culture conditions.

Rat embryos taken at day 9.5 of gestation were exposed in vitro to acetylsalicylic acid (aspirin) using various culture conditions. It was observed that embryos were sensitive to aspirin emulsified in olive oil at concentrations greater than or equal to 150 micrograms/ml. Between 43% and 66% of the embryos exhibited multiple malformations depending on the culture medium, 100% homologous rat serum or Waymouth medium supplemented with 50% rat serum, respectively. At concentrations greater than or equal to 400 micrograms/ml aspirin induced further toxic effects on embryo growth and differentiation. When gelatin was used as the drug-delivery system, aspirin at concentrations of greater than or equal to 150 micrograms/ml induced some malformations (mainly irregular somite shapes) in 57% of the embryos cultured in Waymouth medium, but in only 13% of the embryos grown in 100% serum. At concentrations which were greater than or equal to 400 micrograms/ml aspirin induced dysmorphogenic effects in all embryos, without any concomittant toxicity.

Animals↗
PubMed1980

[Influence of phospholipids and their combination with prothrombin complex and calcium ions on coagulation in mice and rabbits both normal and affected by acetylsalicylic acid (author's transl)].

The influence of phospholipids and their combination with prothrombin and calcium on coagulation both normal and affected by acetylsalicylic acid (ASA) was investigated by determination of the bleeding time of mice, thrombelastographic (TEG) measurements and counting of thrombocytes of rabbits. Bleeding times and times of the TEG were prolonged after oral application of ASA, while thrombus stability was not altered. The number of thrombocytes decreased. Bleeding- and TEG-times normalized after injection of phospholipids. This effect was increased and of longer duration when phospholipids were combined with calcium and prothrombin. Decrease of the number of thrombocytes caused by pretreatment with ASA normalized only after injection of phospholipids together with prothrombin and calcium. The number of thrombocytes was not negatively influenced by the therapy in animals with normal coagulation.

Animals↗
PubMed1997

[Studies on the protective effect of lansoprazole on human gastric mucosa against low-dose acetylsalicylic acid. An endoscopic controlled double-blind study].

In a randomized double-blind parallel study the gastroduodenal tolerability of 300 mg acetylsalicylic acid (ASA) daily has been evaluated in the presence of placebo, 15 mg lansoprazole (CAS 103577-45-3, Agopton) and 300 mg ranitidine daily (8 a.m.) in 30 healthy volunteers using upper gastrointestinal tract endoscopy. The treatment periods lasted 14 days. Endoscopic controls were performed at entry and repeated at day 14. At entry, the mean endoscopic score averaged 1.0 +/- 0.0 (+/- SEM) in the ASA/placebo (n = 10), in the ASA/ lansoprazole 15 mg (n = 10) and the ASA/300 mg ranitidine group. In the placebo experiments 300 mg ASA daily induced marked gastroduodenal lesions at day 14 (lesion score of 10.1 +/- 1.4) (+/- SEM). Concomitant administration of 15 mg lansoprazole daily offered significant protection against 300 mg ASA daily on day 14 (3.6 +/- 1.2) (p < 0.05), 300 mg ASA plus 300 mg ranitidine daily reduced the damaging score to 5.8 +/- 1.3 (p n.s. vs ASA/placebo). Our data suggest that co-administration of 15 mg lansoprazole daily reduces significantly gastroduodenal lesions evoked by 300 mg ASA.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1985

Differential inhibition of platelet thromboxane and lung prostacyclin production by sulphinpyrazone, acetylsalicylic acid and indomethacin by human tissues in vitro.

To compare the inhibition of human platelet and lung cyclo-oxygenases by sulphinpyrazone (SP), acetylsalicylic acid (ASA) and indomethacin, we investigated their effects on platelet thromboxane A2 (TxA2) production during spontaneous clotting and on prostacyclin (PGI2) and TxA2 productions of superfused minced human lung. The synthesis of proaggregatory, vasoconstricting TxA2 and antiaggregatory, vasodilating PGI2 were evaluated by measuring the concentration of their stable metabolites thromboxane B2 (TxB2) and 6-keto-prostaglandin F1 alpha respectively, by radioimmunoassays. The basal platelet TxB2 production was 241.0 +/- 56.3 ng/ml (mean +/- SEM, n = 12). The concentrations needed for 50% inhibition of this production (IC50) were 41.3 mumol/l for sulphinpyrazone, 6.3 mumol/1 for ASA and 0.094 mumol/l for indomethacin. The lung generated 23.8 +/- 5.5 ng/g/min (mean +/- SEM, n = 6) of 6-keto-PGF1 alpha and 8.5 +/- 1.8 ng/g/min of TxB2. The IC50 values for pulmonary 6-keto-PGF1 alpha and TxB2 productions were 530.0 mumol/l for SP, 370.0 mumol/l for ASA and 50.0 mumol/l for indomethacin. Thus pulmonary cyclo-oxygenase, presumably originating from endothelial cells, was 13, 59, and 532 times more resistant to these prostaglandin synthesis inhibitors (PGI's) than platelet cyclo-oxygenase. These data suggest that there are considerable differences in the concentration ranges of various PGI's by which the PGI2/TxA2 balance can be shifted to a dominance of PGI2.

6-Ketoprostaglandin F1 alpha↗