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At least 379 records · Page 21Linked to original sources
PubMed1970

Thrombosis prevention by acetylsalicylic acid in hyperlipemic rats.

In rats, administration of acetylsalicylic acid (ASA) by stomach tube two hours before blood removal, or addition of the drug to platelet-rich plasma in vitro, markedly inhibited platelet aggregation induced by thrombin, ADP and collagen. Addition of ASA in vitro to human platelet-rich plasma also inhibited platelet aggregation by thrombin, ADP and collagen. In hyperlipemic rats, ASA (100 to 200 mg./kg.), administered by stomach tube once or five times, markedly inhibited the production of thrombosis initiated by intravenous injection of S. typhosa endotoxin. In these experiments, thrombosis prevention by ASA was associated with both a decrease in platelet aggregation and an increase in the recalcification plasma clotting time.

Adenine Nucleotides↗
PubMed1975

Acute pulmonary edema and plasma kininogen consumption in the adrenaline-treated rat: inhibition by acetylsalicylic acid and resistance to salicylate and indomethacin.

Pulmonary edema and plasma kininogen consumption caused by intravenously administered adrenaline, were inhibited in rats pretreated with acetylsalicylic acid, but not in rats pretreated with indomethacin or sodium salicylate. The possibility of a connection between this edema and mast cell-linked activation of kallikrein by adrenaline is discussed, as well as the possible role of acetylsalicylic acid acting as an acetylating inhibitor of these processes.

Animals↗
PubMed1975

[The effect of acetylsalicylic acid on the development of infarct-like myocardial necroses experimentally induced in rats by a single administration of novodrin (isopropylnoreadrenaline)].

It appeared that acetylsalicylic acid considerably decreased both development of the infarction-like foci of necrosis and primary damage of the myocardial cells experimentally induced in animals by direct action of novodrin and expressed in the course of the first hour. This led to the supposition that acetylsalicylic acid not only prevented platelet aggregation, but also increased the resistance of the myocardial cells to the injurious action of catecholamines.

Animals↗
PubMed1984

[Effect of acetylsalicylic acid on sulfalene and sulfadimethoxine binding by serum proteins and on their kinetics in rabbits].

The use of sulfalen and sulfadimethoxine in combination with acetylsalicylic acid resulted in the decreased binding of the sulfanilamides by serum proteins, most pronounced with respect to sulfadimethoxine. The decreased binding of the drugs by serum proteins in rabbits was accompanied by decreased elimination of sulfalen and increased excretion of sulfadimethoxine from the host. The different effect of acetylsalicylic acid on the kinetics of sulfalen and sulfadimethoxine in the rabbits was partially due to the unequivalent effect of the decreased binding of the sulfanilamides by the serum proteins on their combined use.

Animals↗
PubMed1980

A placebo-controlled trial of floctafenine (idarac) against enteric-coated acetylsalicylic acid in osteoarthritic patients.

A double-blind placebo-controlled trial was carried out in 30 out-patients with osteoarthritis of knee and hip. The therapeutic value of flactafenine 1.2 g daily, a new oral non-narcotic analgesic agent, was compared with that of enteric-coated acetylsalicylic acid (ACSA) (Rougier Inc.--enteric-coated acetylsalicylic acid, tablets of 650 mg) 2.6 g daily. Every patient successively received the three medications for six weeks according to a Latin-square design. An objective index of improvement of hips and knees was developed and applied to this study. In both objective and subjective assessments of the disease, floctafenine was found to be approximately equivalent to or superior to ACSA and superior to placebo. Both drugs were clinically well tolerated. A consistant but slight decrease in both haemoglobin and red-blood-cell count under floctafenine and ASA was found to be statistically but not clinically significant.

Aspirin↗
PubMedDate not supplied

[Effects of acetylsalicylic acid and diquertin on platelet aggregation and hemorheological parameters in rats with cerebral ischemia].

Rats with model cerebral ischemia were treated over 5 days with acetylsalicylic acid (in a single daily dose of 50 mg/kg via a gastric tube). This treatment decreased the level of platelet aggregation, while producing no statistically significant effect upon hemorheogical indices. The combined treatment with a complex of acetylsalicylic acid and diquertin (50 and 10 mg/kg via a gastric tube, respectively) also produced the antiaggregant effect, but additionally reduced the blood viscosity, erythrocyte aggregation, and fibrinogen content in the blood plasma.

Animals↗
PubMed2003

Effects of acetylsalicylic acid on fresh weight pigment and protein content of bean leaf discs (Phaseolus vulgaris L.).

The effects of 100, 250, and 500 ppm acetylsalicylic acid solutions treatments on weight alteration, pigment and protein amounts in discs from the primary leaves of one month old bean (Phaseolus vulgaris L.) seedlings produced tinder greenhouse conditions are presented. The experiments show that: 100 ppm ASA had no significant influence (P > 0.05) but 250 and 500 ppm ASA caused an increase on weight loss (P < 0.01); ASA at higher concentrations (250 and 500 ppm), generally, caused a decrease on pigment amounts (P < 0.05-P < 0.01) but 100 ppm ASA had no considerably significant influence on them (P > 0.05), none of the ASA treatments caused a statistically significant influence on carotenoid amount (P > 0.05); 100 and 250 ppm ASA treatments did not cause a significant influence on protein amount (P > 0.05). however 500 ppm ASA treatment caused an increase on protein injury (P < 0.05). Consequently, it is supposed that wet weight loss, pigment and protein injury have somewhat increased on leaf discs. depending on the toxic effect of high acetylsalicylic acid concentrations.

Aspirin↗
PubMed2006

Acetylsalicylic acid is compounding to antiplatelet effect of C-reactive protein.

The contribution of inflammatory process to the modulation of platelet response to acetylsalicylic acid (ASA) remains obscure. In our study, we examined the in vitro effect of C-reactive protein (CRP) on the ASA-mediated inhibition of collagen-stimulated platelet reactivity. Influence of CRP on platelet responsiveness to ASA was analysed using classical turbidimetric aggregation and flow cytometry. When acting alone, both C-reactive protein and ASA inhibited collagen-dependent platelet aggregation and reduced the expressions of two platelet surface membrane activation markers: P-selectin and activated GPIIbIIIa complex. Compared to the effects observed for ASA alone, the simultaneous action of both agents lead to further reductions in platelet aggregation (by 56.7+/-1.0% vs. 14.9+/-0.6%, p<0.0001) and lowered the expressions of platelet surface membrane P-selectin (by 72.1+/-5.3% vs. 65.0+/-6.0%, p<0.01) and activated GPIIbIIIa (by 67.0+/-5.6% vs. 47.7+/-8.3%, p<0.01). In general, our findings showed for the first time the augmenting effect of native C-reactive protein in the antiplatelet action of acetylsalicylic acid. Thus, we conclude that the effectiveness of aspirin therapy may strongly depend upon the presence of native CRP in circulation.

Adult↗
PubMed1990

[The effect of acetylsalicylic acid and dipyridamole on glomerular filtration and proteinuria in chronic glomerulonephritis].

The authors treated 14 patients with chronic proliferative glomerulonephritis for one year with acetylsalicylic acid--400 mg/day--and dipyridamole--225 mg/day. They investigated changes of glomerular filtration and proteinuria before treatment, during treatment and one year after its completion. They found that in the course of treatment proteinuria did not change and glomerular filtration declined insignificantly. During the subsequent year proteinuria and glomerular filtration declined significantly. The above findings can be partly explained by changes in the synthesis of renal prostacyclin and thromboxane. The combination of acetylsalicylic acid and dipyridamole in the amounts used did not have a favourable effect on glomerular filtration in patients with chronic proliferative glomerulonephritis.

Adult↗
PubMed1998

Assay of acetylsalicylic acid and three of its metabolites in human plasma and urine using non-aqueous capillary electrophoresis with reversed electroosmotic flow.

The separation of acetylsalicylic acid and three of its metabolites--salicylic acid, salicyluric acid and gentisic acid--is demonstrated in a non-aqueous capillary electrophoresis system with reversed electroosmotic flow. Solvent mixtures of methanol and acetonitrile are used for the electrophoresis media and different electrolytes have been investigated. The flow is reversed by the addition of the polycation hexadimethrine bromide and thus a negative voltage is used. This system provides a fast and effective separation of the four analytes. The separation method was applied to the assay of acetylsalicylic acid and its major metabolites in plasma and urine and the limits of quantification for all of these compounds are about 5 microg ml(-1) in plasma and 25 microg ml(-1) in urine.

Acetonitriles↗
PubMed1993

Effects of pethidine, acetylsalicylic acid, and indomethacin on pain and behavior in the mole-rat.

The antinociceptive and behavioral effects of pethidine (10, 20, or 30 mg/kg), acetylsalicylic acid (200, 400, or 600 mg/kg) and indomethacin (20, 40, or 50 mg/kg) in the naked mole-rat was studied in the hot-plate test. Instead of inducing analgesia, pethidine caused a dose-dependent reduction in response latency. Sensorimotor impairment and aggressive behavior were also observed following administration of pethidine (20 or 30 mg/kg). All animals receiving pethidine (30 mg/kg) died following fighting when kept in colony cages. Aggressive behavior and death was prevented by naloxone or by keeping animals in single cages. Acetylsalicylic acid (600 mg/kg) and indomethacin (40 or 50 mg/kg) caused a significant increase in response latency. It is concluded that in the mole-rat pethidine elicits aggression, sensorimotor impairment, and apparent hyperalgesia.

Aggression↗
PubMed2006

[Tooth extraction under medication with acetylsalicylic acid].

PURPOSE: The purpose of this prospective study was to show and analyze the bleeding complications after teeth extraction under therapy with 100 mg acetylsalicylic acid (ASA) and to compare them to bleeding complications after teeth extraction in patients with a healthy blood profile. PATIENTS AND METHODS: In 65 patients under medication with 100 mg ASA and in 252 healthy patients, 151/ 543 teeth were extracted and the bleeding complications monitored. RESULTS: The postoperative bleeding frequency was 1.54% in the ASA 100 group and 1.59% in the healthy control group without any medication. No serious or uncontrollable postoperative bleedings arose in either group. All bleedings could be easily handled. No obvious difference concerning the bleeding frequency between the two groups was observed. The small number of bleeding events and the complexity of affecting parameters did not permit statistical tests. CONCLUSION: It is not necessary to interrupt the medication of 100 mg acetylsalicylic acid given to prevent thromboembolism before tooth extractions.

Administration, Oral↗
PubMed1976

Gastroscopic evaluation of the effect of a new anti-rheumatic compound, ketoprofen (19.583 R.P.), on the human gastric mucosa. A double-blind cross-over trial against acetylsalicylic acid.

The tolerance of the gastric mucosa to a new anti-inflammatory product, ketoprofen (19.583 R.P., Orudis, Profenid N.D.) was compared to the tolerance of acetylsalicylic acid in a double-blind cross-over trial using selected healthy volunteers. The effect of the medication on the gastric mucosa was examined by the use of a gastrocamera technique. The volunteers received during 2 one-week periods either acetylsalicylic acid 3 g daily or ketoprofen 100 mg daily. The sequential diagram shows that the upper barrier was crossed (preference for ketoprofen) when 10 volunteers had been analysed.

Adolescent↗
PubMed2003

9 alpha,11 beta-prostaglandin F2 in pregnancies at high risk for hypertensive disorders of pregnancy, and the effect of acetylsalicylic acid.

Our purpose was to determine urinary 9 alpha,11 beta-prostaglandin F2, the primary metabolite of prostaglandin D2, in pregnancies at high risk for hypertensive disorders and the effect of acetylsalicylic acid on 9 alpha,11 beta-prostaglandin F2. Ninety high risk women were randomised to acetylsalicylic acid and placebo groups at 12-14 weeks of gestation, with 43 women in both groups followed up successfully. 9 alpha,11 beta-prostaglandin F2 was determined at baseline, at 24-26, and at 32-34 weeks of gestation. Fifteen normotensive non-pregnant women, 17 normotensive pregnant women at 12-14, and 15 at 30-34 weeks of gestation served as controls. Urinary 9 alpha,11 beta-prostaglandin F2 was significantly higher in pregnant women at 12-14 weeks of gestation as compared to non-pregnant women. High risk pregnancies had higher 9 alpha,11 beta-prostaglandin F2 as compared to normotensive pregnancies at 12-14, and at 30-34 weeks of gestation. Urinary 9 alpha,11 beta-prostaglandin F2 increased throughout pregnancy unrelated to the outcome of the pregnancy or to the treatment.

Aspirin↗
PubMed1976

Passive cutaneous anaphylaxis in guinea pigs elicited by gastric absorption of dextran induced by acetylsalicylic acid.

Passive cutaneous anaphylaxis (PCA) was elicited in guinea pigs sensitized with rabbit antidextran by the absorption of dextran macromolecules from the stomach induced by intragastric acetylsalicylic acid. The gastric contents had a pH sufficiently low to maintain the acid mainly in the unionized form since it is the latter which alters gastric permeability. The acid concentration required to induce PCA was below that which caused mucosal cell loss or bleeding. The maximal molecular weight of the absorbed dextran was approximately 25,000. Dextran was chosen as antigen because of its well-characterized physical and immunological properties. It is suggested that ingestion of acetylsalicylic acid may contribute to sensitization and allergic reactions to antigenic food materials by facilitating their absorption from the stomach.

Absorption↗
PubMed1979

[The influence of treatments with a quinine-lithium-salicylate combination or acetylsalicylic acid on hematopoiesis in mice (author's transl)].

The effects of an 8-week treatment with the quinine-lithium-salicylate combination Togal and sole acetylsalicylic acid (ASA) on the hemopoietic bone marrow cells of mice were studied. In general, both substances caused only minor changes. A slight leukopenia caused by higher doses as well as a transitory erythropenia observed a little bit more distinctly in ASA treated animals than in Togal treated animals need more detailed discussion, especially so because after a short two-week Togal treatment some animals showed an increase of hemopoietic cell colonies which a sole ASA dose did not cause. On the other hand, these results indicate a lower toxicity of Togal in comparison with acetylsalicylic acid as has been already shown in several other publications. It was proven that after a several weeks' treatment with therapeutic doses no pernicious influence on blood producing organs or pathological processes of the blood picture occurred. Only doses that border on the toxic region lead to insignificant bone marrow changes. As these over-doses are ten times the highest therapeutical dose the use of Togal does any damage to the blood forming tissue or pathological changes in the blood count are not likely. This has also been proved by other authors by means of long-term tests on humans.

Animals↗
PubMed1979

A comparison of the abilities of acetylsalicylic acid, flurbiprofen and indomethacin to inhibit the release reaction and prostaglandin synthesis in human blood platelets.

1 A quantitative comparison has been made of the abilities of acetylsalicylic acid, flurbiprofen and indomethacin to inhibit the adenosine diphosphate (ADP)-induced platelet release reaction and to inhibit the synthesis of prostaglandins from arachidonic acid. 2 Experiments were carried out on human platelets that had been incubated with the agents in vitro and on platelets obtained from volunteers who had ingested standard doses of the drugs. 3 The results obtained for acetylsalicylic acid show that there is a close relation between the release reaction and the synthesis of prostaglandins in platelets. 4 Flurbiprofen and indomethacin appear to inhibit the release reaction rather more effectively than they inhibit the synthesis of prostaglandins. It is possible that these agents inhibit the release reaction by another mechanism.

Aspirin↗
PubMed1988

Combined low-dose acetylsalicylic acid and dihydroergotamine in migraine prophylaxis. A double-blind, placebo-controlled crossover study.

The efficacy of the combination of dihydroergotamine (10 mg) with acetylsalicylic acid (80 mg) (DHE + ASA) in the prophylaxis of migraine was studied in a double-blind, placebo-controlled crossover trial (8 weeks twice). Of 45 patients who entered the study, 38 completed it. The number of attacks was significantly (p = 0.003) reduced during active treatment (11.5 +/- 6.2) compared with placebo (16.6 +/- 9.9). The mean duration, the mean severity, and the mean score for symptomatic acute medication of attacks did not differ significantly. The overall assessment made by the patients themselves was in favor of DHE + ASA (p = 0.001). These results indicate a moderately beneficial effect of the dihydroergotamine/low-dose acetylsalicylic acid combination in migraine prophylaxis.

Adolescent↗