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PubMed2004

[Acetylsalicylic acid consumption in patients with diabetes mellitus].

BACKGROUND AND OBJECTIVE: Acetylsalicylic acid (ASA) has been recommended for primary (PP) and secondary prevention (SP) of cardiovascular disease (CVD) in diabetic patients. The consumption of ASA among Catalan diabetic people is described here. SUBJECTS AND METHOD: We analyzed 1,718 questionnaires administered to members of the Catalonia's Diabetic Association. ASA intake, history of CVD and medical advice about the use of ASA were evaluated. RESULTS: ASA was taken by 21% subjects (as PP in 14% and as SP in 53%). Medical advice had been received in 23% (15% as PP and 56% as SP). CONCLUSIONS: ASA intake among diabetic patients is low in both PP and SP. Physicians should recommend its use to improve this situation.

Adult↗
PubMed2003

Acetylsalicylic acid reduces perfusion deficit in ischemic injured brain in rats.

Acetylsalicylic acid (ASA) is an antiplatelet agent which has been used in treatment and prevention of stroke in humans. In the present study, the effects of ASA on perfusion deficits in the brain have been studied in an embolic model of stroke. Data showed that perfusion deficits were observed in all rats sacrificed immediately after middle cerebral artery (MCA) occlusion. Treatment with ASA significantly reduced perfusion deficits 1 h but not 3 h after the MCA occlusion. These findings thus support that ASA is useful agent in treatment and prevention of stroke, and show that its mechanism of action is likely through the reopening of cerebral microvessels.

Animals↗
PubMed1984

Plaque-forming cells in man. IV. Influence of acetylsalicylic acid in vivo and dexamethasone in vitro.

The influence of acetylsalicylic acid (ASA) and steroid (ST) on the number of plaque-forming cells (PFC) developed in pokeweed mitogen-activated cultures of peripheral blood lymphocytes (PBL) was investigated. Cultures of 10(6) PBL were established from blood samples of 16 healthy volunteers before and after intake of 2 g of ASA, and parallel cultures were supplemented with ST in vitro. The immunoglobulin secretion was monitored with a protein A assay. Our results show that pharmacological doses of ASA in vivo decrease the number of PFC by 41%, whereas the distribution of the subpopulations was unaltered. In cultures of PBL obtained before the intake of ASA and supplemented with 10, 50 or 100 micrograms/ml of dexamethasone the number of PFC was decreased by 50%, 41% and 44%, respectively. In cultures of PBL obtained after the intake of ASA and supplemented with 10, 50 or 100 micrograms of ST, the number of PFC was further decreased by 22%, 32% and 38%. The effects of ASA in vivo and ST in vitro were additive. The ratio of IgM, IgG and IgA PFC was unaffected by ASA and ST. It is suggested that the modulation of the PFC response induced by ASA and ST is mediated by the prostaglandin system.

Adult↗
PubMed2004

Placebo-controlled comparison of effervescent acetylsalicylic acid, sumatriptan and ibuprofen in the treatment of migraine attacks.

Acetylsalicylic acid (ASA) in combination with metoclopramide has been frequently used in clinical trials in the acute treatment of migraine attacks. Recently the efficacy of a new high buffered formulation of 1000 mg effervescent ASA without metoclopramide compared to placebo has been shown. To further confirm the efficacy of this new formulation in comparison with a triptan and a nonsteroidal anti-inflammatory drug (ibuprofen) a three-fold crossover, double-blind, randomized trial with 312 patients was conducted in Germany, Italy and Spain. Effervescent ASA (1000 mg) was compared to encapsulated sumatriptan (50 mg), ibuprofen (400 mg) and placebo. The percentage of patients with reduction in headache severity from moderate or severe to mild or no pain (primary endpoint) was 52.5% for ASA, 60.2% for ibuprofen, 55.8% for sumatriptan and 30.6% for placebo. All active treatments were superior to placebo (P < 0.0001), whereas active treatments were not statistically different. The number of patients who were pain-free at 2 h was 27.1%, 33.2%, 37.1% and 12.6% for those treated with ASA, ibuprofen, sumatriptan or placebo, respectively. The difference between ASA and sumatriptan was statistically significant (P = 0.025). With respect to other secondary efficacy criteria and accompanying symptoms no statistically significant differences between ASA and ibuprofen or sumatriptan were found. Drug-related adverse events were reported in 4.1%, 5.7%, 6.6% and 4.5% of patients treated with ASA, ibuprofen sumatriptan or placebo. This study showed that 1000 mg effervescent ASA is as effective as 50 mg sumatriptan and 400 mg ibuprofen in the treatment of migraine attacks regarding headache relief from moderate/severe to mild/no pain at 2 h. Regarding pain-free at 2 h sumatriptan was most effective.

Adult↗
PubMed2001

Modified clotting properties of fibrinogen in the presence of acetylsalicylic acid in a purified system.

To assess how treatment with acetylsalicylic acid (ASA) alters the fibrin network structure, clotting was initiated in purified fibrinogen incubated with ASA by adding thrombin. Clotting time and maximum absorbance of the fibrin aggregation curve were used to demonstrate the potential of fibrin generation. The results showed that the clotting properties of fibrinogen decreased and that the affinity of plasminogen to fibrin or thrombin inhibition by antithrombin increased if plasminogen or antithrombin, respectively, were present in the reaction system. The effect of ASA varied in a dose dependent manner. It was concluded that ASA may directly or indirectly confer positive or negative effects on the stability of the fibrin clot and that the balance between these effects may be regulated by the ASA dose.

Aspirin↗
PubMed1978

Acetylsalicylic acid and the cardiovascular effects of ADP in the rat.

Acetylsalicylic acid (ASA) did not prevent the arrhythmias induced in rats by a bolus intravenous injection of ADP, an effect independent of platelets. ASA was also unable to protect the rats from the platelet-mediated cardiovascular effects and myocardial ischaemia induced by a prolonged ADP infusion. It is suggested that the release of vasoactive substances inhibited by ASA does not play a major role in the cardiovascular effects of ADP in rats.

Adenosine Diphosphate↗
PubMed1989

Liver gamma-glutamyl transpeptidase activity following chronic treatment with acetylsalicylic acid in rats.

In the present study, rats were administered acetylsalicylic acid (ASA), at low and high doses, by means of a gastric tube for 30 days. Chronic administration of a high dose of ASA (200 mg/kg body weight) resulted in a significant increase in liver plasma membrane gamma-glutamyl transpeptidase activity, cholesterol, and phospholipid levels. The enzymatic activity and lipid levels appeared not to be affected by ASA when given at a lower dose (50 mg/kg body weight). The changes in the enzymatic activity of plasma membrane were positively correlated to membrane cholesterol content. These findings suggest that the hepatotoxicity of high doses of ASA should not be overlooked during clinical use of the drug.

Animals↗
PubMedDate not supplied

Different patterns of inhibition of adrenaline-induced platelet aggregation and kinetics in vivo by acetylsalicylic acid and indobufen.

The inhibitory effect of 50 mg/kg lysyl acetylsalicylic acid (ASA) intravenously injected 24 and 4 h before 80 micrograms/kg adrenaline, 40 mg/kg indobufen injected 15 min before, or a combination of ASA plus indobufen on the platelet aggregation and kinetics was evaluated in anaesthetized dogs previously injected with 111indium- (111In-) labelled platelets using gamma-camera dynamics studies. The highest degree of inhibition, indicated by the lowest platelet aggregation ratio decrease and the most significant 111In-labelled platelet mobilization from hepatic and splenic stores with a corresponding increase of labelled and unlabelled platelet counts in blood, was obtained in ASA-treated dogs. Such changes were less marked when ASA plus indobufen was injected. In indobufen-treated dogs a similar mobilization of 111In-labelled platelets with an increase in circulating platelet numbers was evident only after the second adrenaline injection. It is concluded that platelet mobilization is mainly dependent on the production of an ASA-sensitive substance.

Animals↗
PubMed1991

Immobilization increases bone prostaglandin E. Effect of acetylsalicylic acid on disuse osteoporosis studied in dogs.

The effect of acetylsalicylic acid (aspirin) on bone mass and bone prostaglandin E (PGE) in immobilization osteoporosis was studied in 12 growing dogs using a unilateral hind limb cast-fixation model. Osteoporosis was induced by fiberglass-cast immobilization of the right hind limb for 4 weeks, with the left hind limb as a control. Six dogs received buffered aspirin at 25 mg/kg body weight per os every 8 hours; 6 dogs received no treatment. All the dogs were killed after 4 weeks, and bone samples were collected. Bone mineral content of the distal tibial metaphysis was measured by single-photon absorptiometry. In vitro release of PGE from the calcaneus, tibial cortical bone, tibial cancellous bone, and ilium were measured using a specific radioimmunoassay for PGE. Compared with the controls, the casted limb of untreated dogs had half the bone mass and a twofold increase in bone PGE. Aspirin treatment was associated with a 65 percent reduction in bone PGE and a 13 percent bone mass sparing effect. These results provide indirect evidence that PGE plays a role in immobilization osteoporosis.

Absorptiometry, Photon↗
PubMed2002

Liver and kidney ultrastructural changes caused by acetylsalicylic acid treatment during pregnancy in rats.

The worldwide use of acetylsalicylic acid (ASA) as an analgesic-antipyretic drug, including during pregnancy, prompted us to investigate its potentially deleterious effects in that condition. Pregnant rats were treated with ASA (1, 10 or 100 mg/kg once a day) from the first day up to term pregnancy. No histological changes were noticed in maternal and fetal livers or kidneys when examined under light microscopy, but some definite dose-dependent effects of ASA were observed on electron microscopy examination. In livers and kidneys of pregnant rats treated with the highest doses of ASA we observed cytoplasmic derangement, mitochondrial cristolysis and abnormally shaped rough endoplasmic reticulum. Similarly, in foetal livers and kidneys from this group we observed degenerative cytoplasmic vacuoles and ballooned mitochondria with cristae derangement and myelin figures. Our data point out the fact that both maternal and foetal tissues can be importantly affected by ASA at the ultrastructural level, without overt signs of toxicity.

Animals↗
PubMed1992

[Long-term medication with acetylsalicylic acid--a problem in regional anesthesia?].

In patients medicated with acetylsalicylic acid (ASA) and undergoing regional anaesthesia there is a risk of traumatically induced haematoma, particularly near the spinal cord. The increased bleeding tendency following aspirin administration is due to a change in thrombocyte aggregation caused by irreversible inhibition of prostaglandin synthesis. In order to assess the bleeding risk, it was investigated whether and how much subaqueous bleeding time (SBT) and aggregation inhibition (AGI) change under low-dose medication, and when these values return to normal after the end of administration. RESULTS. 1. SBT increased significantly with daily ASA medication of 100 mg or of 300 mg. However, only 4.5% of the values measured were within a pathologic range. After discontinuation of the medication SBT significantly dropped on the 2nd day, reaching the initial level on the 4th day at the latest. 2. AGI was significantly reduced, to 20% of the normal value. Depending on the dosage, the 100-mg group reached full aggregation capacity on the 4th day and the 300-mg group on the 7th day following discontinuation of medication. 3. AGI returned to normal 2-3 days later than SBT. CONCLUSIONS. 1. In the case of pathologically increased values (greater than 6 min), the determination of SBT may indicate an increased bleeding risk. 2. If SBT is within the normal range during or shortly after ASA administration, thrombocytic function is still disturbed. Whether there is a correlation between inhibition of thrombocyte aggregation and the occurrence of spinal haematomas is not yet known. 3. In view of these results, the effect of ASA should be investigated by determining SBT prior to scheduled regional anaesthetic procedures near the spinal cord. 4. If SBT is increased (greater than 6 min) and regional anaesthesia near the spinal cord is indicated, the procedure involving the slightest trauma (spinal anaesthesia) should be chosen [31]. Careful postoperative follow-up (1-2 days) should be guaranteed with regard to neurological disorders.

Adult↗
PubMed1992

Tensides from the group of propylene oxide and ethylene oxide copolymers. X. Solubilization of acetylsalicylic acid by polyetherodiol micelles.

The process of structural solubilization of acetylsalicylic acid in balanced systems (weight-balanced) by micelles of Rokopols of 30p160 and 30p60 types and, for comparison, by those of F-68 and F-108 Pluronics was investigated. The determined viscosity and hydrodynamic parameters allowed for the calculation of solubilizing activity of polyetherodiol micelles--n(s(A)). The results of the investigation point at Rokopols as an excipient, which may help to obtain new drug delivery systems.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1990

Secondary prevention of ischemic stroke with low dose acetylsalicylic acid.

In order to evaluate the efficacy of low dose acetylsalicylic acid (ASA) for the secondary prevention of ischemic stroke, this cooperative multicenter clinical trial was conducted on a non-blind basis. Patients having a first transient ischemic attack (TIA), reversible ischemic neurological deficit (RIND) or completed ischemic stroke were eligible for this trial. A total of 590 patients including 47 cases of TIA, 23 cases of RIND and 520 cases of completed stroke entered this study. These patients were allocated by the time of admission to one of the following 5 trial regimens: (1) vasodilators having no known inhibitory effect on platelet function (control group), (2) dipyridamole (DP) 50 mg 3 times a day (DP group), (3) ASA 300 mg once a day (ASA 300 mg group), (4) ASA 300 mg once in combination with DP 50 mg 3 times a day (ASADP group), and (5) ASA 100 mg once a day (ASA1 group). No difference in effect between the control and DP groups was observed, nor between the ASA 300 mg and ASADP groups. Therefore, we combined the control and DP groups to make a non-ASA group, and joined the ASA 300 mg and ASADP groups to make an ASA3 group. The differences in the cumulative event-free rate appeared to be significant between the non-ASA group and the ASA3 group and also between the non-ASA group and the ASA1 group. But the frequency distribution of age, territory of stroke, diabetes mellitus, cardiac disease, hematological disease and hyperuricemia were significantly different among these 3 study groups. We thus included these covariates in the Cox's proportional hazard model to control their possible confounding effects.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1978

Interaction of [14C]acetylsalicylic acid with normal human peripheral blood lymphocytes.

Therapeutic concentrations of acetylsalicylic acid (ASA) have strikingly inhibited in vitro and in vivo mitogen- and antigen-induced blastogenesis by human lymphocytes. These observations may be pertinent to the anti-inflammatory actions of ASA. To investigate further the possible effects of ASA on cellular responses, we studied the in vitro interaction of [14C]ASA with lymphocytes. Results indicated that the [14C]ASA association with cells was (a) proportional to ASA concentrations, (b) non-saturable at high concentrations of ASA, (c) dependent on pH, (d) independent of temperature, (e) dependent on cell concentration, (f) not consistently displaced by unlabelled ASA or other drugs, (g) rapid and unchanged over 1 min to 72 hr incubations and (h) reversed by repeated cell washing. These data confirmed that ASA indeed interacted with lymphocytes. The association was rapid, reversible, pH-dependent and not demonstrably specific under these experimental conditions.

Aspirin↗
PubMed1993

[Intranasal provocation with lysine acetylsalicylic acid].

At present provocation tests are indispensible tools for diagnosing acetylsalicylic acid (ASA) intolerance, which is often associated with nasal polyps. Reliable oral and inhalation provocation tests are time-consuming procedures that often cause the patient discomfort because of accompanying reactions. These tests are therefore best done with the patient hospitalized. Studies concerning the sensitivity, specificity and tolerance of the new intranasal provocation procedure using lysine-ASA were based primarily on cases of bronchial asthma and yielded differing results. Our aim was to examine the above parameters in a large group of patients with nasal polyps (n = 153) and to compare this method with the oral ASA procedure. Intranasal provocation with 2 mg lysine-ASA revealed a sensitivity of 0.47 (n = 30) and a specificity of 0.91 (n = 105), with the test period lasting 40 min. A modified provocation test with 2, 4 and 10 mg lysine-ASA and a 100 min test period resulted in a sensitivity of 0.67 (n = 15) and a specificity of 0.84 (n = 37). All in all, only 2 patients reacted to the test with signs of bronchial asthma. Other reactions to the provocations were limited to the upper respiratory tract or were only found with rhinomanometry. These findings show that nasal provocation with lysine-ASA can be helpful in determining whether an oral provocation test is indicated. The procedure does not take very long, is well-tolerated and can be done in the outpatient department.

Adolescent↗
PubMed1977

Leucocyte migration inhibitory activity of concanavalin-A-stimulated lymphocytes. In vivo and in vitro modifications with dipyridamole and acetylsalicylic acid.

Lymphocytes from 14 patients treated with a combination of acetylsalicylic acid (ASA) and dipyridamole (DIPY) showed a decreased ability to produce leucocyte migration inhibitory activity (LMIA) when stimulated with concanavalin-A (ConA). The combined treatment also produced a decrease of leucocyte response to a standard LMIA-containing culture supernatant. Treatment with only one of the two drugs did not cause detectable alteration of the lymphocyte response to Con-A or the leucocyte response to LMIA. In vitro, both DIPY and ASA were independently effective in decreasing the LMIA production of Con-A-stimulated lymphocytes and the leucocyte response to a standard LMIA-containing culture supernatant.

Adult↗
PubMed1997

Acetylsalicylic acid and vitamin E in prevention of arterial thrombosis.

Both acetylsalicylic acid and vitamin E have been shown to be beneficial in the prevention of stroke and heart attacks. It is implied that their combination in the treatment of thrombotic complications of atherosclerosis may have added benefits. It is suggested that vitamin E may work as a platelet lysosome stabilizing agent.

Arteriosclerosis↗
PubMed1998

In vitro suppression of transforming growth factor-beta induced stimulation of glycosaminoglycan synthesis by acetylsalicylic acid and its reversal by misoprostol.

OBJECTIVE: To determine if acetylsalicylic acid (ASA) suppresses the stimulatory effects of transforming growth factor-beta (TGF-beta) and insulin-like growth factor-1 (IGF-1) on glycosaminoglycan (GAG) synthesis by cultured bovine articular chondrocytes (BAC), and whether such a suppression can be counteracted by the addition of misoprostol, a prostaglandin (PG) E1 analog. METHODS: Confluent cultures of BAC were pre-incubated for 2 days with ASA (Aspirin) (250 microg/ml), TGF-beta (10 ng/ml), IGF-1 (150 ng/ml), and misoprostol (80 ng/ml), separately and in different combinations, and for 2 more days with fresh medium and the same test agents in the presence of 35S-sulfate (10 microCi/ml). The radiolabelled GAG in the medium were then isolated, separated by cellulose acetate electrophoresis, and assayed for incorporated radioactivity, as a measure of GAG synthesis. RESULTS: TGF-beta, IGF-1, at their optimal concentrations, and misoprostol (80 ng/ml) stimulated GAG synthesis 2.6, 1.8, and 2.4-fold, respectively, of the control value, but ASA (250 microg/ml) showed no significant effect. ASA in combination with TGF-beta or misoprostol markedly suppressed the stimulation of GAG synthesis observed with either TGF-beta or misoprostol alone, but had no effect on the stimulation of GAG synthesis by IGF-1. Addition of misoprostol together with TGF-beta potentiated the stimulation of GAG synthesis by TGF-beta and abolished the suppressive effect of ASA on the stimulation of GAG synthesis by TGF-beta. Also, the magnitude of the stimulatory effect of misoprostol varied from batch to batch of misoprostol as well as for the same batch when it was added to the cultures either directly or after diluting with serum-free medium. CONCLUSION: In BAC cultures, ASA suppresses and misoprostol potentiates the stimulation of GAG synthesis by TGF-beta. Misoprostol also counteracts ASA induced suppression of the stimulation of GAG synthesis by TGF-beta.

Animals↗