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PubMed1989

[Cerebral complications in chronic acetylsalicylic acid poisoning].

A 60-year-old woman who for many years had been taking salicylate-containing tablets for headaches, was admitted to hospital, in a somnolent state, because of increasing weakness, tiredness, memory and speech disorders, and tinnitus. Laboratory tests revealed a decompensated metabolic acidosis (pH 7.25), renal insufficiency (creatinine 2.3 mg/dl) and a decreased Quick value (63%). Whole-blood acetylsalicylic acid concentration was markedly elevated to 330 micrograms/ml. After treatment of the acidosis with bicarbonate and forced diuresis she at first regained consciousness, but clouding of consciousness again occurred eight hours later progressing to coma with unequal pupils and seizure potentials in the electroencephalogram. Status epilepticus without motor component was diagnosed, perhaps the result of a dysequilibrium of acid-base balance between blood and cerebrospinal fluid. The signs and symptoms were quickly reversed under treatment with clonazepam.

Aspirin↗
PubMed2002

Application of hydroalcoholic solutions of formaldehyde in preparation of acetylsalicylic acid gastro-resistant capsules.

Enteric coating of hard gelatin capsules by application of hydroalcoholic solutions of formaldehyde was studied and developed in accordance with previous publications. It is possible to affirm that this coating constitutes a simple, stable, reproducible, and inexpensive method, being a valid alternative to those which have been proposed. The aim of the present investigation is the preparation of acetylsalicylic acid gelatin capsules with good conditions of gastro-resistance and enteros solubility.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed2004

Effects of acetylsalicylic acid on experimental atherogenesis induced in rabbits.

AIM: Inflammation related processes play a key role in the current etiologic model of atherosclerosis and its acute complications. In addition, platelet-derived growth factors stimulate the neointimal proliferation of restenosis after coronary interventions. Reducing platelet accumulation at treated sites may attenuate restenosis. The purpose of this experimental study was to investigate the effect of acetylsalicylic acid (ASA), a widely used anti-platelet and anti-inflammatory agent on the development and extent of atherosclerosis. METHODS: Fourty-eight male white New Zealand rabbits were separated in 4 groups (12 animals each group). Group I received a diet of 2% cholesterol and 6% corn oil for 3 months. Group II received a diet of 2% cholesterol and 6% corn oil and in addition received 3 mg of ASA/kg daily intramuscular (i.m.) for 3 months. Group III received the same diet, and in addition received 10 mg of ASA/kg daily i.m. for 3 months. Group IV received the same diet and in addition received 50 mg of ASA/kg daily i.m. for 3 months. Animals were sacrificed after 3 months. RESULTS: ASA reduced the serum levels of total cholesterol, total lipids, triglycerides and LDL cholesterol. There was significant difference in the extent of atherosclerotic lesions between animals which received different doses of ASA and that animals which did not received any ASA. High dose ASA treatment resulted in an increase in fasting plasma glucose, associated with a reduction in total cholesterol and triglycerides. CONCLUSION: Our results suggest that there is a protective effect on atherosclerosis development of ASA down stream from where it lowers plasma fatty acid concentrations. However, further studies are required to verify that effect.

Animals↗
PubMed1987

[A combination of dihydroergotamine and acetylsalicylic acid--prevention of postoperative thromboembolic complications. Clinical study in orthopedics].

202 patients undergoing surgery involving the lower limbs were given antithrombotic treatment for at least 21 days, or until they had regained full mobility. Following subcutaneous prophylaxis with a combination of heparin and dihydroergotamine, two oral regimens were compared in a controlled and randomized prospective study. The first treatment consisted of a combination of acetylsalicylic acid (ASA) and dihydroergotamine (DHE), and the second of acenocoumarol. The radiofibrinogen uptake test was carried out in high-risk patients (i.e. those undergoing hip surgery) to detect deep-vein thrombosis. No statistically significant difference was found between the two groups. However, the ASA/DHE combination enjoyed better patient acceptance and was much easier to use.

Acenocoumarol↗
PubMed1982

Fecal blood loss caused by two differently microencapsulated acetylsalicylic acid preparations in patients with rheumatoid arthritis. A prospective crossover study.

In an investigator-blind crossover study, fecal blood loss determined by 51Cr-labelled red cells was measured in 17 male patients with rheumatoid arthritis and one with anchylosing spondylitis. In two periods, each of one week's duration and separated by a 3-week wash-out period, the patients received microencapsulated acetylsalicylic acid (ASA) 3 g daily--either iwht time-dependent (Acetard) or with pH-depeendent release (Reumyl). With the exception of one patient, who suffered clinically significant bleeding, both preparations produced only moderate bleeding. The bleeding provoked by ASA with pH-dependent release (median blood loss in ml/day: first period 1.6; last period 2.6) was less than with time-dependent release (first period 1.8; last period 3.5).

Adult↗
PubMed2000

Lack of impact of low-dose acetylsalicylic acid on kidney function in type 1 diabetic patients with microalbuminuria.

OBJECTIVE: High-dose treatment with cyclooxygenase inhibitors reduces urinary albumin excretion rate (AER) in type 1 diabetic patients with microalbuminuria and macroalbuminuria. This effect may lead to an incorrect classification of albuminuria (normo-, micro-, and macroalbuminuria) and jeopardize the monitoring of antiproteinuric treatment (e.g., ACE inhibition). Whether similar difficulties exist using low-dose acetylsalicylic acid (ASA), now widely recommended for primary and secondary prevention of cardiovascular events in type 1 diabetic patients with micro- and macroalbuminuria, remains to be elucidated. RESEARCH DESIGN AND METHODS: We performed a randomized double-blind crossover trial in 17 type 1 diabetic patients with microalbuminuria (urinary AER 30-300 mg/24 h). Patients were given ASA (150 mg/daily) for 4 weeks followed by placebo for 4 weeks with at least a 2-week washout period in random order. At the end of each treatment period, AER (enzyme-linked immunosorbent assay), glomerular filtration rate (GFR) (plasma clearance of 51Cr-EDTA), blood pressure (BP) (Hawksley), and HbA1c (by high-performance liquid chromatography) were measured. Patients were advised to follow a normal diabetes diet without sodium restriction and received their usual antihypertensive treatment during the investigation. RESULTS: During the study (ASA vs. placebo), urinary AER (geometric mean 64 [95% CI 39-105] vs. 59 [40-87] mg/24 h), GFR (mean 106 [93-118] vs. 104 [90-117] ml x min(-1) x 1.73 m(-2)), systolic BP (mean 130 [119-141] vs. 130 [119-142] mmHg), diastolic BP (mean 71 [65-78] vs. 71 [64-78] mmHg), and HbA1c (mean 8.4% [8.0-9.0] vs. 8.5% [8.1-9.0]) remained unchanged. CONCLUSIONS: Treatment with 150 mg ASA daily does not have any impact on AER or GFR in type 1 diabetic patients with microalbuminuria. Consequently, primary and secondary prevention of cardiovascular events with low-dose ASA does not interfere with the classification of AER or monitoring of antiproteinuric treatment in such patients.

Adult↗
PubMed2002

[The effect of acetylsalicylic acid on hypotensive action of enalapril in hypertensive patients].

The complex hypotensive action of angiotensin converting enzyme inhibitors (ACEI) results not only from inhibition of converting not active angiotensin I to strong vasoconstrictor-angiotensin II but also from diminution of inactivation of potent vasodilator-bradykinin. Bradykinin promotes generation by endothelium such substances as endothelium-derived hyperpolarizing factor, prostacyclin and nitric oxide. Simultaneous therapy with acetylsalicylic acid, which inhibits synthesis of prostanoids, and ACEI may block one of potent hypotensive mechanisms of ACEI. This study indicates that concomitant therapy with 150 mg of aspirin per day does not reduce hypotensive efficacy of enalapril.

Adult↗
PubMed1991

Evaluation of the buccal bleeding time and platelet glass bead retention as assays of hemostasis in the dog: the effects of acetylsalicylic acid, warfarin and von Willebrand factor deficiency.

The study evaluated two hemostatic assays in the dog, a modified version of the buccal mucosal bleeding time (BMBT) and the platelet glass bead retention (PR), to describe the aspects of hemostasis measured by these assays. Von Willebrand factor (vWf)-deficient Doberman pinscher dogs were used in evaluating the effects of altered platelet adhesion. Normal dogs were treated with either acetylsalicylic acid (ASA) or warfarin to evaluate the effects of altered platelet aggregation and coagulation. There was significant prolongation of the BMBT and reduction of the PR in vWf-deficient dogs as compared to normal dogs. In ASA treated dogs the BMBT was slightly prolonged; the PR was significantly reduced. The change in ASA-induced BMBT did not correlate with the sensitivity of the dog platelets to arachidonic acid. In warfarin treated dogs there was no change in the BMBT; however, the PR was significantly reduced. The BMBT is a test of hemostasis that is sensitive to platelet adhesion and aggregation deficits. The PR is useful in detecting general abnormalities in hemostasis including platelet adhesion defects due to reduced vWf.

Animals↗
PubMed2003

Dissolution testing of acetylsalicylic acid by a channel flow method-correlation to USP basket and intrinsic dissolution methods.

A new modification of the channel flow dissolution method is introduced together with the theoretical basis to extract the solubility and mass transfer parameters from the dissolution experiments. Correlation of drug dissolution profiles in the channel flow apparatus was evaluated with respect to USP basket and intrinsic dissolution methods at pH 1.2 or 6.8. Acetylsalicylic acid (ASA) was studied as a pure drug substance and as three simple tablet compositions with microcrystalline cellulose (MCC) and/or lactose as excipients. The channel flow measurements of 100% ASA tablets correlated well with the results of intrinsic dissolution tests. In the channel flow method as well as in the USP basket method the release of ASA was fastest from the tablet compositions containing lactose, while the slowest dissolution rate was observed with the composition containing MCC as the only excipient. As presumed, the dissolution rate of the weak acid was decreased as the pH of the medium was lowered, which was clearly confirmed also by the three dissolution methods. MCC forms matrix tablets and in the USP basket method the dissolution profiles followed square root of time kinetics indicating that diffusion was the rate-controlling step of ASA dissolution. Also the channel flow results indicated that the dissolution of ASA was controlled by mass transfer. The swelling behaviour of the tablets is different in the channel flow method as compared to the basket method: only one tablet surface is exposed to the dissolution medium in the channel flow system. The contact between the tablet surface and the dissolution medium is more similar between the channel flow and intrinsic dissolution methods.

Algorithms↗
PubMed1981

Effect of various doses of acetylsalicylic acid in combination with dipyridamole on the balance between prostacyclin and thromboxane in human serum.

1 Thirty-six healthy human subjects were randomly divided into six groups which were treated with a single dose of 75 mg (1.3 mg/kg) of dipyridamole alone, or 75 mg of dipyridamole in combination with 30 mg (0.5 mg/kg), 50 mg (0.8 mg/kg), 160 mg (2.6 mg/kg) and 330 mg (5.7 mg/kg) of acetylsalicylic acid (ASA), or with placebo. 2 The concentrations of prostacyclin (PGI2) and thromboxane A2 (TxA2) metabolites, 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) and TxB2 respectively, were measured in serum with specific radioimmunoassays before and 1 and 3 h afer the ingestion of the test dose. 3 The basal concentrations of 6-keto-PGF1 alpha and TxB2 correlated significantly (r = 0.588, P less than 0.001). 4 Dipyridamole alone did not change PGI2 or TxA2 production. 5 Dipyridamole-ASA combinations with ASA doses between 0.5 and 0.8 mg/kg inhibited TxB2 production by 48 to 74% and with the ASA doses between 2.6 and 5.7 mg/kg by about 90%. None of these combinations changed PGI2 production. 6 The ratio of 6-keto-PGF1 alpha to TxB2 increased 3.5 to 6 times with ASA doses of 0.5 to 0.8 mg/kg and 21 to 29 times with doses between 2.6 to 5.7 mg/kg. 7 These results suggest that the anti-thrombotic effect of dipyridamole in vivo is not mediated through direct changes in PGI2 and/or TxA2 production.

Adult↗
PubMed1997

Effect of acetylsalicylic acid on pulmonary gas exchange in patients with severe pneumonia: a pilot study.

BACKGROUND: It has been hypothesized that local release of prostacyclin in acute pneumonia may ablate hypoxic pulmonary vasoconstriction, thus contributing to the impairment of pulmonary gas exchange in these patients. Inhibition of cyclooxygenase pathway could prevent this phenomenon by reducing the release of these metabolites. METHODS: A study was designed to assess the effect of I.V. acetylsalicylic acid (ASA) (2 g) on pulmonary gas exchange in seven patients (age, 64+/-11 [mean+/-SD] years) with unilateral severe pneumonia (PaO2/fraction of inspired oxygen, 168+/-67) needing mechanical ventilation. Respiratory gases, pulmonary and systemic hemodynamics, and ventilation-perfusion (VA/Q) distributions were studied before and 15 and 60 min after the infusion of ASA. RESULTS: At baseline, the amount of shunt (VA/Q ratios <0.005) was 28+/-17% of cardiac output, blood flow to areas with low VA/Q ratios (<0.1, excluding shunt) was 8+/-7%, and the dispersion of pulmonary blood flow distribution (second moment, log SD Q) was 1.45+/-0.49 (normal range, 0.3 to 0.6). Sixty minutes after the infusion of ASA, we observed a mild reduction of the amount of shunt, from 28+/-17% to 23.5+/-13% (p<0.05) without changes in arterial oxygenation. This was associated with a significant increase in mean pulmonary artery pressure (from 21.9+/-3.6 to 24.4+/-5.1 and 23.9+/-5.3 mm Hg, p<0.025 and p=0.1) and pulmonary vascular resistance (from 1.4+/-0.9 to 1.8+/-0.8 and 1.8+/-1.3 mm Hg x min x L(-1) , p<0.002 and p=0.11) 15 and 60 min after ASA, respectively. The ASA plasma levels were within the normal therapeutic range (120+/-7 microg/mL, 15 min, and 113+/-11 microg/mL, 60 min after ASA infusion). CONCLUSIONS: Although there was a modest improvement in intrapulmonary shunt, our results suggest that perfusion of ASA in this small sample of patients with severe pneumonia appears to be of little benefit as complementary treatment for severe hypoxemia.

Adult↗
PubMed1977

[Quantitative assessment of drug-induced prophylaxis of postoperative thromboembolism. Comparison of frequencies of deep vein thrombosis and pulmonary embolism using acetylsalicylic-acid, dextran, dihydroergotamine, low-dose heparin and the fixed combination of heparin and dihydroergotamine (author's transl)].

2136 patients in general surgery, gynaecology and urology were investigated by the 125I-fibrinogen-uptake-test for detection of postoperative deep vein thrombosis (DVT). They received at random one of low-dose heparin, dihydroergotamine, the fixed combination of both drugs (Heparin-Dihydergot), low molecular weight dextran and acetylsalicylic-acid (ASS). When DVT was detected repeated lung perfusion scintigraphies were carried out for diagnosis of embolic pulmonary perfusion defects. Results demonstrate the outstanding effect of Heparin-Dihydergot, which is not only 2-3 times better than the anti-thrombotic standard low-dose heparin but also eliminates almost completely the risk of postoperative embolism. The preventive efficacy of ASS and dextran must be considered to be poor and not comparable to that obtained when using heparin, dihydroergotamine or the combination. Now Heparin-Dihydergot is the new standard with which all prophylactic procedures should be compared.

Adult↗
PubMedDate not supplied

Clinical evidence of an interaction between imipramine and acetylsalicylic acid on protein binding in depressed patients.

The binding of imipramine to plasma proteins was studied in 20 adult patients with endogenous depression, with the purpose of assessing the effect produced by its simultaneous administration with an analgesic. Patients were administered 150 mg/day imipramine for 5 days and the binding to plasma proteins was determined. This was repeated 2 days later, after simultaneous administration of imipramine with 1,000 mg/day acetylsalicylic acid (ASA). Adverse effects for each patient were registered during both phases and were classified as mild, moderate, or severe. Results showed 84.4 +/- 7.07% of imipramine bound to plasma proteins and 72.18 +/- 6.5% when imipramine was administered with ASA (p < 0.05). When imipramine was administered alone, 1.95 mild adverse events per patient were registered. When imipramine was administered with ASA, the mild adverse events increased to 3.1 (p < 0.01) and the severe adverse events increased from 0.6 to 1.5 (p < 0.01). The levels of free imipramine increased when ASA was administered, indicating a displacement on the binding to plasma proteins. When adverse events were compared for each treatment, the accumulation of the free fraction of imipramine caused an increase in adverse events as well as in their clinical severity.

Adolescent↗
PubMedDate not supplied

Effects of different doses of acetylsalicylic acid on platelet aggregation: an experimental study of prosthetic materials in dogs.

Laminar flow is the condition best suited to the study of platelet thrombi. This type of thrombus is predominant in arteries, in the tubes of cannulas used in artificial circulatory systems, in cardiac valve prostheses and in prosthetic arterial implants. Antiplatelet drugs could, in these cases, reduce the extent of thrombus formation. At present the optimal dose of acetylsalicylic acid (ASA) to achieve the best antithrombotic effect is unknown; some papers show that high doses augment experimental thrombosis. By means of autologous platelets labelled with 111In-oxine, we have quantified the accumulation on different materials used in cardiovascular surgery (woven, knitted and double velour Dacron, Avcothane 51 elastomere and smooth surface and rough surface pericardium). Samples of these fabrics were placed in a laminar flow chamber connected between the right atrium and femoral artery of the experimental animals (dogs). The animals were divided into four groups of eight dogs: Group I: no treatment Group II: animals treated one week earlier with ASA (1 mg/kg/day) Group III: as in Group II, but at a dose of 5 mg/kg/day Group IV: as in Group II, but at a dose of 20 mg/kg/day. The materials upon which the least amount of platelets were accumulated were the smooth, epicardial surface of pericardium (SP) and Avcothane (AV). The least deposition was produced in Group III, with the exception of SP. In the case of this material, there was no difference between Groups I and III. In Group IV, the deposit was greater with respect to the untreated group (Group I), except in the case of AV, in which there was no difference between Groups I and IV.

Animals↗
PubMed1983

[Drug concentrations in blood, synovial fluid, synovial membrane, periarticular bone, muscle and adipose tissue in patients with rheumatoid polyarthritis receiving a single intramuscular injection of ketoprofen or acetylsalicylic acid (3 hours after the injection)].

The therapeutic activity of antiinflammatory agents in rheumatic joint disease is related to their presence at the target site of action, i.e. the joints. Tissue concentrations of such agents have been previously determined in patients with rheumatic disorders under long-term treatment with acemetacin and indomethacin (Köhler et al., 1981). The purpose of the present study was to determine concentrations of ketoprofen and acetylsalicylic acid in blood as well as synovial fluid, synovial membrane and periarticular bone and adipose tissue, three hours after administration of a single dose. Drug concentrations found in each of these tissues following a single intramuscular injection were sufficient to ensure therapeutic efficiency.

Adipose Tissue↗
PubMed1989

Modulation of phenytoin teratogenicity and embryonic covalent binding by acetylsalicylic acid, caffeic acid, and alpha-phenyl-N-t-butylnitrone: implications for bioactivation by prostaglandin synthetase.

Teratogenicity of the anticonvulsant drug phenytoin is thought to involve its bioactivation by cytochromes P-450 to a reactive arene oxide intermediate. We hypothesized that phenytoin also may be bioactivated to a teratogenic free radical intermediate by another enzymatic system, prostaglandin synthetase. To evaluate the teratogenic contribution of this latter pathway, an irreversible inhibitor of prostaglandin synthetase, acetylsalicylic acid (ASA), 10 mg/kg intraperitoneally (ip), was administered to pregnant CD-1 mice at 9:00 AM on Gestational Days 12 and 13, 2 hr before phenytoin, 65 mg/kg ip. Other groups were pretreated 2 hr prior to phenytoin administration with either the antioxidant caffeic acid or the free radical spin trapping agent alpha-phenyl-N-t-butylnitrone (PBN). Caffeic acid and PBN were given ip in doses that respectively were up to 1.0 to 0.05 molar equivalents to the dose of phenytoin. Dams were killed on Day 19 and the fetuses were assessed for teratologic anomalies. A similar study evaluated the effect of ASA on the in vivo covalent binding of radiolabeled phenytoin administered on Day 12, in which case dams were killed 24 hr later on Day 13. ASA pretreatment produced a 50% reduction in the incidence of fetal cleft palates induced by phenytoin (p less than 0.05), without significantly altering the incidence of resorptions or mean fetal body weight. Pretreatment with either caffeic acid or PBN resulted in dose-related decreases in the incidence of fetal cleft palates produced by phenytoin, with maximal respective reductions of 71 and 82% at the highest doses of caffeic acid and PBN (p less than 0.05). Caffeic acid and PBN also significantly reduced the incidence of fetal resorptions produced by phenytoin, but not the fetal weight loss. In viable embryos, ASA pretreatment reduced the covalent binding of phenytoin to embryonic protein by 43% (p less than 0.05). Binding of phenytoin to embryonic resorptions was equally high with and without ASA pretreatment, and within each treatment group was 3- to 10-fold higher than that in the respective placentas and associated viable embryos (p less than 0.05). These results suggest that prostaglandin synthetase may contribute to the enzymatic bioactivation of phenytoin to a teratogenic free radical intermediate.

Abnormalities, Drug-Induced↗
PubMed2000

Influence of acetylsalicylic acid on oxidation of native and glycated low-density lipoprotein.

It is generally accepted that oxidation of low-density lipoproteins (LDL) is a causal factor in the development of atherosclerosis. Non-enzymatic glycosylation of LDL, i.e."glycation", plays a central role in late complications of diabetes mellitus and may initiate and/or accelerate the oxidation process. Therefore, the inhibition of this processes is of major therapeutic relevance. The influence of acetylsalicylic acid (ASA) on the oxidation of native and glycated LDL was studied in vitro. LDL (0.25 mg protein/ml ) was oxidatively modified with 5.0 microM CuSO4. Only at "supratherapeutical" ASA concentrations in the range 0.06-2.0 mg /ml we found a significant concentration-dependent inhibition of LDL oxidation both for native and glycated LDL, which was from 0.2 mg/ml upwards significantly more marked for native LDL than for glycated LDL. The maximal inhibitory effect occurred at 2.0 mg/ml with 89.6% inhibition of LDL-oxidation for native LDL and 64.4% for glycated LDL. At 0.2 mg/ml ASA the respective inhibitory values were 38.5% and 31.0%. For glycated LDL the ASA doses of maximal- and approximately 50%-inhibition, as found for native LDL, were chosen to investigate the inhibitory effect on 2,4,8 and 24 hours oxidation of glycated LDL to monitor the time-dependency of inhibition by ASA. This revealed that ASA only delayed, not permanently inhibited LDL oxidation.

Adult↗
PubMed1985

Enteric-coated acetylsalicylic acid plus dipyridamole compared with anticoagulants in the prevention of ischemic events in patients with transient ischemic attacks.

From December 1976 through March 1982, 188 patients entered an open non-random study carried out on hospitalized patients with a history of transient ischemic attacks or amaurosis fugax. Ninety-two patients received peroral anticoagulants usually combined with heparin treatment during the first days of treatment, and 96 patients enteric-coated acetylsalicylic acid 0,5 g twice daily plus dipyridamole 75 mg twice daily. The patients were followed up to March 1983, irrespective of whether treatment was changed or not. Recurrent transient ischemic attack or amaurosis fugax occurred more frequently (P less than 0.01) from 2 months of follow-up and throughout the observation period in the antiplatelet-treated group. There were no statistically significant differences between the 2 groups on the originally given treatment for endpoints such as stroke (6 patients on anticoagulants, 12 patients on antiplatelet therapy) or stroke or death (11 patients on anticoagulants, 17 patients on antiplatelet therapy). The findings from this trial suggest that anticoagulant treatment is superior to antiplatelet therapy given in the prevention of ischemic attacks and that this difference mainly exists during the first one to 2 months after onset of transient ischemic attacks or amaurosis fugax.

Aged↗