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PubMed1995

[Protective effect of omeprazole against low-dose acetylsalicylic acid. Endoscopic controlled double-blind study in healthy subjects].

Protective Effects of Omeprazole against Low-dose Acetylsalicylic Acid/An endoscopic controlled double-blind study in healthy volunteers. In a randomized double-blind parallel study the gastroduodenal tolerability of 300 mg acetylsalicylic acid (CAS 50-78-2, ASA) daily (8 p.m.) has been evaluated in the presence of 20 mg and 40 mg omeprazole (CAS 73590-58-6) daily (8 p.m.) or placebo in 36 healthy volunteers using upper GI-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 0.9 +/- 0.08 in the ASA/placebo (n = 12), the ASA/omeprazole 20 mg (n = 12) and the ASA/omeprazole 40 mg group (n = 12). The median values were 1.0. In the placebo experiments 300 mg ASA daily induced marked gastroduodenal lesions at day 14 (12.4 +/- 1.7). The median value was 10.0. Concomitant administration of 20 mg omeprazole daily afforded significant protection against 300 mg ASA daily on day 14 (2.9 +/- 0.9) (p < 0.0005 vs. ASA/placebo). 300 mg ASA + 40 mg omeprazole daily reduced the damaging score to 1.8 +/- 0.5 (p < 0.00002 vs. ASA/placebo). The median values in the ASA/omeprazole 20 mg and in the ASA/omeprazole 40 mg group were 1.0. The difference in the damaging score between ASA/omeprazole 20 mg and ASA/omeprazole 40 mg after 14 days did not reach statistical significance. Our data suggest that coadministration of 20 mg omeprazole daily reduces almost completely gastroduodenal lesions evoked by 300 mg ASA.

Adult↗
PubMed1994

Effects of ibuprofen lysinate and acetylsalicylic acid on gastric and duodenal mucosa. Randomized single-blind placebo-controlled endoscopic study in healthy volunteers.

Acetylsalicylic acid (ASA, CAS 50-78-2) and ibuprofen (IB) are commonly used over-the-counter drugs for short-term treatment of pain of different origin. Ibuprofen lysinate (IBL, CAS 57469-76-8) is a water soluble form of ibuprofen for rapid absorption. This single blind, randomized, controlled study compared the incidence and severity of irritation of gastric and duodenal mucosa in normal healthy subjects (n = 45) following administration of IBL (Dolormin) 800 mg/d, ASA 2000 mg/d or placebo for 3 consecutive days. Gastric and duodenal mucosal injury were assessed endoscopically using a severity scale of 0-4 for mucosal erosions and mucosal hemorrhages. Mean gastric hemorrhage and erosion scores for ASA and IBL were significantly higher than those for placebo. In addition, ASA was found to be significantly more irritating to gastric mucosa than IBL, in both the incidence and severity of gastric erosions. No duodenal hemorrhages were detected in this study. The incidence of duodenal erosions was significantly higher in the ASA group (64%) than in both the IBL (6%) and placebo groups (0%) which were not significantly different. Only one subject (in the placebo group) reported an adverse experience (mild headache) during the study. The data suggest that both active treatments are more injurious to the gastric mucosa than placebo when given for 3 days to normal healthy volunteers, but that IBL 800 mg/d is significantly less injurious to the gastric and duodenal mucosa than ASA 2000 mg/d.

Adult↗
PubMed1997

Acetylsalicylic-acid-containing drugs and nonsteroidal anti-inflammatory drugs available in Canada.

A large number of drugs containing acetylsalicylic acid (ASA) and nonsteroidal anti-inflammatory drugs (NSAIDs) are available by prescription and over the counter in Canada. The possibility of serious side effects and drug interactions is therefore high. The authors have compiled a comprehensive list of products containing these drugs from information supplied by pharmaceutical databases, independent marketing researchers and Health Canada's Drug Directorate. Physicians should ensure that additional ASA-containing drugs or NSAIDs are not inadvertently taken by patients, especially those receiving oral anticoagulant therapy or those with a qualitative platelet defect. Patients at risk should be cautioned to check with their physician before taking any new medication, even over-the-counter products.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMedDate not supplied

Intravenously administered acetylsalicylic acid in combination with low-dose heparin in acute ischemic stroke: a safety analysis.

Although therapy with acetylsalicylic acid (aspirin, ASA) is well established in secondary prevention of stroke, efficacy and side effects of this substance in acute stroke treatment are undetermined. ASA may be useful in acute cerebral ischemia because of its potential to prevent thrombus propagation and neuronal damage. A total of 268 patients with an acute cerebral ischemia, who were admitted to our stroke unit within 24 hours after stroke, were treated with intravenously administered ASA (0.5 g/day) in combination with low-dose heparin. The functional status of the patients was assessed after 1 month using the modified Rankin Scale. Eighteen (6.7%) patients died during the observation period. The functional status according to Rankin Scale was classified as stage 0 in 76 (28.3%), 1 in 59 (22.0%), 2 in 39 (14.6%), 3 in 32 (12.3%), 4 in 36 (13.4%), and 5 in 7 (2.6%) patients. A symptomatic secondary intracerebral hemorrhage was seen in one patient. Gastrointestinal symptoms were observed in 13 (4.8%) patients, including five instances of gastrointestinal bleeding. Further complications were allergic reactions to aspirin (one) and hematuria (one). Recurrent cerebral ischemia occurred in nine (3.3%) patients (five with transient ischemic attack or minor stroke) during the observation period. We conclude that treatment of acute ischemic stroke with intravenously applied aspirin in combination with low-dose heparin is safe. Efficacy of this therapy should be elucidated in a controlled trial.

Acute Disease↗
PubMed1987

Pulmonary haemodynamics during exercise after low and high doses of acetylsalicylic acid in sheep.

Despite comparable increases in cardiac output there is a greater reduction in pulmonary vascular resistance (PVR) in sheep during exercise than in dog or man. The mechanism for this marked reduction in PVR in sheep is unknown. To assess the role of arachidonic acid metabolites in producing this low PVR we measured the effect of intravenous acetylsalicylic acid (ASA, 10 mg/kg) on PVR at rest and during exercise in sheep. ASA caused a slight rise in resting PVR (p less than 0.05), but did not affect the exercise-induced decrease in PVR. High-dose ASA (100 mg/kg), presumably sufficient to block the lipoxygenase pathway produced the same responses as low-dose ASA which should only block the cyclo-oxygenase pathway. Products of the cyclo-oxygenase and lipoxygenase pathways which include vasodilator prostaglandins, have only a minor role in maintaining low pulmonary vascular resistance at rest and have no demonstrable role in the reduced PVR that occurs during exercise in sheep.

Animals↗
PubMed2004

Life-history traits of standard and autochthonous cladocerans: I. Acute and chronic effects of acetylsalicylic acid.

Pharmaceuticals have been recognized as an important group of aquatic micropollutants, mainly because of their biologically active nature. Acetylsalicylic acid (ASA), which is the active compound of Aspirin and many other pharmaceuticals, is consumed in large quantities every year. Therefore, its acute and chronic effects on standard (Daphnia magna) and autochthonous (Daphnia longispina) daphnids were investigated. The results showed that ASA impaired the survivorship, reproduction, and growth of the cladoceran species. The standard daphnid was the more tolerant species in acute assays (48-h EC(50) = 1293.05 mg/L; D. longispina: 48-h EC(50) = 647.31 mg/L); whereas the autochthonous daphnid seemed to be more resistant under chronic exposure to ASA, mainly its population-level traits. Despite this, the observed effect concentrations were much higher than the environmental concentrations of ASA. Notwithstanding this, the impairment of individual-level traits is likely to occur at environmental levels as an ultimate response to long-term exposure.

Animals↗
PubMed1993

Anorectal stenosis in patients with prolonged use of suppositories containing paracetamol and acetylsalicylic acid.

We report five cases in which anorectal stenosis was associated with chronic administration of suppositories containing paracetamol and acetylsalicylic acid. All patients were females taking suppositories for chronic migraine. Patients experienced anal pain, tenesmus, fecal incontinence, and, in two cases, intestinal obstruction. Lesions were characterized by a severe circular narrowing of the distal rectum with superficial ulcerations. Radiographs demonstrated the presence of sinus-tract-like formations in the diseased segment and thickening of the rectal wall. Histologic examination showed signs of chronic inflammation with deep ulcerations associated with obliteration of the lamina propria by a fibromuscular proliferation, as was described in the solitary ulcer syndrome of the rectum. Rectal administration of suppositories was discontinued in all the patients. Two patients were improved by anorectal dilatation, but the remaining three required a left proctocolectomy with subsequent coloanal anastomosis. The use of such suppositories must be restricted.

Acetaminophen↗
PubMed1994

Effects of acetylsalicylic acid on parameters related to peroxisome proliferation in mouse liver.

Male C57 BL/6 mice were exposed to 1.0% (w/w) acetylsalicylic acid (ASA) in their diet for 10 days and effects related to peroxisome proliferation were subsequently examined. A 2.2-fold increase in mitochondrial protein content was obtained. The activities of the peroxisomal enzymes, lauroyl-CoA oxidase, palmitoyl-CoA oxidation and catalase, were enhanced 4.5-, 4.0- and 2.1-fold, respectively. There was a dramatic increase (9.1-fold) in microsomal cytochrome P450 IVA-catalysed activity, a 1.6-fold induction of total microsomal P450 content and a 2-fold induction of microsomal cytochrome P450 reductase activity (measured as NADPH-cytochrome c reductase). Catalase activity in the cytosol was induced 5.2-fold and DT-diaphorase activity was increased 3.5- and 3.2-fold in the cytosol and mitochondria, respectively. There was a significant increase in the susceptibility of microsomes to lipid peroxidation. Smaller increases in superoxide dismutase, glutathione transferase and glutathione peroxidase activities were also observed. The possible relevance of these effects to the pharmacology of ASA is discussed.

Animals↗
PubMed2004

N-way PLS applied to simultaneous spectrophotometric determination of acetylsalicylic acid, paracetamol and caffeine.

In this work, a simple and rapid analytical procedure was proposed for simultaneous determination of acetylsalicylic acid (ASA), paracetamol (PRC, also known as acetaminophen) and caffeine (CAF) in pharmaceutical formulations based on multivariate calibration and UV spectrophotometric measurements (210-300 nm). The calibration set was constructed with nine solutions in the concentration ranges from 10.0 to 15.0 microg x ml(-1) for ASA and PRC and from 2.0 to 6.0 microg x ml(-1) for CAF, according to an experimental design. The procedure was repeated at four different pH values: 2.0, 3.0, 4.0 and 5.0. Partial least squares (PLS) models were built at each pH and used to determinate a set of synthetic mixtures. The best model was obtained at pH 5.0. An N-way PLS model was applied to a three-way array constructed using all the pH data sets and enabled better results. This calibration model provided root mean squares errors of prediction (RMSEP) from 11.5 to 35% lower than those obtained with PLS at pH 5.0, depending on the analyte. The results achieved for the determination of these drugs in commercial tablets were in agreement to the values specified by the manufactures and the recovery was between 94.7 and 104.5%.

Acetaminophen↗
PubMed1996

Effect of acetylsalicylic acid on radiation and cosmetic results after conservative surgery for early breast cancer: a randomized trial.

BACKGROUND AND PURPOSE: Acetylsalicylic acid (ASA) can reduce the incidence of stroke and myocardial infarction by inhibiting platelet-fibrin thrombi in small blood vessels. To determine if ASA could reduce late effects of radiation therapy mediated by damage to small blood vessels, a prospective, placebo-controlled, double-blind trial was conducted in women with early breast cancer, receiving radiotherapy to the conserved breast. MATERIALS AND METHODS: Cosmetic outcome and late radiotherapy effects were recorded prospectively for 186 women with T1 or T2, pathologically node-negative breast cancer treated with breast conservation and randomized to receive ASA (325 mg daily) or placebo for 1 year from the start of radiation therapy. Radiation was a tangent pair to the breast alone delivering a modal dose of 44 Gy in 16 daily fractions in 22-25 days. RESULTS: Median follow-up is 6.5 years. The use of ASA has not had any effect on the acute (erythema, edema or discomfort) or late (induration, telangiectasia) effects of radiotherapy (all P > 0.10), the patients' or physicians' assessment of the cosmetic outcome (all P > 0.25) or rates of breast recurrence (P > 0.25). CONCLUSION: ASA cannot be recommended to improve the outcome of radiotherapy complementing breast conserving surgery.

Aspirin↗
PubMed1984

Dose-related effect of acetylsalicylic acid on replication of varicella zoster virus in vitro.

Cultivation of human embryonic lung (HEL) cells in media containing acetylsalicylic acid (ASA) at 100 micrograms/ml and maintenance at this level after inoculation with either cell-free varicella zoster virus (VZV) or virus-infected cells resulted in a 2- to 4-fold increase in yields of cell-free virus released by sonication. The degree of enhancement was dependent upon multiplicity of infection and time of harvest. Enhanced viral yields were not consistently accompanied by an increase in the number of infected cells, nor was VZV plaque formation in HEL indicator cells significantly increased in the presence of ASA at 100 micrograms/ml. In the presence of ASA at 500-1000 micrograms/ml, VZV plaque formation was inhibited; this inhibition was partially reversible, depending on concentration and period of exposure to ASA. These findings may bear on the apparent association between ASA ingestion and the development of Reye syndrome after infection with varicella virus.

Aspirin↗
PubMed2000

Influence of acetylsalicylic acid on development of radiation-induced nephropathy.

PURPOSE: Previous studies have demonstrated that long-term treatment with acetylsalicylic acid (ASA) can significantly reduce the renal functional impairment that develops after high doses of irradiation. The effect is hypothesized to be mediated by selective inhibition of thromboxane A2 synthesis and inhibition of platelet aggregation. The present study was undertaken to investigate this phenomenon further using more clinically relevant fractionated and re-irradiation schedules. METHODS AND MATERIALS: Groups of mice were given bilateral renal irradiation with a series of four or 20 daily fractions of X-rays, or 10 daily fractions with a single dose of re-irradiation (0-10 Gy) after 27 weeks. Half the mice received ASA in drinking water (2.4 g x l(-1)) from 1 week before the start of irradiation and continuously throughout the follow-up period. Renal function was assessed by clearance of [51Cr]EDTA, about every 4 weeks for up to 80 weeks after the start of treatment. Histological damage in representative groups of mice was also assessed. RESULTS: Oral administration of ASA caused inhibition of thromboxane A2 synthesis (to < 36% of controls) and a strong inhibition of platelet aggregation in whole mouse blood (ex vivo). Prolonged treatment with ASA also resulted in a small, non-significant reduction of radiation-induced renal functional damage. No reduction in histological damage was seen in the ASA treated mice. CONCLUSION: Long-term oral administration of ASA gave only a modest, non-significant reduction of renal radiation injury after clinically relevant fractionated irradiation schedules.

Animals↗
PubMed2006

Shortened onset of action of antidepressants in major depression using acetylsalicylic acid augmentation: a pilot open-label study.

Based on our preclinical data showing a potential accelerating effect of acetylsalicylic acid (ASA) in combination with fluoxetine in an animal model of depression, we examined the effect of ASA augmentation therapy on selective reuptake inhibitors (SSRI) in major depressed non-responder patients. Twenty-four non-responder patients having received at least 4 weeks of an adequate SSRI treatment were included in a pilot open-label study. Participants were treated openly during 4 weeks with 160 mg/day ASA in addition to their current antidepressant treatment. The combination SSRI-ASA was associated with a response rate of 52.4%. Remission was achieved in 43% of the total sample and 82% of the responder sample. In the responder group, a significant improvement was observed within week 1 (mean Hamilton Depression Rating Scale-21 items at day 0=29.3+/-4.5, at day 7=14.0+/-4.1; P<0.0001) and remained sustained until day 28. Despite limitations due to the open nature of this study, our preliminary results confirm our preclinical findings and are in favour of an accelerating effect of ASA in combination with SSRIs in the treatment of major depression. Potential physiological and biochemical mechanisms may involve an anti-inflammatory and/or neurotrophic effect.

Adult↗
PubMed1993

Effects of acetylsalicylic acid on pulmonary vascular tone and membrane permeability in blood-perfused dog lung.

We studied the effects of acetylsalicylic acid (ASA) on pressor response, microvascular filtration coefficient (Kf), extravascular lung water, and plasma concentrations of cyclooxygenase- and 5-lipoxygenase-derived products in 21 blood-perfused dog lungs with constant flow. The lungs were perfused for 1 h with an intrapulmonary injection of saline as vehicle (n = 5), a low dose of ASA [136 +/- 25 (SD) micrograms/ml perfusate; n = 5], a high dose of ASA (1,006 +/- 278 micrograms/ml perfusate; n = 6), or alloxan (1,000 mg; n = 5). Alloxan significantly increased Kf and extravascular lung water, whereas neither the low nor high dose of ASA increased Kf or extravascular lung water. The ASA-induced increase in vascular resistance did not correlate with the extent of the decrease in perfusate 6-keto-prostaglandin F1 alpha or the ratio of perfusate 6-ketoprostaglandin F1 alpha to thromboxane B2. Moreover, ASA did not enhance the generation of perfusate leukotrienes B4, D4, or E4. We conclude that pulmonary microvascular permeability is unaltered by ASA and that neither the decrease in plasma prostacyclin nor the increase in plasma sulfidopeptide leukotrienes may account for ASA-induced pulmonary vasoconstriction.

6-Ketoprostaglandin F1 alpha↗
PubMed1984

Asthma relieved by acetylsalicylic acid and nonsteroid anti-inflammatory drugs.

The authors report 2 typical asthmatic cases in whom the administration of acetylsalicylic acid (ASA) and nonsteroid anti-inflammatory drugs (NSAID) resulted in bronchodilatation. 500 mg of ASA were administered intravenously to 1 patient and the other was treated with ASA, indomethacin, noramidopyrine intravenously and acetaminophen orally during a bronchospastic attack. FEV1 and SRAW were measured before and after drug administration. The test was repeated with placebo (physiological saline). FEV1 increased rapidly after ASA and NSAID administration. Although the pathogenesis of asthma reversed by aspirin is not entirely clear, the authors suggest an alteration of sensitivity of the cyclo-oxygenase enzyme due to the inhibitory action of ASA and NSAID.

Anti-Inflammatory Agents↗
PubMed1977

Influence of acetylsalicylic acid and paracetamol on menstrual blood loss.

In a double-blind cross-over study the influence of acetylsalicylic acid (ASA) and paracetamol on menstrual blood loss has been investigated in 23 women without an intrauterine loop or birth control pills. After intake of ASA there was no significantly, increased blood loss compared with intake of placebo or paracetamol.

Acetaminophen↗
PubMed2002

Antioxidative properties of acetylsalicylic Acid on vascular tissues from normotensive and spontaneously hypertensive rats.

BACKGROUND: The mechanisms of the beneficial cardiovascular effects of acetylsalicylic acid (ASA, aspirin) therapy are not completely understood. Oxidative stress and inflammation play important roles in the development of cardiovascular diseases. METHODS AND RESULTS: In this study, we tested the hypothesis that ASA treatment could reduce superoxide anion (O(2)(-)) generation in aortic ring and in cultured aortic smooth muscle cells (SMCs) from normotensive (WKY) and hypertensive (SHRs) rats by means of the Lucigenin-enhanced chemiluminescence method. Although ASA did not show any short-term effect in vitro and in vivo, long-term oral treatment (100 mg/kg/day, 12 days) significantly reduced the basal O(2)(-) production by 27% and 45% in aorta of normotensive and hypertensive rats, respectively, in association with a reduction of the NAD(P)H oxidase activity in both groups. These effects were dose-dependent from 10 to 100 mg/kg/day. Similar effects were observed in SMCs following long-term incubation (48 hours) with ASA. ASA treatment also completely inhibited the angiotensin II-induced hypertension and O(2)(-) production. Moreover, ASA treatment significantly improved the impaired aortic relaxation response to acetylcholine and markedly attenuated the age-dependent development of hypertension in SHRs. CONCLUSION: Long-term ASA treatment in vivo markedly reduced vascular O(2)(-) production through lowering the NAD(P)H oxidase activity in both normotensive and hypertensive rats. These antioxidative properties of ASA are likely involved in the restoration of aortic vasorelaxation, in the attenuation of the development of hypertension in young SHRs, and in the prevention of hypertension following long-term angiotensin II infusion.

Acetylcholine↗
PubMed2001

Inhibition of thrombus formation by low-dose acetylsalicylic acid, dipyridamole, and their combination in a model of platelet-vessel wall interaction.

Effects of low-dose acetylsalicylic acid (ASA, 50 mg/day), dipyridamole (sustained-release preparation 400 mg/day), and their combination were investigated in a model of human platelet-vessel wall interaction. In a randomized, double-blind clinical pharmacology trial in 96 healthy subjects, the inhibition of mural platelet thrombus was measured ex vivo using blood samples collected both before and 2 hours after a 3.5-day treatment with ASA, dipyridamole, ASA combined with dipyridamole, or placebo. Both the size and the number of platelet thrombi adherent to a thrombogenic matrix after a 15-minute flow experiment were identified by automated fluorescence microscopy. ASA treatment alone reduced the mean size of all thrombi by about 45%, and dipyridamole alone achieved an approximate 17% reduction in the mean size of all thrombi. The combination of both agents had an additive effect. Formation of the subpopulation of very large thrombi was reduced by ASA and dipyridamole to a similar extent, with their combination producing an effect at least twice as strong as that witnessed in a single treatment. These results suggest that ASA and dipyridamole affect platelet thrombus growth by different mechanisms of action. These findings provide the pharmacologic rationale for the combination of ASA (suppressing the synthesis of prothrombotic thromboxane A2) and dipyridamole (by feedback inhibition of platelet activation via local accumulation of adenosine) as a highly effective and safe combination for secondary prevention of stroke. They are consistent with the clinical findings of the Second European Stroke Prevention Study (ESPS-2). In this large trial, the addition of dipyridamole (400 mg/day in a sustained-release preparation) to aspirin (50 mg/day) doubled the efficacy of aspirin in the secondary prevention of stroke without increasing the risk for bleeding.

Aspirin↗