[Electrolytes, protein and sialic acid in gastric contents during treatment with Ibuprofen and acetylsalicylic acid].
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Adult↗
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Skin and plasma levels of acetylsalicylic acid: a comparison between topical aspirin/diethyl ether mixture and oral aspirin in acute herpes zoster and postherpetic neuralgia.
OBJECTIVE: The aim of this investigation was to elucidate whether the analgesic effect was due to the local aspirin or to the systemic drug. This was done by comparing skin and plasma levels of acetylsalicylic acid (ASA) and salicylic acid (SA) after topically administered ASA/diethyl ether (ADE) mixture in acute herpetic neuralgia (AHN) and postherpetic neuralgia (PHN). The analgesia and the plasma and skin levels of ASA were also determined after oral administration of aspirin. METHODS: Nineteen patients, 11 (57.9%) with AHN and 8 (42.1 %) with PHN were given, on different days, a single 500-mg oral dose of ASA or a topical dose (750 mg) of (ADE) daubed onto the painful skin. The analgesic effect was assessed by means of a visual analogue scale (VAS). Overall pain relief was graded as: excellent, good, fair, or poor. AHN as well as PHN patients had severe pain at baseline (6.83 and 5.93). Levels of ASA and SA in plasma and in the stratum corneum after adhesive tape stripping of the treated area were determined by HPLC. RESULTS: After ADE application, the analgesic effect was very rapid and VAS scores were lower than at baseline. Pain significantly decreased by 82.6% after topical and 15.4% after oral ASA. After ADE, 95% of the patients had excellent or good pain relief, but after oral administration 79% of the patients had a poor response. Pain relief was similar in the two subgroups after ADE. Skin concentrations of ASA, but not of SA, after ADE were about 80- to 100-fold those after oral administration. Levels of ASA and SA in plasma after oral administration were similar to those previously found, but after ADE were undetectable or very low. Patients with excellent pain relief showed a trend towards higher ASA skin concentrations. CONCLUSIONS: The analgesic effect can be obtained only after topical administration, because by this route the skin levels of ASA are much higher than after oral administration. The mechanism is exclusively local; there are no active drugs in plasma after topical administration.
Acute Disease↗
Plasma acetylsalicylic acid and salicylic acid levels during aspirin provocation in aspirin-sensitive subjects.
The ability of aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) to inhibit the cyclo-oxygenase which catalyzes formation of prostaglandins appears to be central to the mechanisms involved in aspirin sensitivity. We have investigated whether the plasma levels of acetylsalicylic acid (ASA) and its main metabolite salicylic acid (SA) at the time of intolerance reactions correspond with the concentrations required for enzyme inhibition in vitro. Twelve aspirin-sensitive and 15 aspirin-tolerant subjects were followed during provocation with aspirin. ASA and SA concentrations in plasma were determined by HPLC. After oral provocation (up to 460 mg cumulative dose), the levels of ASA and SA in plasma were equivalent in aspirin-sensitive and aspirin-tolerant subjects. For the aspirin-sensitive subjects, at the time of adverse reaction, the concentration range was 2.9-33.3 microM for ASA and 18.1-245 microM for SA. Oral provocation with sodium salicylate yielding 10-fold higher SA levels did not elicit intolerance reactions. Statistically significantly lower levels of ASA and SA (P < or = 0.01) evoked airway obstruction, as compared with merely extrapulmonary symptoms. Bronchial absorption of aspirin was found after inhalation of lysine-aspirin and was comparable in asthmatic and nonasthmatic subjects. In three aspirin-sensitive subjects who developed airway obstruction, the plasma levels for ASA and SA were 0.9-2.6 microM and 0.0-6.7 microM, respectively. In conclusion, the plasma levels of ASA reached at the time of a positive reaction are of the magnitude known to inhibit cyclo-oxygenases. Neither differences in bioavailability of ASA nor the formation of SA seems to contribute to the aspirin-elicited reactions.
Administration, Oral↗
Analgesic potency of a new anticonvulsant drug versus acetylsalicylic acid via laser somatosensory evoked potentials. Randomized placebo-controlled double-blind (5-way) crossover study.
A randomized, double-blind crossover study was performed with three different acute oral dosages of CM 40907 (3-(4-hydroxypiperidyl)-6-(2'-chlorophenyl)-pyridazine) (600, 900 and 1200 mg), a newly developed anticonvulsant drug, vs acetylsalicylic acid (ASA, 1000 mg) and placebo in 12 male healthy volunteers to check analgesic potency. Objective algesimetry was done by Laser Somatosensory Evoked Potentials (LSEP). Subjective pain intensities were measured by retrospective visual analog scale ratings (VAS). Effects on objective vigilance were checked by Auditory Evoked Potentials (AEP). For both types of evoked potentials there was a simultaneous control of alterations in vigilance by means of the adaptive pursuit tracking task (APTT). A vigilance-controlled EEG (V-EEG) and a resting (R-EEG), visual analog scales (VAS) on sedation, excitation and anxiety as well as vital parameters (blood pressure and heart rate under supine and upright conditions) and adverse event scales were included in this trial as well. CM 40907 showed distinct analgesic effects on objective and subjective algesimetric parameters, which for the highest dosage (1200 mg) were superior in ("central") P2-amplitude suppression of LSEPs to those of ASA in ("peripheral") N1-amplitudes suppression and ongoing for more than 6 h. Subjective sedation was decreased, however, AEP-findings indicated a decreased vigilance after CM 40907. Some EEG-patterns, specifically related with CM 40907--although being ambiguous in classification terms--resembled features of benzodiazepines. Blood pressure and heart rate were raised in a clinically irrelevant manner.
Acoustic Stimulation↗
Increased tendency towards gingival bleeding caused by joint effect of alpha-tocopherol supplementation and acetylsalicylic acid.
Alpha-tocopherol (vitamin E) may play a role in the treatment of arterial thromboembolic disease, possibly by inhibiting platelet aggregation. Thus far, no clinical evidence exists for this effect. The objective of this study was to assess the effect of alpha-tocopherol supplementation on gingival bleeding either in combination with acetylsalicylic acid (ASA) or without it. This study was an end-point examination of a random sample of male smokers who had participated in a controlled clinical trial, the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study (ATBC Study) for 5-7 years. The study included 409 men aged 55-74 years of whom 191 received alpha-tocopherol supplementation (50 mg/day); 56 used ASA, 30 received both and 132 received neither. Gingival bleeding was examined by probing with a WHO probe and reported as a percentage of bleeding sites adjusted by the logistic regression model. Gingival bleeding was more common in those who received alpha-tocopherol compared with nonreceivers among subjects with a high prevalence of dental plaque (P < 0.05). ASA alone increased bleeding only slightly. The highest risk of gingival bleeding was among those who took both alpha-tocopherol and ASA (33.4% of probed sites bleeding vs 25.8% among subjects taking neither alpha-tocopherol nor ASA, P < 0.001). In the ATBC Study, more deaths from haemorrhagic stroke and fewer from ischaemic heart disease were observed among those participants who received alpha-tocopherol compared with those who did not. Based on the results of the present study and the ATBC Study, we conclude that alpha-tocopherol supplementation may increase the risk of clinically important bleedings, particularly when combined with ASA.
Aged↗
Acetylsalicylic acid inhibits platelet PAI-1 antigen release without affecting circulating PAI-1 antigen in plasma.
An important plasminogen activator-inhibitor (PAI-1) is present in plasma and concentrated in alpha-granules of platelets. PAI-1 is released during platelet stimulation in vitro. It is presently unknown to what extent the treatment with acetylsalicylic acid (ASA) inhibits platelet PAI-1 release and if release inhibition has an effect on plasma PAI-1 levels. We therefore investigated by a double-blind placebo-controlled crossover study the effects of oral ASA (500 mg/day for 3 days) on platelet PAI-1 release and on plasma PAI-1 levels of healthy male volunteers. The PAI-1 release from platelets stimulated by arachidonic acid and collagen was significantly reduced by ASA: from average values of 88 and 80% to 14 and 17%, respectively (p less than 0.01). However, plasma PAI-1 levels were not modified by this treatment. We can conclude that platelet PAI-1 release does not play a role in modulating the plasma PAI-1 levels in healthy volunteers.
Adult↗
Hypothesized treatment for migraines using low doses of tryptophan, niacin, calcium, caffeine, and acetylsalicylic acid.
The author hypothesized that existing agents known to influence serotonin blood level, vascular tone, and inflammatory reactions might terminate migraines. The author presented the rationale for using five different agents therapeutically and avoiding two other agents during a migraine. The proposed treatment is to use low doses of tryptophan, niacin, calcium, caffeine, and acetylsalicylic acid (ASA) soon after migraine symptoms are noticed and to avoid during a migraine high-potassium food and magnesium supplements. Preliminary results from 12 migraine patients indicated that 9 of 12 (75%) had significant benefit from this approach. Using these five agents together is a novel combination and a new idea for treating migraines.
Adult↗
Residual platelet function under acetylsalicylic acid and the risk of restenosis after coronary angioplasty.
Restenosis after percutaneous transluminal coronary angioplasty (PTCA) was shown not to be preventable by antiplatelet therapy; residual platelet function under treatment with platelet inhibitors could be one cause of this. Therefore, in a prospective investigation, residual platelet function was assessed in 98 patients treated with acetylsalicylic acid (ASA) on three occasions during the first 3 months after successful PTCA. Control cardiac catheterization was obtained in 75 of these patients (77%) with 82 dilated stenoses 173 +/- 117 days after PTCA. Restenosis, defined as diameter stenosis greater than or equal to 50% at control angiography, occurred in 41% of the dilated vessels, and 43% of patients experienced restenosis in at least one vessel. The in vitro platelet aggregatory response to either ADP (0.5, 1, and 10 microM) or collagen (1 and 5 mg/L) as aggregating agents did not differ between patients with and without restenosis. In addition, neither the collagen-stimulated in vitro synthesis of thromboxane nor the basal or prostaglandin E1-stimulated concentrations of cyclic AMP in platelet-rich plasma (PRP) was different in the two groups. There was no significant correlation between any of the parameters of platelet function assessed and the change in coronary luminal diameter observed between immediately after PTCA and control coronary angiography. The mean dose of ASA ingested during follow-up was also not a determinant of the occurrence of restenosis. Thus, residual platelet function under treatment with ASA as measured in vitro in this study, did not influence the occurrence of restenosis after successful PTCA.
Angioplasty, Balloon, Coronary↗
Effects of acetylsalicylic acid on peripheral hemodynamics in patients with chronic heart failure treated with angiotensin-converting enzyme inhibitors.
Cyclooxygenase inhibitors may affect the hemodynamic status of patients with heart failure adversely and may also block the vasodilatory effects of angiotensin-converting enzyme (ACE) inhibitors in such patients. Relatively low doses of the cyclooxygenase inhibitor acetylsalicylic acid (ASA) are now used routinely in ischemic heart disease, the most important cause of heart failure. Therefore, we investigated the hemodynamic interaction between ASA and captopril in heart failure. In a randomized, cross-over study, 13 patients with congestive heart failure (CHF) who were already receiving maintenance treatment with an ACE inhibitor received a single dose of 25 mg captopril combined with 236 mg ASA or placebo. Peripheral blood flow was studied noninvasively by venous occlusion plethysmography of the calves. Liver blood flow was estimated from indocyanine green (ICG) clearance. Administration of captopril alone significantly decreased blood pressure (BP), and ICG clearance. Calf blood flow remained unchanged. However, after arterial occlusion, hyperemic calf blood flow persisted for longer. Captopril alone did not significantly change the plasma levels of the vasodilating prostaglandins PGI2 and PGE2 or the vasoconstricting thromboxane A2 (TXA2). In contrast, captopril combined with ASA reduced the plasma levels of these vasoactive substances, with significant decreases in PGE2 and TXA2 as compared with captopril alone, yet the hemodynamic alterations after captopril plus ASA were similar to those observed after captopril alone. A single antithrombotic dose of ASA (236 mg) in 13 patients with CHF [New York Heart Association (NYHA) class II-IV] undergoing chronic treatment with ACE inhibitors had no discernible effect on hemodynamic status.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Differential effect of acetylsalicylic acid and dipyrone on prostaglandin production in human fibroblast cultures.
Human skin fibroblasts incubated with arachidonic acid in culture show basal release of prostaglandins. They produce the same prostaglandins after stimulation with bradykinin. Basal release of prostaglandins I2 (6-oxo-PGF1 alpha), F2 alpha and E2 is inhibited dose-dependently by both acetylsalicylic acid (ASA) and dipyrone (P less than 0.05). The examined dose-range was 10(-7) to 10(-4) M for both drugs. During the first 5 min after removal of the drugs from the incubation medium, bradykinin-stimulated release remains dose-dependently inhibited (P less than 0.001) in ASA-, but not in dipyrone-treated cultures. The difference between the effects of ASA and of dipyrone is highly significant (P less than 0.0001), whereas the dipyrone-treated cultures are not different from controls. The findings are consistent with cyclo-oxygenase inhibition by ASA as well as by dipyrone. However, the data demonstrate rapid reversibility of the effect of dipyrone. This suggests that in contrast to ASA, dipyrone does not inhibit cyclo-oxygenase by binding covalently to the enzyme.
Aminopyrine↗
Differential effects of two analgesic drugs, morphine chlorhydrate and acetylsalicylic acid, on thalamic mast cell numbers in rat.
Thalamic mast cells (TMCs), the only immunocytes known to infiltrate the brain in physiological conditions, respond to pharmacological agents including sumatriptan - a serotonergic anti-migraine agent - that increases their number. We analysed the effects of two other main analgesics: morphine chlorhydrate, a micro opioid agonist, and acetylsalicylic acid (ASA), a non-steroidal anti-inflammatory drug. All three drugs have specific modes of action, and morphine and ASA, unlike sumatriptan, are also known to interact with peripheral mast cells. Only ASA was effective in promoting TMC number decrease. TMCs, unlike other mast cells, do not express cyclooxygenase (COX) - the key enzyme in the production of prostanoids and the main site of action of ASA - thus dismissing a direct local cellular COX-mediated action. Direct TMC COX-independent mechanisms or effects mediated via distant populations of COX-positive cells such as platelets, leptomeningeal, endothelial and peripheral mast cells are thus probable. ASA, morphine and sumatriptan have distinct TMC effects, suggesting that the TMC number variations they induce are more likely to derive from systemic vasoactive actions than from pharmacological mechanisms devoted to pain relief.
Analgesics↗
Effect of acetylsalicylic acid and dipyridamole in primary membranoproliferative glomerulonephritis type I.
Primary membranoproliferative glomerulonephritis (MPGN) has a poor long-term prognosis, with 40 per cent of patients reaching end-stage renal failure after 10 years of observation. Approximately 35 per cent of patients die due to complications of the nephrotic syndrome. This study investigates the effect of acetylsalicylic acid (ASA) combined with dipyridamole on proteinuria and renal function in nephrotic MPGN patients with normal/moderately reduced glomerular filtration rate (GFR). Fourteen patients with biopsy-proven type I MPGN received ASA (1000 mg/day) and dipyridamole (300 mg/day) for 24 months. Proteinuria was reduced from 6.8 +/- 2.4 g/day to 1.1 +/- 0.6 g/day (p < 0.001). Serum albumin levels increased from 2.2 +/- 0.5 g/dL to 3.7 +/- 0.4 g/dL (p < 0.001) during the study period after 24 months compared to baseline. Serum creatinine and GFR did not significantly change in patients treated with acetylsaliclylic acid and dipyridamole during the observation period (p < 0.05). Our study suggests that ASA combined with dipyridamole significantly reduces proteinuria without impairing renal function in patients with MPGN.
Adolescent↗
The effect of combined treatment with dextran 40 and acetylsalicylic acid on patency in severely traumatized small veins and arteries: an experimental study in the rabbit.
The effects of pharmacologic intervention on the fates of severely traumatized small veins and arteries have been studied in a rabbit model. Controls were given bolus doses of saline and a group treated with a combination of dextran 40 and acetylsalicylic acid starting prior to traumatization and continuing until postoperative day 5. Relative to controls, bleeding times in the treated group were significantly lengthened in arteries but not in veins, and venous patency significantly improved throughout the interval ending 2 weeks postoperatively. Arterial patency was at first highly improved but by 2 weeks, occlusion was virtually 100 percent. Since some of the occlusions took place more than a week after traumatization, the effects of antithrombotic agents on patency may need to be evaluated over considerably longer time periods than has previously been the rule.
Animals↗
Effect of a prostaglandin E1 derivative (OP-1206) and acetylsalicylic acid on electrically induced thrombosis in guinea-pig mesenteric artery and its modification by an inhibitor of prostaglandin I2 synthetase, tranylcypromine.
The antithrombotic effect of a prostaglandin E1 derivative, OP-1206 (17S-20-dimethyl-trans-delta 2-PGE1) X alpha-cyclodextrin clathrate (OP-1206 X alpha-CD), was compared with that of acetylsalicylic acid (ASA) in a electrically induced thrombosis model of guinea-pig mesenteric arteries using intact animals and animals subjected to the superfusion of tranylcypromine (TC, 15 mM) over their mesentery. The drug-effect was assessed by the change of the threshold voltage for the thrombus formation. 1) TC (1.5-15 mM) lowered the threshold voltage, and the effect was comparable to its inhibitory effect on PGI2 formation in vitro, suggesting that PGI2 generated in mesenteric arteries acts to prevent thrombus formation. 2) In intact animals, OP-1206 X alpha-CD at doses of 0.01-0.3 mg/kg, p.o. (as OP-1206), significantly and dose-dependently elevated the threshold voltage. ASA (30-1000 mg/kg, p.o.) significantly elevated the threshold voltage, but the effect reached to its maximum at 100 mg/kg and lessened with further increase of ASA. 3) In TC-treated animals, OP-1206 X alpha-CD elevated the threshold voltage dose-dependently, but the elevation of threshold voltage by ASA reached to its plateau level which was significantly lower than that obtained with OP-1206 X alpha-CD at 0.3 mg/kg, indicating that the antithrombotic effect of ASA is incomplete in this model.(ABSTRACT TRUNCATED AT 250 WORDS)
Alprostadil↗
[Plasma carbonyl group concentration in pregnant women with IUGR treated by L-arginine and acetylsalicylic acid].
OBJECTIVES: Carbonyl groups are the elements connecting protein structure, they influent into biological activity. High concentration of carbonyl groups means high risk of protein destruction. DESIGN: The aim of this study was the evaluation of carbonyl group concentration in blood serum in normal pregnancy and in women with IUGR treated by L-arginine and acetylsalicylic acid. MATERIAL AND METHODS: The study was done at the Department of High Risk Pregnancy, Department of Gynaecology and Obstetrics, Medical University of Łódź, in 1999-2002. The study group included 80 pregnant women hospitalised due to foetal growth restriction, between the 32-th and 38-th weeks of pregnancy. The treatment was conducted for twenty days and consisted of everyday low dose aspirin (Acard) and L-arginine (NO precursor). The ultrasound and laboratory examinations were done on the first day of hospitalisation in both groups, and at 20-th day of treatment in the group of IUGR. The carbonyl groups concentration was measured by Levine method and expressed in mmol/1 mg proteins. RESULTS: In controls mean value of carbonyl groups concentration was 1.848 +/- 0.291 mmol/1 mg proteins and after 20 days of observation 1.897 +/- 0.439. In the group with IUGR before treatment was 2.193 +/- 0.658. After 20 day of the therapy and the value decreased to 2.078 +/- 0.679. There is a significant difference between the value of carbonyl-groups concentration in normal pregnancy and IUGR. The carbonyl-groups concentration decreased after 20 days of treatment by L-arginine, and the value is still higher than in normal pregnancy. CONCLUSIONS: Oxidative protein damage in IUGR decreased in the process of treatment.
Adult↗
Acetylsalicylic acid in the prevention of stroke in patients with reversible cerebral ischemic attacks. A Danish cooperative study.
Two hundred and three patients, 148 males and 55 females, who during the last month before admission had experienced at least one reversible cerebral ischemic attack of less than 72 hours duration, were randomly assigned to treatment with either acetylsalicylic acid (ASA) 1000 mg daily (101 patients) or placebo (102 patients). The average follow-up period was 25 months. The two treatment groups were comparable with respect to age, sex, associated diseases, risk factors, number and duration of cerebral ischemic attacks. No statistically significant differences were found between the treatment groups as to the primary end point: stroke or death (ASA group 20.8%, placebo group 16.7%). Occurrence of transient ischemic attacks during the treatment period was not reduced by ASA treatment, whereas there was a trend suggesting fewer myocardial infarctions in the ASA group (5.9%) than in the placebo group (13.7%). The difference, however, was not statistically significant (p = 0.10). We were thus unable to demonstrate any favorable influence of ASA 1000 mg daily in patients with reversible ischemic attacks. This study does not, of course, prove that ASA treatment is ineffective in stroke prevention.
Adult↗
The effect of O-acetylsalicylic acid on lipid synthesis by guinea pig gastric mucosa in vitro.
The aim of this work was to investigate the involvement of lipids as possible components of the gastric mucosal barrier by studying the synthesis and secretion of lipids by the epithelial cell lining of gastric mucosa and the effect of salicylate on these processes. O-Acetylsalicylic acid reversibly reduced in vitro incorporation of [U-14C]acetate and of DL-[2-14C]mevalonic acid into lipids by isolated epithelial cells and by intact mucosa of guinea pig stomach, indicating reversible inhibition of lipid synthesis by the tissue in the presence of the drug. Inhibition of incorporation of both precursors into total lipids, into their fatty acid components, and into cholesterol is demonstrated.
Animals↗
Antithrombotic effects of some flavonoids alone and combined with acetylsalicylic acid.
In the rat, a selection of two experimental models of "prethrombotic states", one of venostatic thrombosis and one of arterial thrombosis was used to compare the antithrombotic of three flavonoid preparations: O,-(beta-hydroxyethyl)-rutosides (HR), an association of trihydroxyethylrutoside and coumarin (troxerutin) and 7-mono-hydroxyethylrutoside (7-Mono-HR), as well as acetylsalicylic acid (ASA). The flavonoids were very effective "protectors" on the prethrombotic models, but only ASA was active on the model of arterial thrombosis. No compound showed a clear protection on the venostatic model if direct activation by kaolin was used. However, if an indirect activation by vessel wall stimulation was used, 7-Mono-HR possessed a marked protective effect. The most favourable results were obtained with an association of 7-Mono-HR and ASA, which could be considered for investigation in clinical thrombosis prophylaxis.
Animals↗