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At least 523 records · Page 29Linked to original sources
PubMed1993

Acetylsalicylic acid and misoprostol combination in adjuvant arthritis of rats.

The combined effect of acetylsalicylic acid (ASA) and misoprostol (MISO) on adjuvant arthritis was investigated on rats. Alteration by various doses of MISO and fixed dose of ASA was studied. Drugs were given by the nasogastric route each day beginning from the day of adjuvant injection (day 0) and continued until the 16th day. Paw swelling was measured on days 4, 17, and 29, and secondary lesions were assessed on days 17 and 29. Pathological examination of tibiodorsal junction was also evaluated on the 29th day. The results clearly showed that the combination of MISO with ASA did not inhibit the antiinflammatory effect of ASA. Unexpectedly, MISO increased the antiinflammatory effect of ASA at some dosage regimens.

Animals↗
PubMed1983

Effect of acetylsalicylic acid on plasma thromboxane B2 and platelet aggregation in man.

The effect of acetylsalicylic acid (ASA) on plasma thromboxane A2 (TXA2) and platelet aggregation was studied in 12 healthy, non-smoking, male students, in a double-blind, cross-over study, after single doses and 14-days on ASA 50, 100, 250 and 1000 mg/day. Platelet production of TXA2 was assessed by measuring the thromboxane B2 (TXB2) content of clotted venous blood by RIA. Platelet aggregation induced by ADP and adrenaline was studied by the method of Born. All doses of ASA completely suppressed the production of TXB2 within 3 h, with the exception of the 50 mg dose, which effected only 61% suppression (p less than 0.001). After administration for 14 days the suppression was complete, even including the lowest dose. At that time ASA had blocked the secondary phase of adrenaline- and ADP-induced platelet aggregation. It is concluded that the maximal antithromboxane and antiaggregatory effects, which last for at least 24 h, can be achieved by continuous daily administration of ASA 50 mg.

Adult↗
PubMed2003

Pharmacokinetics and pharmacodynamics of melagatran, the active form of the oral direct thrombin inhibitor ximelagatran, are not influenced by acetylsalicylic acid.

OBJECTIVE: The aim of this study was to evaluate the effect of acetylsalicylic acid (ASA or aspirin) on the pharmacokinetics (PK) and pharmacodynamics (PD) of melagatran in healthy volunteers. Melagatran is the active form of the oral direct thrombin inhibitor, ximelagatran. METHODS: This was a double-blind, randomised, two-way, crossover study consisting of two treatment periods separated by a washout period of at least 2 weeks. Twelve subjects received, in a randomised order, either melagatran plus ASA in the first treatment period and melagatran plus placebo in the second treatment period or vice versa. Two single doses of ASA were given, first 450 mg on the day before (day 1) and then 150 mg just before administration of melagatran on day 2. Melagatran 4.12 mg was administered as an intravenous (i.v.) infusion over 4 h on day 2 of both treatment periods. Serial blood samples were collected over the course of the study for the determination of melagatran plasma concentration and coagulation analyses [activated partial thromboplastin time (APTT) and activated clotting time (ACT)]. Capillary bleeding time was measured before ASA/placebo on day 1 and before and after the start of the melagatran infusion on day 2. RESULTS: The plasma concentration of melagatran during the i.v. infusion was maintained at about 0.2 micro mol/l, and ASA did not influence the PK parameters of melagatran. APTT and ACT increased with increasing melagatran plasma concentration, and the observed increases were similar whether melagatran was administered on top of ASA or placebo. Administration of ASA significantly prolonged the capillary bleeding time (by 41% relative to placebo). Melagatran also prolonged the bleeding time significantly (by 25% relative to placebo alone), but this prolongation was not significantly different from the observed prolongation when melagatran was administered on top of ASA (by 17% relative to ASA alone). CONCLUSION: In young healthy volunteers, ASA had no effect on the PK or PD properties of melagatran at the studied dose. That the combination of ximelagatran with ASA may be used with acceptable safety must be verified in the relevant patient populations.

Administration, Oral↗
PubMed1984

One milligramme of acetylsalicylic acid daily inhibits platelet thromboxane A2 production.

To seek the lowest dose of acetylsalicylic acid (ASA) capable of inhibiting platelet thromboxane A2 (TxA)2 production, 18 healthy volunteers ingested 9 mg, 3 mg or 1 mg of ASA/day for twenty days and the release of TxB2 (a metabolite of TxA2) during the spontaneous clotting of blood was measured by radioimmunoassay. In addition, the production of prostacyclin (epoprostenol, PGI2) was investigated by measuring the urinary excretion of its break-down product, 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) by radioimmunoassay. Significant inhibition of platelet TxA2 production was seen from the 15th day of treatment onwards with 1 mg of ASA (maximally 15%), from the 4th day of treatment onwards with 3 mg of ASA (maximally 40%), from the 1st day of treatment onwards with 9 mg of ASA (maximally 67%). No ASA dose changed platelet counts or urinary 6-keto-PGF1 alpha excretion. One mg of ASA daily, is the lowest dose ever shown to inhibit platelet TxA2 production.

Aspirin↗
PubMed2005

Increased blood plasma hydrolysis of acetylsalicylic acid in type 2 diabetic patients: a role of plasma esterases.

Hydrolysis of acetylsalicylic acid (ASA, aspirin), an antiplatelet drug commonly used in the prevention of stroke and myocardial infarction, seems to play a crucial role in its pharmacological action. Thirty-eight healthy volunteers and 38 type 2 diabetic patients were enrolled to test the hypothesis that the enhanced plasma degradation and lowered bioavailability of ASA in diabetic patients is associated with the attenuation of platelet response. Aspirin esterase activities were tested at pH 7.4 and 5.5. A significantly higher overall aspirin esterase activity was noted at pH 7.4 in the diabetic patients (P<0.003), corresponding to faster ASA hydrolysis (P<0.006). This increased activity was attributable to butyrylcholinesterase and probably to albumin, because it was effectively inhibited by eserine and 4-bis-nitrophenyl phosphate (P<0.01). No significant differences between control and diabetic subjects were found at pH 5.5 in either enzymatic activities or ASA hydrolysis rates. The enhanced plasma ASA degradation in diabetic subjects was significantly associated with the refractoriness of blood platelets to ASA (P<0.05) and modulated by plasma cholesterol (P<0.01). No direct effects of plasma pH or albumin were observed. In conclusion, higher aspirin esterase activity contributes to the lowered response of diabetic platelets to ASA-mediated antiplatelet therapy.

Adult↗
PubMed1998

Effect of acetylsalicylic acid on formalin test and on serotonin system in the rat brain.

1. Acetylsalicylic acid (ASA; 400 mg/kg, i.p.) increased serotonin (5-HT) content in rat brain but did not modify the number or the affinity of 5-HT1A receptors in the pons and the cerebral cortex, whereas the number of cortical 5-HT2 receptors decreased significantly. 2. Pretreatment with parachlorophenylaline (100 mg/kg/day for 4 days) depleted 5-HT brain content but modified neither the serum levels of salicylates nor the 5-HT2 cortical receptor characteristics, and it abolished the antinociceptive effect of ASA, 400 mg/kg, in the first phase of the formalin test. 3. These data support the involvement of the central serotonergic system in the antinociceptive activity of ASA.

Animals↗
PubMed1998

Risk of haemorrhage from transurethral prostatectomy in acetylsalicylic acid and NSAID-treated patients.

Postoperative bleeding in patients who regularly ingest acetylsalicylic acid (ASA) has been reported after several types of surgery. However, data on the influence of ASA on the risk of haemorrhage from transurethral prostatectomy (TUR-P) have been conflicting. We have studied retrospectively the unselected clinical records of all patients undergoing TUR-P in the Department of Urology at Hvidovre Hospital (during 1992-1994) with special focus on the use of ASA and non-steroidal anti-inflammatory drugs (NSAIDs). In total, 457 records were examined: 99 patients on ASA/NSAID received 42 units of blood, while 358 patients free from such medication received 68 units of blood, a significantly smaller amount (p = 0.0390). We conclude that ASA and NSAIDs increase the risk of bleeding during and after TUR-P, and we recommend the withdrawal of these drugs for one week before TUR-P.

Aged↗
PubMed1984

Effects of Salicylic and Acetylsalicylic Acids on the Scotonastic and Photonastic Leaflet Movements of Cassia fasciculata.

Salicylic and acetylsalicylic acids applied on excised leaves of Cassia fasciculata modify the dark-induced (scotonastic) and light-induced (photonastic) leaflet movements. They inhibit the scotonastic movements in a dose-dependent manner from 1 x 10(-4) to 1 x 10(-3) molar and they promote the photonastic movements at an optimum concentration of 5 x 10(-4) molar. These results suggest that these phenolic compounds do not act specifically on the K(+) uptake, which was shown to be inhibited by their action on other materials.

Journal Article↗
PubMed1985

The effects of age and sex on the disposition of acetylsalicylic acid and its metabolites.

The disposition of a low dose (600 mg) of acetylsalicylic acid (ASA) and its metabolites (salicylate, salicyluric acid and salicyl glucuronides) was studied in 25 male and female patients of different ages. Plasma levels of ASA and salicylate were found to be significantly higher in the females (young and elderly), whereas plasma levels of salicyluric acid were found to be significantly higher in the elderly (male and female) groups. The higher plasma levels of ASA and salicylate in the females appear to be due to an intrinsically lower metabolic activity in that sex, while the lower clearance of salicyluric acid leads to the accumulation of that compound in the aged. No age and sex effects were found to influence the volumes of distribution of ASA, salicylate and salicyluric acid.

Adult↗
PubMed1983

Interactions between ethanol and acetylsalicylic acid in damaging the rat gastric mucosa.

The interactions between ethanol (EtOH) and acetylsalicylic acid (ASA) in damaging the gastric mucosa were investigated in urethane-anaesthetised rats upon intragastric irrigation. The addition of 5, 10 or 20 mM ASA to 1 and 4 M EtOH instillates strongly aggravated lesion formation in the gastric mucosa and mucosal bleeding. ASA enhanced the back-diffusion of hydrogen ions into the mucosa induced by 1 M EtOH, whereas gastric mucosal blood flow, which is thought to dispose of the back-diffused acid from the mucosa, remained unchanged, thus resulting in an accumulation of acid within the gastric mucosa. ASA did not further enhance the strongly increased back-diffusion of hydrogen ions induced by 4 M EtOH, but it effectively inhibited EtOH-induced stimulation of the gastric mucosal blood flow, thus causing an increase in the ratio between hydrogen ion back-diffusion and gastric mucosal blood flow. The simultaneous presence of EtOH and ASA did not enhance the rates of absorption of each from the instillates. The results indicate that EtOH and ASA have a strong synergistic action in damaging the gastric mucosa in the rat. The mechanism of this interaction may be an increased accumulation of hydrogen ions within the gastric mucosa, resulting in excessive acidification of the mucosal tissue.

Animals↗
PubMed1997

Acetylsalicylic acid increases tolerance against hypoxic and chemical hypoxia.

BACKGROUND AND PURPOSE: Treatment with acetylsalicylic acid (ASA) is established for secondary stroke prevention. Recent studies showed neuroprotection of ASA against glutamatergic excitants. The goal of this study was to investigate the time course of neuroprotection of ASA against indirect excitotoxicity by hypoxic hypoxia and chemical hypoxia. METHODS: Population spike amplitude (PSA) and ATP content were measured in hippocampal slices from untreated control animals (c-slices) and slices prepared from animals pretreated in vivo with a single intraperitoneal injection of 20 mg/kg body wt ASA 1 to 48 hours before slice preparation (p-slices). RESULTS: Posthypoxic recovery of PSA was 30% in c-slices (15 minutes of hypoxia, 45 minutes of recovery). When c-slices were treated in vitro for 15 minutes with 20 mg/L ASA 30 minutes before hypoxia, posthypoxic recovery improved to 82 +/- 4% (mean +/- SE, P < .01). In p-slices, posthypoxic recovery of PSA improved in a time-dependent manner. With a time interval of 1 hour between in vivo pretreatment with ASA and slice preparation, posthypoxic recovery of PSA was 64 +/- 16% (P < .05). With time intervals of 6 hours, 24 hours, and 48 hours, posthypoxic recovery of PSA was 87 +/- 19% (P < .01), 59 +/- 12%, and 40 +/- 9%, respectively. Pretreatment with ASA in vitro or in vivo decreased the decline of ATP content during hypoxic hypoxia and chemical hypoxia (inhibition of succinic dehydrogenase by 3-nitropropionic acid). When extracellular glucose was reduced to 4 mmol/L, no difference was observed between c-slices and p-slices. CONCLUSIONS: We conclude that ASA is neuroprotective against hypoxic hypoxia and chemical hypoxia and delays the decline of intracellular ATP content.

Action Potentials↗
PubMed1979

Diflunisal, a new-acting analgesic and prostaglandin inhibitor: effect of concomitant acetylsalicylic acid therapy on ototoxicity and on disposition of both drugs.

Intermittent and concomitant acetylsalicylic acid (ASA) therapy was superimposed onto a 21-day regimen with diflunisal 250 mg b.i.d. Low doses of ASA (600 mg single dose or 300 mg q.i.d.) did not influence signficantly diflunisal blood levels whereas a 600 mg q.i.d. dosing caused a small significant drop, especially at trough level. This drop is not expected to be clinically significant. No ototoxicity could be demonstrated with any treatment of diflunisal though four of fourteen subjects reported mild tinnitus during concomitant therapy at the higher doses of ASA. Diflunisal at 375 mg b.i.d. failed to alter the metabolism of a single dose of labelled ASA (600 mg) as judged by plasma levels, urinary excretion and plasma binding. Daily urinary excretion of prostaglandins E1 and E2 major metabolite was decreased by about 70% by diflunisal.

Adult↗
PubMed1996

Effect of acetylsalicylic acid on metabolism and contractility in the ischemic reperfused heart.

The effect of acetylsalicylic acid (ASA) on high-energy phosphates (adenosine triphosphate: ATP, creatine phosphate: CrP, inorganic phosphate: Pi) and intracellular pH during myocardial ischemia and reperfusion was studied using phosphorus 31-nuclear magnetic resonance (31P-NMR) in the isolated rabbit hearts. Coronary flow, left ventricular systolic developed pressure (LV Dev.P) and left ventricular end-diastolic pressure (LVEDP) were also measured. Langendorff hearts perfused at 37 degrees C with the perfluorochemical emulsion Fluosol-43 were subjected to 15 min and 30 min of zero-flow ischemia and to 15 min of low-flow ischemia (coronary perfusion pressure = 20 mmHg) followed by 65 min of reperfusion (control, Group I). ASA (0.28 mmol/L) was infused either for the entire experimental period from beginning 45 min prior to ischemia (Group II) and infused immediately after reperfusion (Group III). During ischemia, Group II showed a significant suppression of the decrease in the ATP level and pH with both zero-flow and low-flow ischemia compared to those in the other groups, and moreover the increase in Pi and the decrease in CrP in low-flow ischemia were also suppressed. In Group III, the ATP level during reperfusion was significantly higher than that in Group I, but was not significantly different from that in 30 min zero-flow ischemia. In 30 min zero-flow ischemia, Pi, CrP and coronary flow after reperfusion in Group II tended to recover to preischemic values. There were no differences in LV Dev.P among the 3 groups. In conclusion, ASA has a protective effect on myocardial high-energy phosphates during ischemia and reperfusion in rabbit hearts.

6-Ketoprostaglandin F1 alpha↗
PubMed1991

Thrombopoietin production in mice treated with acetylsalicylic acid.

Recent work revealed that mice in which platelet function was inhibited by acetylsalicylic acid (ASA) treatment showed evidence of increased platelet production. It was proposed that poorly functioning platelets gave rise to elevated thrombocytopoiesis by causing the release and action of thrombopoietin. However, direct evidence is lacking. Therefore, in the work reported here, plasma from mice treated with ASA was injected into normal recipient mice in an attempt to document the existence of the humoral factor. Compared with control mice given normal plasma, the injection of mice with plasma from ASA-treated mice resulted in increased thrombocytopoiesis, as evidenced by significant increases in the percentage of 35S incorporation into platelets, larger platelet size, and elevated megakaryocyte precursor cells (the small acetylcholinesterase-positive cell). For a positive control, additional mice were treated with plasma from animals made thrombocytopenic by an injection of antiplatelet serum. These mice also showed significant increases in thrombocytopoiesis. The results support the hypothesis that platelet production in ASA-treated mice is elevated by release and action of thrombopoietin.

Animals↗
PubMed1992

[Acetylsalicylic acid in unstable angina, after coronary revascularization and in prevention of cardiac thromboembolism].

Acetylsalicylic acid (ASA) inhibits platelet function via cyclooxygenase inhibition. The selective inhibition of platelet cyclooxygenase is possible with the use of low doses of ASA due to presystemic acetylation of the platelet enzyme in the portal circulation. The clinical efficacy of ASA has been demonstrated for a number of indications. ASA reduces the rate of myocardial infarctions and cardiovascular deaths in patients with unstable angina. Simultaneous intravenous infusion of heparin has an additional positive effect. The prevention of acute coronary thromboses during PTCA and of early bypass graft occlusion has been convincingly demonstrated, if therapy is initiated immediately after surgery. Neither ASA nor any other drug has been effective in the prevention of late restenosis following PTCA and of late bypass graft occlusions. Thromboembolic complication after implantation of biological valve prostheses is significantly reduced by ASA, if no rheumatic valve disease is present. The rate of peripheral or cerebral thromboembolic events is markedly increased in patients with lone atrial fibrillation. In contrast to the very positive results obtained for anticoagulants, the reports with ASA were contradictory. ASA may be effective in preventing thromboembolic complications in younger patients with a lower risk or in elderly patients with contraindications for anticoagulation. For most clinical indications the efficacy of ASA has been demonstrated for doses of 75-324 mg/d. Following a loading dose of 300 mg on the first day, continuation of therapy with 100 mg/d should combine maximal therapeutic efficacy with a low rate of unwanted drug effects.

Angina, Unstable↗
PubMed1992

Pharmacokinetics and relative bioavailability of a new chewable, buffered acetylsalicylic acid tablet formulation in comparison to a conventional plain tablet.

The pharmacokinetics of acetylsalicylic acid (ASA) and its main metabolite salicylic acid (SA) following single dose administration of a new chewable, buffered ASA tablet formulation and a conventional plain ASA tablet formulation were investigated in 12 healthy male subjects. The volunteers received in a randomized, crossover design two pharmaceutical units of both formulations containing 500 mg ASA each after an overnight fast on an empty stomach. ASA and SA in the collected plasma and urine samples were determined using an internally standardized validated HPLC method. Regarding the normalized extent parameters for ASA, an increase of about 114% for the maximum concentration (Cmax,norm) and about 16% for the area under the curve (AUC0----infinity,norm) was found for the new chewable, buffered tablet formulation as compared to the plain tablet. Comparing the corresponding parameters for the main metabolite, both formulations were statistically equivalent. The quotient of normalized areas (QAUC0-20min, norm/AUC0----infinity,norm) for ASA was higher by about 124% for the new formulation, indicating an increased and faster absorption during the first 20 min after administration. The time of the concentration maximum did not differ statistically. These data indicate that the new chewable, buffered ASA tablet formulation shows a significant benefit as compared to the plain ASA tablet. The new tablet produced higher plasma ASA concentrations in a shorter time, which is clinically important since higher ASA concentrations are assumed to be related to an improved analgesic efficacy.

Adolescent↗
PubMed1985

Comparison of the concentration-effect relationship of a local antiinflammatory agent and oral acetylsalicylic acid: the value of local application.

Using a pharmacological model, the comparison between acetylsalicylic acid (ASA), administered orally, and a solution combining two salicylate derivatives (ethyl 5-methoxy-salicylate and 3-phenyl-propyl-salicylate), applied locally, demonstrated the value of the local application. Indeed, the pharmacological activity was highly significant and directly related to the tissue concentration of salicyl ions, which was higher after local application of the solution than after oral administration of ASA. The local solution also resulted in a lower plasma concentration of salicylate ions, allowing high plasma salicylate concentrations to be avoided.

Administration, Topical↗
PubMedDate not supplied

[Gonadotoxic action of acetylsalicylic acid].

It has been established in experiments on white rats that administration of acetylsalicylic acid (ASA) in a dose of 1/10 LD50 for 1 1/2 months is accompanied by a decrease in the functional activity of spermatozoids. Repeated inhalation of ASA dust at a concentration of 25 mg/m3 for 4 months produces morphological changes in the spermatogenic epithelium and abnormal antenatal development of the progeny of male animals under test.

Animals↗