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PubMed1983

Recovery of acetylsalicylic acid and indalpine (LM 5008) after buccal partitioning.

The recoveries were compared of acetylsalicylic acid (ASA) and indalpine (1) after buccal absorption in three trained human volunteers. Recovery of the poorly lipid soluble ASA was less than 1% at pH 5 or 8, while that of the lipid soluble I was 19% and 13% at pH 5 and 8 respectively. This difference in recovery may represent a difference in their storage within the buccal mucosa dependent on their different lipid solubilities.

Absorption↗
PubMed1982

Effect of acetylsalicylic acid on insulin sensitivity in subjects with impaired glucose tolerance.

The effect of acetylsalicylic acid (ASA) on tissue sensitivity to insulin was studied in 14 non-obese subjects with impaired glucose tolerance. For the determination of insulin sensitivity a 1 h priming dose-constant insulin infusion technique was used. The percent decrease of plasma glucose and non-esterified fatty acid (NEFA) concentration at comparable steady-state insulin levels was taken as a measure of body sensitivity to insulin. Patients were restudied after daily treatment with 3.0 g ASA over 3 days. The decrease in plasma glucose and NEFA concentration was in the same range prior to and after ASA treatment (20.1 +/- 3.4 vs 20.8 +/- 4.9% and 54.2 +/- 4.8 vs 54.2 +/- 5.4%), indicating no change of insulin sensitivity by ASA treatment. The mean C-peptide concentration during the insulin infusion test did not differ between the two studies. The metabolic clearance rate of insulin was slightly reduced and the disappearance time of insulin was increased after treatment with ASA. In conclusion ASA did not exert any effect on tissue sensitivity to insulin in subjects with impaired glucose tolerance.

Adult↗
PubMedDate not supplied

Pharmacokinetics of acetylsalicylic acid and its metabolites at low doses: a compartmental modeling.

The pharmacokinetics of acetylsalicylic acid (ASA) and its metabolites salicylic acid (SA) and salicyluric acid (SUA) were studied in 12 healthy young volunteers after oral administration of low (30 and 100 mg) and moderate (400 mg) doses. Plasma and urine were assayed for the above drugs by high-performance liquid chromatographic method. Individual pharmacokinetic parameters were estimated by compartmental modeling (ASA and SA) and by model-independent methods (SUA). ASA parameter values estimated in this study were in agreement with those reported by other authors after administration of higher doses, which confirms the linearity of ASA pharmacokinetics in a broad dose range. On the contrary, both metabolic and renal elimination routes for SA were found to be saturable. The relative changes in SA renal clearance with the dose were more pronounced than those in metabolic clearance. Particularly, there was no statistically significant difference in SA metabolic clearance between 30 and 100 mg doses, indicating the linear kinetics in this dose range. Further increase in the dose resulted in significant decrease in SA metabolic clearance. At the same time, both SA excretion rate constant and fraction excreted significantly diminished across the entire dose range studied. The dependence of SUA renal clearance upon the dose was shown to be complex, reflecting possible saturability of its excretion.

Administration, Oral↗
PubMed1995

[Effect of acetylsalicylic acid on platelet aggregation and capillary bleeding in healthy cats].

The influence of acetylsalicylic acid (ASA) in vitro and in vivo on several parameters of the hemostatic system was evaluated in healthy cats. The aggregation response of cat platelets in vitro was not influenced by 10 micrograms ASA/ml plasma, whereas ASA concentrations of 35, 70, 100 micrograms/ml and of 1 mg/ml consistently inhibited the platelet aggregation induced by 0.1 (n = 4 cats) and 0.25 micrograms collagen/ml (n = 6 cats). The aggregation response to ADP and thrombin was partially (n = 2) or completely (n = 8) inhibited by an ASA concentration of 5 mg/ml. Administration of ASA at a dosage of 10 and 25 mg/kg BW orally and intravenously yielded a plasma concentration of salicylic acid of 30-42 micrograms/ml (10 mg/kg BW) and 50-70 micrograms/ml (25 mg/kg BW). All the dosages of ASA produced an inconsistent inhibition of the collagen-induced platelet aggregation (1/5 and 2/5 for the respective groups), whereas the response to ADP and thrombin was not altered. Capillary bleeding time was not significantly altered after the ASA administration. Platelet count and screening tests were not influenced by ASA application. According to the results of this study, ASA as a platelet aggregation inhibitor is not useful for the prophylaxis of thromboembolism in cats.

Adenosine Diphosphate↗
PubMed1998

Relative bioavailability of rapidly dispersing, plain, and microencapsuled acetylsalicylic acid tablets after single dose administration.

UNLABELLED: Extent and rate of absorption of acetylsalicylic acid (ASA) from rapidly dispersing (Acesal Extra) and plain tablets (Acesal) relative to reference 1 (plain tablets, Aspirin) and from microcapsuled tablets (Micristin) relative to comparable listed tablets (reference 2, Colfarit) were assessed in 2 single-dose (0.5 g ASA), open, randomized, crossover studies with intervals of 14 days between 2 periods. Both studies were performed in 24 male and female healthy volunteers each (age 18-32 years, body weight 48-90 kg, body height 161-190 cm). ASA and its metabolite salicylic acid (SA) were measured with an HPLC method validated for ASA between 0.2 and 20 microg/ml and for SA between 0.4 and 40 microg/ml. The test tablets were considered bioequivalent with reference in extent of absorption if the 90% confidence limits of the AUC0 to infinity ratio were within the range of 0.80-1.25, and in rate of absorption if the confidence limits of the Cmax/AUC0 to infinity ratios were within 0.70-1.43. RESULTS: Geometric means and 90% confidence limits for the test/reference ratios of the comparisons Acesal vs reference 1, Acesal Extra vs reference 1 and Micristin vs reference 2 were 1.05 (0.97-1.13), 1.13 (1.05-1.22), 1.02 (0.92-1.14) for ASA AUC0 to infinity and 1.02 (0.96-1.07), 1.05 (0.99-1.11), 0.98 (0.91-1.04) for SA AUC0 to infinity, respectively. The results for Cmax/AUC of ASA were 1.16 (1.00-1.34), 1.72 (1.49-1.99), 0.83 (0.73-0.94) and of SA 1.02 (0.98-1.07), 1.07 (1.02-1.12), 0.93 (0.88-0.97). CONCLUSION: Acesal and Micristin were bioequivalent with the respective references in both extent and rate of absorption. Acesal Extra and reference 1 were bioequivalent with regard to extent only. Acesal Extra was absorbed faster.

Adult↗
PubMed1984

Effect of cimetidine on net ion fluxes across the rat gastric mucosa during mucosal damage after gastric ischemia and after intravenous acetylsalicylic acid.

This study was performed to determine the relationship between net ion fluxes across the rat gastric mucosa and gastric mucosal damage after gastric ischemia and after intravenous administration of acetylsalicylic acid, and to determine the effect of cimetidine on these parameters. Gastric mucosal blood, albumin, and fluid loss that occurred after gastric ischemia was not associated with an increase in net H+ flux from mucosa to serosa. A significant increase in net Na+ and K+ flux from serosa to mucosa occurred. In the presence of cimetidine (150 mg/kg X h, i.v.), which reduced gastric damage, net H+ flux increased significantly, whereas there was an inhibition of Na+ and K+ fluxes. Acetylsalicylic acid-induced gastric hemorrhage preceded an increase in net H+ flux from serosa to mucosa, although net Na+ and K+ fluxes were unaffected. Cimetidine (150 mg/kg X h, i.v.) potentiated gastric hemorrhage and this was associated with an increase in net K+ flux from serosa to mucosa. These studies demonstrate that overt damage to the rat gastric mucosa can occur without changes in net ion fluxes across the gastric mucosa.

Animals↗
PubMedDate not supplied

Sex differences in the enzymatic hydrolysis of acetylsalicylic acid by microsomes from various rat tissues.

We studied the in vitro hydrolysis of acetylsalicylic acid (ASA) to salicylic acid (SA) catalysed by microsomal preparations from liver, kidney, small intestine and stomach mucosas and blood serum of adult female and male rats. Hepatic microsomes from male rats had the highest specific activity: 42.3 +/- 6.0 nmol SA mg(-1) min(-1) (mean +/- SEM). Kidney, intestine, stomach and serum activities were 60, 30, 14 and 0.7% with regard to the liver. In contrast, gastric microsomes from female rats showed the highest specific activity: 53 +/- 22.1 nmol SA mg(-1) min(-1) (mean +/- SEM) whereas intestine, liver, kidney and serum activities were 60, 43, 40 and 1.7% with regard to the stomach mucosa. Hepatic, renal and intestinal microsomes had a pH optimum of 5-6. Male rats had Vmax and Km values of 95.5, 83.4 and 29.4 nmol SA mg(-1) min(-1) and 2.9, 1.27 and 6.4 mM, while for female rats they were 54.8, 75.8 and 59.4 nmol SA mg(-1) min(-1) and 2.6, 1.35 and 3.4 mM for hepatic, renal and intestinal microsomes, respectively. Parathion inhibited the hydrolysis of ASA with an IC50 of 1.2 x 10(-5) M for liver and kidney and 5 x 10(6) M for intestine from male rats.

Animals↗
PubMed1982

Bioavailability of acetylsalicylic acid and salicylic acid from rapid-and slow-release formulations, and in combination with dipyridamol.

Acetylsalicylic acid (ASA) is a strong, irreversible inhibitor of platelet aggregation, but loses this activity following first-pass deacetylation to salicylic acid (SA). In order to compare the bioavailability of unchanged ASA from rapid- and slow-release formulations, the single-dose concentration profiles of ASA and SA were studied in healthy volunteers following intake of two different rapid-release (conventional and effervescent tablets) and three different slow-release (microencapsulated ASA in tablets and in capsules, and enteric-coated tablets) formulations of ASA, and of one slow-release formulation of sodium salicylate. Since anti-platelet therapy with ASA is often combined with dipyridamol, the influence of this drug was also examined. The concentrations of ASA and SA were measured by high-pressure liquid chromatography. While the bioavailability of SA from the 5 ASA formulations was essentially equal and similar to that of the salicylate formulation, the bioavailability and peak concentrations of ASA appeared to be the much greater after rapid-release than after slow-release formulations. Indeed, ASA was only rarely detected in systemic blood following intake of slow-release ASA. Co-administered dipyridamol did not significantly influence the kinetics of ASA or SA. It appears that rapid-release formulations of ASA should be prefered in anti-platelet therapy, either alone or in combination with dipyridamol.

Adult↗
PubMed1977

Acute effects of acetylsalicylic acid on renal function in normal man.

The acute effects of therapeutic doses of acetylsalicylic acid (ASA) on renal water and solute output, and the possible interaction of ASA with the diuretic effects of furosemide, have been studied in a double blind double cross over study in healthy human subjects. There was a significant decrease in 24 h sodium excretion and Na/K ratio in urine in the ASA-treated subjects. The effect of ASA on urinary sodium excretion was most prominent during day time (8 a.m.-10 p.m.) and on days with low sodium intake, as confirmed by control sodium excretion and plasma renin activity. A decrease in urine volume and an increase in tubular reabsorption of free water were caused by ASA, the antidiuretic effect being most marked at night (10 p.m.-8 a.m.). No action of ASA on the effect of furosemide on urinary sodium excretion was found. Creatinine clearance remained unaltered by ASA treatment, and ASA did not interfere with the increase in urinary creatinine excretion after furosemide treatment.

Aspirin↗
PubMed1998

The influence of acetylsalicylic acid on cognitive processing: an event-related potentials study.

The central effects of acetylsalicylic acid (ASA) are discussed controversially. In animal models, it has been shown that ASA can interact with the central serotonergic and catecholaminergic neuronal system. However, the relevance of this interaction for humans is still unknown. We performed a study on the influence of ASA on central cognitive processing. In 25 healthy subjects (age 21-56 years), visually evoked event-related potentials (ERP) and reaction time under IV ASA medication were recorded. ERP were evoked by an oddball paradigm. As compared to placebo, ASA decreased the latency of the P3 component significantly in a time interval of 20-40 min after administration. The latency of the N2 component was significantly decreased about 25 min after administration; the latency of the exogenous P2 component was not influenced by ASA. The mean choice reaction time was significantly decreased by ASA 35 min after administration. At this time point, there was a significant correlation between decrease in reaction time and increase in ASA plasma level. The data show that IV administration of ASA has an accelerating effect on the endogenous components of visual ERP and on reaction time. This finding suggests that ASA can influence central cognitive processing, possibly by ASA induced changes of neurotransmitters. Since serotonin can be released by ASA and serotonin release leads to a decrease of ERP latencies. we assume that ASA most likely influences cognitive processing via the central serotonergic transmitter system.

Adult↗
PubMed1976

Gastro-intestinal microbleeding under acetylsalicylic acid, ketoprofen and placebo.

A quantitative comparison of gastro-intestinal microbleeding induced by acetylsalicylic acid (ASA), 3.6 g daily, ketoprofen (KETO), 200 mg daily and placebo (P) was undertaken in 12 normal volunteers using a double-blind factorial design with repeated measures. We conclude that KETO induces less gastro-intestinal bleeding than ASA but more than placebo and that there is a significant residual bleeding under placebo following ASA.

Anti-Inflammatory Agents↗
PubMed1995

The effect of acetylsalicylic acid on fibrin gel lysis by tissue plasminogen activator.

The in vitro effect of acetylsalicylic acid (ASA) on fibrin gel lysis by exogenous t-PA was studied in 13 patients with angina pectoris. Six patients received 75 mg, and seven patients 160 mg of ASA. Plasma clots were formed and lysed in microtiter plate wells and turbidity monitored spectrophotometrically. Mean lysis times in the 75 mg group were 8.7, 11.4 and 11.2 min during ASA treatment, and after 1 and 2 weeks ASA withdrawal respectively. Reduced changes were observed in the 160 mg group. Additionally, a relationship was found between the fibrin fiber mass/length ratio, i.e. fiber thickness in mature clots and lysis times after ASA administration (P = 0.0015). Importantly, fibers are thicker during treatment with ASA. It was subsequently demonstrated that the potential to produce thicker fibers by varying the thrombin concentration has a noticeable effect on turbidimetric profiles in the presence of exogenous t-PA. This effect was similar to the changes observed during and after ASA treatment. Thus, these results suggest that the enhancement of fibrin gel lysis during ASA treatment may be due to alterations in gel structure. In addition, a reduction in the fibrin mass in lower turbidity clots, suggests an added mechanism by which ASA may enhance lysis.

Angina Pectoris↗
PubMedDate not supplied

Effects of duration of acetylsalicylic acid administration on patency and anastomotic hyperplasia of ePTFE grafts.

Effects of duration of acetylsalicylic acid (ASA) administration on the patency and development of distal anastomotic intimal hyperplasia (DAIH) of endothelial cell (EC) seeded and unseeded prosthetic aortoiliac grafts were studied in a canine model. ASA, 5 gr po qd, was administered to dogs 1 day prior to placement of bilateral, 12 to 17 cm long, 5 mm inside diameter expanded polytetrafluoroethylene (ePTFE) aortoiliac grafts and continued for 2 wk (Group 1, n = 12 dogs) or 16 wk (Group 2, n = 12 dogs). Six dogs in each group received autologous EC seeded grafts, while the others received unseeded grafts. Prosthesis patency was assessed weekly. At the conclusion of the study, DAIH was measured on serial sections using a computer-linked digitizer. The 16 wk patency for Group 1 grafts was 67%, while that for Group 2 grafts was 88% (p less than 0.09). Luminal narrowing due to DAIH was not significantly different between Groups 1 and 2 (7.7 +/- 8.3% [means +/- SD] and 9.0 +/- 7.8% respectively). EC seeding improved the 16 wk combined patency from 62 to 92% (p less than 0.02). A more complete luminal endothelial cell lining was correlated with reduced DAIH (r = -0.4, p less than 0.05). Chronic ASA administration prevented graft thrombosis between 2 and 4 wk postimplantation in this study but was not associated with decreased DAIH.

Anastomosis, Surgical↗
PubMed1982

Systemic availability of acetylsalicylic acid in human subjects after oral ingestion of three different formulations.

Systemic availability of acetylsalicylic acid (ASA) in normal human subjects after oral ingestion of 1 g in three different formulations was determined by using high-pressure liquid chromatography for ASA assay. For an effervescent, a plain and a sustained release preparation systemic availabilities expressed in percent of the ingested dose were 16.9 +/- 3.2, 8.6 +/- 1.2 and 2.6 +/- 0.4%, respectively. All subjects had clearly measureable amounts of ASA in plasma after oral intake of a sustained release preparation with an average peak concentration of 15 mumol/l. Peak concentration after an effervescent and plain formulation was on the average 80 and 40 mumol/l, respectively. Half-life of ASA in plasma was 18.1 +/- 1.2 min. for the effervescent and 28.7 +/- 5.3 min. for the plain preparation, while the elimination phase was too ill defined for the sustained release formulation. Average plasma half-life of salicylic acid (SA) was similar after the three different administration forms with values between 3.0 and 3.7 hrs. Further, no difference in SA distribution volumes or amounts of SA absorbed was found. The present study demonstrates that oral ingestion of ASA in effervescent, plain and sustained release formulations gives rise to significant amounts of ASA in plasma. Concentrations found indicate that long-term antithrombotic therapy with ASA in a sustained release formulation may be possible.

Administration, Oral↗
PubMed1982

Reduction of the bradykinin-induced activation of feline group III and IV muscle receptors by acetylsalicylic acid.

1. In chloralose-anaesthetized cats, the influence of systemically or locally applied acetylsalicylic acid (ASA) on the responses of thin-fibre muscle receptors to close-arterial injections of bradykinin was studied. 2. Many of the slowly conducting (group III and IV) muscle afferents had a background activity of low frequency. This discharge was either unaffected or slightly increased by the ASA doses used. In two units which had a very high discharge rate ASA led to a marked decrease in background activity. 3. On local (I.A. or I.M.) injection of ASA, doses below 1 mg were sufficient for reducing the bradykinin-induced activations of group III and IV muscle receptors. The reduction lasted for about 15-30 min. 4. On systemic (I.V.) administration of ASA (50 mg/kg body weight) the reduction in response magnitude to bradykinin became significant 8 min after injection of the analgesic. The effect was maximal about 10 min later and lasted for more than 60 min. 5. Five receptors were found which gave a repeated response to 5-hydroxytryptamine (5-HT) injected at 10 min intervals. The 5-HT-induced activations could not be reduced by ASA (50 mg/kg I.V.). 6. Most of the receptors responding to bradykinin had a high threshold on mechanical stimulation and thus were probably nociceptors. It is concluded that the reduction of their bradykinin-induced activations reflects the suppression of nociceptive information by an analgesic. Since the recordings were obtained from primary afferent units the data constitute direct evidence for a peripheral action of ASA.

Action Potentials↗
PubMed1975

Influence of intravenously administered acetylsalicylic acid on platelet functions. A pharmacodynamic and pharmacokinetic study.

The influence of intravenously administered acetylsalicylic acid (ASA) on the kinetics of platelet function was examined in 10 patients. Simultaneously, assays of salicylate in plasma were performed. A significant inhibition of platelet aggregation as well as PF 3 and PF 4 availabilities could be demonstrated 2 min after injection. A decrease of platelet adhesion was significant after 15 min. The inhibition of platelet functions was still present after 24 h and was partially demonstrable after 72 h. The concentration of salicylate in plasma 2 min after injection of ASA was only about two thirds of the level calculated from mere distribution in circulation. After 1 h, half of the initial salicylate had disappeared from plasma. No salicylate could be found after 24 hours. ASA also depressed platelet functions when added to platelet-rich plasma in vitro in a concentration of 100 mug/ml. Inhibition of platelet aggregation and of PF 4 availability were dependent on the time of incubation. Their onset was much slower in vitro than in vivo. No inhibition of the PF 3 availability could be found in vitro. The inhibition of platelet functions by ASA is demonstrable almost immediately after injection while the duration of this inhibition is considerably longer than the elimination time of salicylate from plasma. This allows the conclusion that a direct intravascular reaction between ASA and platelets occurs and that the inhibition of platelet functions is irreversible.

Aspirin↗
PubMed1999

Rapid decline of cerebral microemboli of arterial origin after intravenous acetylsalicylic acid.

BACKGROUND AND PURPOSE: The present study investigated the influence of the antiplatelet agent acetylsalicylic acid (ASA) on cerebral microembolism as detected by transcranial Doppler sonography (TCD). METHODS: Nine patients with recent transient ischemic attack or minor stroke of arterial origin were investigated. Eight had not received an antiplatelet or anticoagulant medication before TCD, and in 1 patient a preexisting ASA medication (100 mg/d) had not been changed since the onset of stroke symptoms. An initial 1-hour TCD monitoring was extended for an additional 2.5 hours after an intravenous bolus injection of 500 mg ASA and was repeated for 1 hour on the following day. RESULTS: Microembolic signals (MES) were detected in all patients only on the symptomatic side. After the ASA bolus injection, a significant drop of the MES rate was found in 7 patients, all without previous medication, starting 30 minutes after the application (mean per hour=25.1 [range, 6 to 66] versus mean per hour=6.4 [range, 0 to 14]). In 3 of these patients, platelet aggregation tests were performed that demonstrated normal aggregation before bolus injection and inhibited aggregability as early as 30 minutes after bolus injection. The rate of MES remained unchanged in 1 patient without antiplatelet medication. The ninth patient, who had suffered an ischemic event on ASA, showed only a transient decrease of MES frequency. CONCLUSIONS: In patients with recent stroke of arterial origin, intravenous ASA can rapidly reduce cerebral microemboli as detected by TCD. Microemboli might be a useful parameter to monitor early effects of antiplatelet therapy.

Adult↗
PubMed1998

Different dosages of acetylsalicylic acid lead to adverse modifications of the reaction of rat pancreas to ethanol.

CONCLUSION: Acetylsalicylic acid (aspirin, ASA) in a therapeutic dose prevents lipid peroxidation and damage of cell organelles in pancreatic tissue of rats chronically fed with ethanol. In contrast, higher ASA dosages lead to enhanced biochemical and morphological signs of pancreatic damage different from findings in rats fed by ethanol alone. METHODS: Two groups of rats received 20% alcohol as drinking fluid plus a diet containing either 6 (S6) or 10 g/kg (S10) ASA. Two control groups received no ASA (CA) and neither ASA nor alcohol (CW), respectively. Feeding was performed by the interrupted feeding regimen with four 18-h periods of food and fluid withdrawal weekly. After 7 mo, pancreatic tissue was examined by light and electron microscopy. In pancreas homogenates, the contents of malondialdehyde (MDA), protein, trypsinogen, lipase, pancreatic secretory trypsin inhibitor, acid phosphatase (AcPh), cathepsin B, beta-glucuronidase, and desoxyribonucleic acid were determined. RESULTS: In the pancreas of group CA, we found a 100% increase of MDA compared with group CW, increased fat deposition, as well as damaged mitochondria (Mito) and endoplasmic reticula (ER) in acinar cells, decreased protein content, decreased AcPh activity, and unchanged secretory parameters. The ASA-fed groups showed MDA contents indistinguishable from group CW. Protein and secretory parameters were decreased. Lysosomal enzymes were decreased in S6, but in S10, they were always higher than in group S6 and mostly as high as in group CW. Fat deposits were as frequent as in group CA. Mito and ER were mostly well preserved, but more autophagosomes and residual bodies occurred, particularly in group S10.

Animals↗