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PubMedDate not supplied

[Effect of a course of dosages of acetylsalicylic acid and sodium salicylate on the indices of the tonus of vessels of differing functional importance in cats].

The experiments on 42 adult male and females cats showed that acetylsalicylic acid and sodium salicylate (daily orally in 7-day and 14-day courses in a dose of 100 mg/kg) increase the tension of some visceral (of the myocardium, liver, stomach) and major (of the abdominal aorta, femoral and carotid) arteries, sodium salicylate effect being more pronounced. The maximum changes were noted in the vessels of the gastric mucosa and submucous layer.

Animals↗
PubMed1988

Effects of acetylsalicylic acid on electromechanical activity of in vivo rabbit ileum.

Aspirin has antisecretory and ulcerogenic properties in the gastrointestinal tract. The aim of this study was to determine the effects of acetylsalicylic acid (ASA) on the electrical and mechanical activity of the ileum in anesthetized New Zealand White rabbits. Ileal electromechanical activity was recorded from serosal electrodes and a miniature intraluminal balloon. Thirty minutes after injection of ASA (30, 60 and 100 mg/kg intravenous) significant and dose-dependent increases in the percentage of slow waves with action potentials were observed when compared with saline-infected animals. The onset of action potentials correlated with phasic increases in intraluminal pressure, indicating the onset of circular muscle contractions. Injection of 15 mg/kg ASA, sodium salicylate (100 mg/kg intravenous) or saline had no effect on baseline action potential activity. Prostaglandin E2 (PGE2) (5 and 10 micrograms/kg intravenous) significantly increased slow-wave frequency and decreased ASA-induced action potential activity. This study demonstrates that (1) ASA, but not sodium salicylate, stimulates phasic ileal action potential and contractile activity and (2) in ASA-treated animals, PGE2 produces differential effects on in vivo slow-wave frequency and action potential activity.

Action Potentials↗
PubMed1989

Effect of low dose acetylsalicylic acid on the frequency and hematologic activity of left ventricular thrombus in anterior wall acute myocardial infarction.

In this prospective, randomized, placebo-controlled trial the effect of 100 mg acetylsalicylic acid (ASA) once daily on the incidence, hematologic activity and embolic potential of left ventricular (LV) thrombosis was studied in 100 consecutive patients with a first anterior wall acute myocardial infarction (AMI). Patients were randomized to ASA or placebo less than 12 hours after onset of symptoms. Heparin, 5,000 IU subcutaneously twice daily, was given to all patients during immobilization. Echocardiography was performed less than 24 hours, 48 to 72 hours and 1, 2, and 12 weeks after AMI. LV thrombosis was detected by echocardiography in 30 (33%) of the 92 evaluable patients (15 patients given ASA and 15 given placebo). Indium-111 platelet scintigraphy was done in 17 of the 22 patients with an LV thrombus at the second week echocardiogram. Among 7 ASA-treated patients, 4 had positive images; among 10 placebo patients, 5 had positive images. LV thrombus resolution was noted in 3 of 9 patients with a positive scan and in 5 of 8 patients with a negative platelet scan. In 7 of 10 ASA-treated patients and 5 of 12 placebo-treated patients thrombus resolution was observed (difference not significant). Systemic embolism occurred in 2 patients, both given ASA, during the first week after AMI. Thus, low dose ASA has no effect on the incidence, hematologic activity and embolic potential of LV thrombosis in anterior wall AMI.

Adult↗
PubMed1986

Effects of acetylsalicylic acid and indomethacin on single groups III and IV sensory units from acutely inflamed joints.

In cats with an acute experimental inflammation in the right knee joint the effects of acetylsalicylic acid (ASA) and indomethacin on the discharge properties of single fine myelinated and unmyelinated articular afferent units were tested. The knee joint was inflamed by injection of kaolin and carrageenan into the joint cavity some hours before the recording period. Before drug application the single afferent fibres showed resting activity and responses to movements of the joint within its working range which is common for units from the inflamed knee. Resting activity was reduced significantly in most units within 0.5 h after the intravenous injection of the drugs. Within the observation time of about 1-2 h there was no recovery. In a few units a transient increase of resting activity was observed immediately after the injection of a drug. After the initial observation period of 1-2 h the responses to movements were tested. They were reduced in all units except one myelinated afferent. Also during this testing period the resting discharges did not recover. Intra-arterial injection of prostaglandin E2 in low doses close to the joint temporarily nullified the depressing effects of aspirin and indomethacin. Resting activity and movement evoked responses were increased up to the level before the treatment with analgesic drugs. The effects of prostaglandin E2 lasted for several minutes to more than 1 h. The depression of resting and evoked activity in single afferent articular units from inflamed joints is discussed in relation to the analgesic properties of aspirin and indomethacin.

Afferent Pathways↗
PubMed1996

European Stroke Prevention Study. 2. Dipyridamole and acetylsalicylic acid in the secondary prevention of stroke.

In 1988, we undertook a randomized, placebo-controlled, double-blind trial to investigate the safety and efficacy of low-dose acetylsalicylic acid (ASA), modified-release dipyridamole, and the two agents in combination for secondary prevention of ischemic stroke. Patients with prior stroke or transient ischemic attack (TIA) were randomized to treatment with ASA alone (50 mg daily), modified-release dipyridamole alone (400 mg daily), the two agents in a combined formulation, or placebo. Primary endpoints were stroke, death, and stroke or death together. TIA and other vascular events were secondary endpoints. Patients were followed on treatment for two years. Data from 6,602 patients were analysed. Factorial analysis demonstrated a highly significant effect for ASA and for dipyridamole in reducing the risk of stroke (p < or = 0.001) and stroke or death combined (p < 0.01). In pairwise comparisons, stroke risk in comparison to placebo was reduced by 18% with ASA alone (p = 0.013); 16% with dipyridamole alone (p = 0.039); and 37% with combination therapy (p < 0.001). Risk of stroke or death was reduced by 13% with ASA alone (p = 0.016); 15% with dipyridamole alone (p = 0.015); and 24% with the combination (p < 0.001). The treatment had no statistically significant effect on the death rate alone. Factorial analysis also demonstrated a highly significant effect of ASA (p < 0.001) and dipyridamole (p < 0.01) for preventing TIA. The risk reduction for the combination was 36% (p < 0.001) in comparison with placebo. Headache was the most common adverse event, occurring more frequently in dipyridamole-treated patients. All-site bleeding and gastrointestinal bleeding were significantly more common in patients who received ASA in comparison to placebo or dipyridamole. We conclude that (1) ASA 25 mg twice daily and dipyridamole, in a modified-release form, at a dose of 200 mg twice daily have each been shown to be equally effective for the secondary prevention of ischemic stroke and TIA; (2) when co-prescribed the protective effects are additive, the combination being significantly more effective than either agent prescribed singly; (3) low-dose ASA does not eliminate the propensity for induced bleeding.

Adult↗
PubMed1986

A double-blind, randomized study of naproxen and acetylsalicylic acid after surgical removal of impacted lower third molars.

100 patients had an impacted lower 3rd molar surgically removed in a double-blind study. Naproxen (500 mg b.i.d.) or acetylsalicylic acid (ASA) (1 g t.i.d.) were administered to the patients. Paracetamol was allowed as escape medication. 49 patients received naproxen and 51 ASA. 4 patients from each group were excluded because they took other analgesics, took too few tablets, were lost to follow-up or had misunderstood the instructions. There was a significantly better over all analgesic effect of naproxen than ASA (p = 0.004). More patients in the naproxen group than in the ASA group (p less than 0.01) would accept treatment with the same drug again. 4 patients, all from the ASA group, complained spontaneously about side effects.

Adolescent↗
PubMed2005

The influence of acetylsalicylic acid intake by healthy volunteers on duplicate PFA-100 measurements.

The PFA-100 device is increasingly used for assessing platelet function. Its use to monitor anti-platelet therapy, like acetylsalicylic acid (ASA), has been described. In most studies single PFA-100 measurements were used. In this study, we evaluate the influence of ASA on duplicate measurements using collagen/epinephrine cartridges. Twelve healthy volunteers received a single dose of 160 mg ASA and 12 other healthy volunteers received 30 mg ASA during 10 days followed by 80 mg ASA during 10 days. PFA-100 measurements were performed in duplicate 1 and 24 h after the final intake of medication. The mean coefficient of variation of duplicate measurements before medication was 8.4% and at least two times higher after the intake of a single dose of 160 mg ASA or 30 mg ASA during 10 days. Per individual, huge differences between duplicate measurements were observed after ASA ingestion. Differences were less pronounced after ingestion of 80 mg ASA during 10 days, because six of 12 volunteers had a maximum PFA-100 value>300 s in both measurements. As a consequence, one should be cautious to use the PFA-100 to monitor ASA therapy in individual patients.

Adult↗
PubMed1978

A single dose study comparing the analgesic effects of diflunisal, acetylsalicylic acid, and placebo in pain following meniscectomy.

A single dose experiment was used to evaluate the analgesic effect of diflunisal, a new salicylic acid derivative. Three dose levels of diflunisal (125 mg, 250 mg, and 500 mg) were compared to one dose level of acetylsalicylic acid (ASA) (600 mg) and placebo. The maximal analgesis induced by 500 mg diflunisal was comparable to that of 600 mg ASA. The onset of action was slightly more rapid with ASA but the duration of the analgesic effect was far longer for diflunisal, extending beyond 8 hours after administration. Diflunisal is a promising drug for the treatment of post-operative pain because of its long-lasting effect.

Adult↗
PubMed1976

Gastrointestinal microbleeding in normal subjects receiving acetylsalicylic acid, placebo, and R-803, a new antiinflammatory agent, in a design balanced for residual effects.

This study was undertaken to compare the relative gastrointestinal toxicity of equipotent doses of acetylsalicylic acid (ASA), 900 MG q.i.d., and a new anti-inflammatory agent, R-803, 300 mg q.i.d., against placebo. Gastrointestinal micro-bleeding was quantitated with the 61Cr-labeled erythrocyte assay. The experimental design was balanced for residual effects in the first week following any treatment. An interesting relationship between stool weight and blood loss was found to influence the microbleeding independently of the treatments themselves. All observed blood loss values were corrected by regression to a reference stool weight of 100 Gm. Final analysis of corrected values was done on arithmetic and logarithmic scales. On both scales, R-803 induced much less blood loss than ASA. A difference of 1.3 ml/day between R-803 and placebo was not statistically significant on the arithmetic scale. On the log scale, a statistically significant difference was found; but since it corresponds to 0.4 ml/day, it was not considered to be clinically significant at this dosage.

Anti-Inflammatory Agents↗
PubMed1992

Optimal low dosage of acetylsalicylic acid (ASA) for the prevention and treatment of ischemic cerebrovascular disease in geriatric patients.

A series of 108 geriatric patients with ischemic cerebrovascular disease were treated with low dose aspirin (acetylsalicylic acid, ASA). Daily doses of 100 mg, 50 mg and 25 mg were administered to three groups of 36 patients. Changes in platelet aggregation responses were dynamically observed in 64 (22 normal subjects, 42 patients). Monitoring of 22 normal subjects revealed inhibition of platelet aggregation at a dose of 300 mg or 100 mg which could last as long as 7 days. This suggests that 100 mg or less could be clinically effective. Satisfactory inhibitory effects on platelet aggregation were observed in all three groups, with 14 patients in each group given daily doses of 100 mg, 50 mg and 25 mg during four weeks' observation. The most effective inhibition was obtained in the 50 mg group. Therefore, the authors recommend 50 mg/d as the optimal dosage for low dose aspirin therapy in geriatric patients.

Aged↗
PubMed1984

The pharmacokinetics of meprobamate following its oral and rectal administration as a series of combinations with diphenhydramine, acetylsalicylic acid, codeine and pentaerythritol tetranitrate.

Studies in human volunteers of the pharmacokinetics of the active drugs in the formulations Visano-mini (meprobamate and diphenhydramine HCl), DoloVisano (meprobamate, diphenhydramine HCl, acetylsalicylic acid and codeine phosphate) and VisanoCor (meprobamate, diphenhydramine HCl and pentaerythritol tetranitrate (PETN], have demonstrated systemic absorption of each of the drugs from all of the formulations. Bioequivalence of meprobamate is indicated despite the drug combinations involved. Some differences in diphenhydramine pharmacokinetics are, however, apparent. The bioavailability of meprobamate administered rectally to human volunteers as the marketed preparations DoloVisano Suppositories and Dolo-Visano Suppositories sine codeino, is similar to that observed following oral administration.

Administration, Oral↗
PubMedDate not supplied

[Prevention of pre-eclampsia by low-dose acetylsalicylic acid--a critical appraisal].

Pre-eclampsia has been shown to be associated with platelet activation and excessive release of vasoconstricting thromboxane preceding the onset of the disease. Low-dose acetylsalicylic acid (ASA) substantially inhibits thromboxane formation and may thus prevent pre-eclampsia from developing. In agreement with this hypothesis early randomised trials reported on promising reductions in pre-eclampsia risk and possible fetal growth retardation. Subsequent multicentre trials during the nineties failed to confirm a large benefit, which may in part be explained by late initiation of treatment, low dosages, low patient compliance and wide inclusion of women with concomitant disorders such as chronic hypertension, diabetes mellitus and kidney disease. A recent systematic review of all randomised trials showed an acceptable safety profile and a significant but only moderate reduction in the risk of pre-eclampsia regardless of gestation at trial entry or dose of ASA. There is now growing evidence that the earlier ASA treatment is started, the greater the reduction in the risk of pre-eclampsia is. Moreover, ASA has much stronger effects at higher (80 - 150 mg/day) than at lower doses in the protection against pre-eclampsia and the prevention of severe fetal growth retardation. No clinically important effects, however, have been found in patients with chronic hypertension, kidney disease or diabetes mellitus. In contrast, low dose ASA (100 mg/day) might benefit women with unfavourable obstetric history, in particular those with severe fetal growth retardation or pre-eclampsia with onset at < 32 weeks. The crucial time for starting treatment may be before 16 weeks and daily ingestion before bedtime appears useful. To start low-dose ASA at 20 - 24 weeks gestation seems only justified in women with abnormal uterine Doppler flow.

Aspirin↗
PubMed2004

Prevention of angiotensin II-induced hypertension, cardiovascular hypertrophy and oxidative stress by acetylsalicylic acid in rats.

BACKGROUND: Angiotensin II (Ang II)-induced oxidative stress has been suspected to play an important part in the pathogenesis of many cardiovascular diseases. Our previous study demonstrated that acetylsalicylic acid (ASA) possesses potent antioxidative properties. OBJECTIVE: To evaluate the pathogenetic role of oxidative stress in Ang II-induced hypertension and cardiovascular hypertrophy. METHODS AND RESULTS: Chronic infusion of Ang II (200 ng/kg per min for 12 days) increased the aortic and cardiac tissue production of superoxide anion (O2) (lucigenin-enhanced chemiluminescence method) by 77 and 35%, respectively. These effects were associated with progressive increases in systolic blood pressure (from 135 to 194 mmHg) and heart/body weight ratio (from 2.25 to 2.69). Chronic treatment with oral ASA alone (100 mg/kg per day for 12 days) significantly reduced aortic and cardiac production of O2 (by 31 and 33%, respectively), without alteration in blood pressure and heart/body weight ratio in control normotensive animals. However, concurrent treatment with ASA in Ang II-infused rats completely prevented the Ang II-induced production of O2, in addition to hypertension and cardiac hypertrophy. Similar protective effects were observed in cultured aortic smooth muscle cells, in which increases in O2 production and [H]leucine incorporation (221 and 38%, respectively) induced by Ang II (10 mol/l) were totally prevented by concurrent incubation with ASA (10 mol/l). Losartan, but not PD 123319, also blocked the Ang II-induced oxidative and hypertrophic effects in those cells. Other anti-inflammatory drugs, such as salicylic acid, indomethacin and ibuprofen, did not show similar anti-Ang II and antioxidative effects in vivo. CONCLUSIONS: Oxidative stress plays a major part in chronic Ang II-induced hypertension and cardiovascular hypertrophy. Chronic concurrent treatment with ASA was found to prevent those Ang II-induced effects on the cardiovascular system, presumably through its antioxidative properties.

Angiotensin II↗
PubMed1987

Similar effects of acetylsalicylic acid and morphine on immediate responses to acute noxious stimulation.

The formalin and writhing tests in mice were employed to investigate a possible delay in the onset of antinociceptive action of acetylsalicylic acid (ASA). Drugs were given 30 min. before the noxious stimulation by either formalin or acetic acid. In the formalin test, the difference between the drug treated groups and the control group reach statistical significance within 30 sec. of noxious stimulation. ASA (400 mg/kg intraperitoneally) and morphine (5 mg/kg intraperitoneally) treated groups were not significantly different in any of the ten periods (30 sec. each) that were analysed during the first 5 min. In the writhing test, the number of writhings in response to intraperitoneal injection of acetic acid was counted during the first 20 min. The difference between the drug treated groups and the control group reached statistical significance after 3 min. both for ASA (400 mg/kg subcutaneously) and morphine (2 mg/kg subcutaneously) and no significant differences between the drug treated groups were found in any of the one min. periods that were analysed. Thus no delay of onset in the action of ASA compared to morphine could be demonstrated, and ASA seems to be antinociceptive also in acute non-inflammatory pain. Actions apart from inhibition of the synthesis of prostaglandins are suggested for this effect of ASA.

Analgesics↗
PubMed1989

Reduction by acetylsalicylic acid of paracetamol-induced hepatic glutathione depletion in rats treated with 4,4'-dichlorobiphenyl, phenobarbitone and pregnenolone-16-alpha-carbonitrile.

The role of enzyme induction in the reduction by acetylsalicylic acid (ASA) of paracetamol-induced hepatic glutathione (GSH) depletion has been studied in rats. Administration of an overdose of paracetamol to control rats resulted in an appreciable decrease of GSH concentration. Pretreatment with the enzyme inducers phenobarbitone, 3-methylcholanthrene (3-MC), pregnenolone-16-alpha-carbonitrile (PCN) and 4,4'-dichlorobiphenyl (4,4'-DCB) significantly potentiated the paracetamol-induced depletion of GSH. Simultaneous administration of an equimolar dose of ASA resulted in a reduction of the paracetamol-induced depletion of GSH in all instances except for those rats that were not pretreated and those given 3-MC. Benorylate, the ASA ester of paracetamol, depressed rat liver GSH to levels comparable to those produced by the combination of paracetamol and ASA. ASA itself caused only minor changes in liver GSH concentrations. The results demonstrate that ASA causes a diminution of paracetamol-induced GSH depletion in rats with phenobarbitone type of enzyme induction. Inhibition of the formation of the reactive metabolite of paracetamol or reduction of the absorption rate of paracetamol seem to be unlikely as mechanisms underlying the ASA-induced effect. An ASA-mediated effect via changes of the hepatic thiol status is proposed.

Acetaminophen↗
PubMed1991

[Pharmacokinetics of acetylsalicylic acid for the prophylaxis of cardiovascular pathology].

BACKGROUND: The metaanalysis of clinical trials on the secondary prevention of myocardial infarction and cerebrovascular disease with antiplatelet drugs suggests that low doses of acetylsalicylic acid (ASA) reduce cardiovascular mortality and morbidity. The ideal galenic formulation should contain a low dose of ASA, should be enteric-coated--to reduce gastrointestinal toxicity--and should be slowly absorbed--to facilitate selective inhibition of thromboxane synthesis by platelets. METHODS: The kinetics of a single dose of an enteric-coated sustained-release preparation containing 300 mg of ASA were studied in 6 healthy volunteers. Plasma concentrations of ASA and salicylic acid (SA) were measured during 12 hours after its administration. RESULTS: The time elapsed to achieve maximum plasma concentrations in the systemic circulation was 1 to 4 hours, as compared with 0.25 to 1.5 hours with other conventional preparations of ASA. The maximum plasma concentration recorded in one subject was 1.2 micrograms/ml, as compared with 4.8, 12, and 14 micrograms/ml with other preparations. CONCLUSIONS: The pharmacokinetic profile of this new preparation fits that proposed by others to produce a selective inhibition of thromboxane synthesis by platelets.

Adult↗