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PubMed1983

[Animal experiments on the gastric mucosa and demonstration of analgesic and antipyretic effects after combined administration of acetylsalicylic acid and sodium pyruvate].

Animal experimental examinations in guinea pigs and rats demonstrate the positive influence of sodium pyruvate on lesions of the gastric mucosa induced by acetylsalicylic acid. As compared to pure acetylsalicylic acid a combination of acetylsalicylic acid and sodium pyruvate reduces significantly the numbers of erosions, ulcers and hemorrhages on the gastric mucosa. Sodium pyruvate protects effectively against the undesired side-effects by acetylsalicylic acid. The analgetic and antipyretic effect of acetylsalicylic acid is not impaired by the addition of sodium pyruvate.

Analgesics↗
PubMed1994

Low dose acetylsalicylic acid in the antithrombotic treatment of patients with stable angina pectoris and acute coronary syndromes (unstable angina pectoris and acute myocardial infarction).

Acetylsalicylic acid has an antithrombotic effect by inhibition of thromboxane A2 synthesis in platelets. Thromboxane A2 is a potent stimulator of platelet aggregation and vasoconstriction and synthesis may be completely inhibited by a single oral dose of 150 mg acetylsalicylic acid or an intravenous dose of 100 mg. A daily maintenance dose of 75 mg acetylsalicylic acid is sufficient to effectively inhibit thromboxane A2 synthesis in long-term treatment. Acetylsalicylic acid therapy reduces acute myocardial infarction and sudden death in patients with stable angina pectoris and the drug is equally effective in patients with symptomatic and 'silent' angina pectoris. Early intervention with acetylsalicylic acid in patients with unstable angina pectoris reduces the risk of acute myocardial infarction and death. In patients with acute myocardial infarction, acute therapy with acetylsalicylic acid significantly reduces mortality both in monotherapy and in combination with thrombolytics. In the secondary prophylaxis following acute myocardial infarction, acetylsalicylic acid reduces the incidence of reinfarction and coronary death. Treatment of 100 patients with acute coronary syndrome (unstable angina pectoris or acute myocardial infarction) for 2 years may hinder the development of 3-4 fatal and 4 non-fatal vascular events. The risk of gastrointestinal side-effects and bleeding during acetylsalicylic acid therapy is dose-dependent and the incidence is low with a daily dose of 75-150 mg.

Administration, Oral↗
PubMed1991

Induction of omega-oxidation of monocarboxylic acids in rats by acetylsalicylic acid.

The accumulation of dicarboxylic acids, particularly long chain, is a prominent feature of Reye's syndrome and diseases of peroxisomal metabolism. We assessed the omega-oxidation of a spectrum of fatty acids in rats and asked whether pretreatment of rats with aspirin, which is known to predispose children to Reye's syndrome, would affect omega-oxidation of long chain fatty acids. We found that aspirin increased liver free fatty acids and increased the capacity for omega-oxidation three- to sevenfold. Omega-oxidation of long chain substrate was stimulated to a greater degree than medium chain substrate and was apparent within one day of treatment, at serum aspirin concentrations below the therapeutic range in humans. The apparent Km for lauric acid was 0.9 microM and 12 microM for palmitate. We also found a difference in the storage stability of activity toward medium and long chain substrate. Saturating concentrations of palmitate had no effect on the formation of dodecanedioic acid, whereas laurate decreased but never eliminated the omega-oxidation of palmitate. 97% of the total laurate omega-oxidative activity recovered was found in the microsomes, but 32% of palmitate omega-oxidative activity was present in the cytosol. These results demonstrate that aspirin is a potent stimulator of omega-oxidation and suggest that there may be multiple enzymes for omega-oxidation with overlapping substrate specificity.

Animals↗
PubMed1980

Protein-binding of ascorbic acid 2. Interaction with acetylsalicylic acid.

The effect of aspirin (ASP) on the binding of ascorbic acid (AA) to bovine serum albumin (BSA) has been investigated by the method of dynamic dialysis. Scatchard plots were constructed which confirmed that binding with AA occurred in the presence of BSA. When ASP was also present, greater curvature of the plot was demonstrated indicating that less binding of AA to BSA was taking place. The limiting slopes of the plots showed that ASP displaces both primary and secondary sites previously occupied by AA and that the strengths of both primary and secondary sites increased as a result of interaction with ASP. It is concluded that primary sites for binding of AA to BSA consist of two or more types of similar binding strengths, and that secondary binding also may involve binding on two or more sites. The pathophysiological implications are discussed.

Animals↗
PubMed1975

Patho-physiological studies on lactic acid-induced pulmonary thrombosis in rat. I. Effect of heparin, acetylsalicylic acid, urokinase and tranexamic acid.

The role of platelet aggregation and coagulo-fibrinolytic systems in thrombogenesis of lactic acid-induced pulmonary thrombosis in rat were studied using an anti-coagulant, platelet aggregation inhibitor, fibrinolytic or anti-fibrinolytic agents. In normal rat, heparin (2.5 mg/kg), acetylsalicylic acid (30 mg/kg) and tranexamic acid (100 mg/kg) suppressed specifically coagulation, platelet aggregation induced by collagen or thrombin and fibrinolysis respectively. Urokinase (10,000 units/kg) activated powerfully fibrinolytic system in addition to suppressing slightly platelet aggregation. The pretreatment with heparin, acetylsalicylic acid or urokinase markedly prevented the formation of thrombus initiated by the infusion of lactic acid at the doses used. Additive effect was also obtained by combined administration of these agents. On the other hand, it was interesting to note that tranexamic acid (100 mg/kg) did not affect the thrombus formation at all despite a potent anti-fibrinolytic effect of this agent. These results indicate that both platelet aggregation and enhancement of coagulation activity are important factors responsible for the formation of thrombi in DIC, while the fibrinolytic activity in blood seems not to be involved in it. On the basis of the findings, mechanism for triggering activation of coagulation and platelet aggregation is also discussed here.

Animals↗
PubMed1998

Better increase in fibrin gel porosity by low dose than intermediate dose acetylsalicylic acid.

AIM: To investigate the influence on plasma fibrin gel structure of low and intermediate doses of acetylsalicylic acid in healthy individuals. The influence of acetylsalicylic acid on thrombin formation, fibrinolytic capacity and plasminogen inhibitor-1 in plasma was also investigated. METHODS: Nineteen subjects were treated with 75 mg and 11 with 320 mg acetylsalicylic acid daily; eight subjects received both doses. Fibrin gel structure was determined by a permeability technique yielding a porosity constant (Ks), and the thromboxane metabolite 11-dehydro-thromboxane B2 (TxM) was determined by an ELISA. RESULTS: Acetylsalicylic acid increased fibrin porosity by 65% at 75 mg (P<0.001, n=19), whereas lower increases were found at 320 mg (+22%, P<0.05, n=11). One week after withdrawal Ks had essentially returned to baseline (ns). Urinary thromboxane metabolites were suppressed during treatment (-61%, P<0.001 at 75 mg, n=19; -46%, P<0.01 at 320 mg, n=11). The intra-individual comparison showed similar results (Ks +92%, TxM -62% at 75 mg; Ks +5%, TxM -52% at 320 mg). Fibrinolytic capacity, plasminogen inhibitor-1 levels and thrombin generation (in platelet-poor citrated plasma) were not influenced. CONCLUSION: Low dose acetylsalicylic acid causes the greatest increase in fibrin gel porosity; this may well be of therapeutic importance.

Adult↗
PubMed2003

Effects of acetylsalicylic acid and metamizol on hyaluronidase activity and sperm characteristics in rams.

The effects of acetylsalicylic acid and metamizol on hyaluronidase activity of semen and sperm characteristics in rams were investigated. Acetylsalicylic acid and metamizol at the doses of 75 and 50 mg/kg were administered to the rams, respectively and then semen samples were taken at 1, 2, 4, 24, 48, 96, 120 and 144 h. The hyaluronidase activities of semen in rams treated with acetylsalicylic acid and metamizol were determined to increase significantly (P<0.001) when compared with control groups at all times. Additionally, the spermatozoa motilities in both groups were measured to increase significantly (P<0.05) when compared with control group. Furthermore, there were significant (P<0.01, <0.05) decreases in the sperm concentrations and semen volumes of rams treated with acetylsalicylic acid and metamizol at all times, respectively. In conclusion, although the use of acetylsalicylic acid and metamizol cause an increase in the hyaluronidase activities and spermatozoa motilities, these drugs decrease the sperm concentrations and semen volumes along 6 days. For these reason, the use of these drugs in breeding rams during ramming season is not suitable.

Animals↗
PubMed1979

Stability of acetylsalicylic acid in divided powders in the presence of aminophenazone.

The combination of acetylsalicylic acid with aminophenazone, often prescribed in divided powders, is considered to be incompatible. High performance liquid chromatography was applied to determine the content of salicylic acid which is the main known product from the decomposition of acetylsalicylic acid. The analysis of model samples containing a 1:1 (by weight) mixture of acetylsalicylic acid and aminophenazone, after having been stored under usual conditions in starch capsules, showed that the decomposition of acetylsalicylic acid into salicylic acid did not exceed 0.8% even after ten weeks.

Aminopyrine↗
PubMed1975

Oral antipyretic therapy: evaluation of benorylate, an ester of acetylsalicylic acid and paracetamol.

The capacity of benorylate, an ester of acetylsalicylic acid and paracetamol, to reduce fever in children was compared with that of the components as such or as a combination. The series of cases studied consisted of 66 patients between the ages of 4 months and 12 years with rectal temperatures above 38.5 degrees C. Temperatures were recorded at 15 and 20 min and 1, 2, 4 and 6 hrs after the administration of the drug. The antipyretic effect of combined acetylsalicylic acid (11 mg/kg) and paracetamol (14 mg/kg) was superior to the effect of benorylate with a dose of 25 mg/kg and even of 50 mg/kg as well as better than the effect of either drug alone. Acetylsalicylic acid (10 mg/kg) and paracetamol (12.5 mg/kg) alone produced a significantly greater antipyretic effect than benorylate with a dose of 25 mg/kg. Given in a dose of 35--40 mg/kg, benorylate seems to have a significant antipyretic effect. However, this effect is clearly smaller than that of either of its components, acetylsalicylic acid or paracetamol. Therefore benorylate is probably not suitable to be used as a general antipyretic agent in children.

Acetaminophen↗
PubMedDate not supplied

Comparative study of antithrombotic and antiaggregatory activity of acetylsalicylic acid, ticlopidine and a new noncarboxylic acid antiinflammatory pyrazine derivative HF90.

The action of acetylsalicylic acid, ticlopidine and a new pyrazine derivative HF90 selected in preliminary screenings (11, 18, 19) was studied by using the mouse antithrombotic assay according to DiMinno and Silver (22) and in vitro blood platelet aggregation method according to Born (23). Acute pulmonary thromboembolism was induced by injection of a mixture of collagen and epinephrine into the mouse tail vein. The effect of HF90, an acidic pyrazine derivative possessing active methylene moiety, administered at doses of 50 and 100 mg/kg, was compared to the action of the well established antithrombotic agents: ticlopidine (100 mg/kg) and acetylsalicylic acid (20 mg/kg). The compounds were administered i.p. in single doses 1 h and 24 h before the thrombotic challenge or once a day per three consecutive days before the thrombotic challenge. Ticlopidine appeared to provide the better protection against microembolism than acetylsalicylic acid although its effect has not manifested itself immediately after administration. The pyrazine derivative examined has a lower but significant antithrombotic activity. The chemical class of pyrazine derivatives with active methylene moiety (the so called pyrazine CH/NH-acids) (16) provides a new original antiinflammatory pharmacophore and HF90 may serve as the "lead compound" in the search for new agents of pharmacological interest.

Animals↗
PubMed2006

Simultaneous determination of acetylsalicylic acid and caffeine in pharmaceutical formulation by first derivative synchronous fluorimetric method.

A sensitive, rapid, and specific assay has been developed for the simultaneous determination of acetylsalicylic acid and caffeine in commercial tablets based on their natural fluorescence. The mixture of these drugs was resolved by first derivative synchronous fluorimetric technique using two scans. At Deltalambda=106 nm, using first derivative synchronous scanning, only acetylsalicylic acid yields a detectable signal at 316 nm (peak to zero method) which is unaffected by caffeine. At Deltalambda=30 nm, the signal of caffeine at 288 nm (peak to zero method) is not affected by acetylsalicylic acid. The range of application is between 0.021 and 41.62 microg ml(-1) (correlation coefficient, R=0.9995) for acetylsalicylic acid and between 0.4486 and 44.86 microg ml(-1) (correlation coefficient, R=0.99786) for caffeine. The recovery range of 98.40-102% for acetylsalicylic acid and 90-100.5% for caffeine from their synthetic mixture was reported. Overall recovery of both compounds about 97-99% for acetylsalicylic acid and 97-98% for caffeine was obtained from real sample analysis. The detection limits are 0.0013 microg ml(-1) and 0.0306 microg ml(-1) for acetylsalicylic acid and caffeine, respectively. The relative standard deviation (n=10) for 20 microg ml(-1) of acetylsalicylic acid is 2.75% and for 2.2 microg ml(-1)of caffeine is 1.7%.

Aspirin↗
PubMed1981

A study on constrictor response of dog coronary arteries to acetylsalicylic acid.

The present study was designed to investigate the effects of acetylsalicylic acid at a high dose on dog coronary arteries. In the isolated and perfused dog hearts, an intracoronary injection of acetylsalicylic acid (10 mg) decreased coronary blood flow concomitant with diminution of myocardial contractile force, but did not change heart rate. In the isolated dog coronary arterial strips, acetylsalicylic acid (10-4 M) produced the contractions of them, which were significantly inhibited by calcium-free solution, diltiazem, nifedipine, phospholipase A2, arachidonate and prostaglandin E1. The results indicate that acetylsalicylic acid at a high dose produces coronary arterial contracture probably through inhibition of intravascular synthesis of vasodilating prostaglandins.

Animals↗
PubMed1985

[The bioavailability of combination preparations of acetylsalicylic acid and codeine phosphate].

Plasma levels time curves of acetylsalicylic acid, salicylic acid, salicyluric acid and codeine were monitored after intravenous, oral and rectal application (single dose) of preparations containing acetylsalicylic acid and codeine. The mean absolute bioavailability of acetylsalicylic acid was 68% after oral application and 60% after rectal application. The corresponding bioavailability data of codeine were 59% and 63%, respectively.

Administration, Oral↗
PubMed1975

[Hemostasis suppression by a combination of heparin and acetylsalicylic acid].

The effect of a combined application of acetylsalicylic acid and heparin on haemostasis is examined on 7 healthy test persons. Apart from the change of the plasmatic coagulation and the platelet function by the pharmaca a prolongation of the bleeding time which is larger than the values of the individual application can be established. In the in-vitro-experiment could be proved that the prolonged bleeding time is based on the prevented by acetylsalicylic acid release of the heparin neutralising factor 4 from the platelets. An improvement of the therapeutic effect of heparin when at the same time acetylsalicylic acid is given is discussed.

Aspirin↗
PubMed1994

Two distinct mechanisms of inhibition of platelets aggregation by acetylsalicylic acid.

The von Willebrand Factor-Ristocetin adduct activates Platelets aggregation and secretion. Acetylsalicylic acid inhibits Platelets activation by two distinct mechanisms indicating that the adduct activates Platelets by triggering at least two distinct intraplatelet metabolic pathways. The first starts from the activation of Phospholipase A-2 that produces Arachidonic acid, which, in turn, undergoes the metabolic pathway leading to Thromboxane A-2; this pathway can be blocked by the intraplatelet Acetylsalicylic acid by irreversible inactivation of Cyclooxygenase but it is insensitive to the extra-platelet Acetylsalicylic acid. The second pathway is triggered by intact von Willebrand Factor, but not by the Acetylsalicylic acid-treated one; it is insensitive to intraplatelet Acetylsalicylic acid and therefore unrelated to the Arachidonic acid metabolism.

Arachidonic Acid↗
PubMed1997

[Acetylsalicylic acid after myocardial infarct].

There is no doubt about the positive influence of acetylsalicylic acid on vascular disease. The antithrombotic therapy with acetylsalicylic acid is a fundamental of secondary prevention of vascular events, especially in nonfatal myocardial infarction, instable angina pectoris, stroke and in patients with amaurosis fugax. Clinical studies done since 1990 about the effect of a low-dose therapy confirmed the experimental results, which showed that 25-50 mg acetylsalicylic acid per day are enough, to suppress platelet function as far as necessary, without influencing the protective function of prostacyclin synthesis. Side-effects can be reduced to a minimum with a reduced dosage. The wide-spread use of a low-dose acetylsalicylic acid therapy in primary prevention especially in patients at high risk has to be reevaluated in further studies.

Aspirin↗