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PubMed1993

Intrathecal injection of lysine acetylsalicylic acid in the rat: a neurotoxicological study.

Lysine acetylsalicylic acid has been reported to induce analgesic effects in humans after intrathecal (i.t.) injection. Before conducting further studies in humans with this drug, it is important to evaluate potential toxicological effects on the spinal cord in animals. In the present study the effects of chronic intrathecal administration of provocative doses of lysine acetylsalicylic acid (L-ASA) on the rat spinal cord were evaluated using light and electron microscopy and a quantitative morphometric method. We also investigated the effects of single doses of the drug on the spinal cord blood flow (SCBF) using the laser-Doppler flowmetry technique. No histopathological changes or differences in number or density of neuronal cells could be seen after chronic administration of L-ASA as compared to controls. The SCBF decreased immediately after i.t. injection of a large dose (4 mg) of L-ASA and returned to predrug levels within 10 min. At the end of the experiment metabolic acidosis was detected, indicating a systemic effect of acetylsalicylic acid. It is concluded that no neurotoxic effects on the spinal cord were seen after chronic i.t. injection of L-ASA. From a neurotoxicological point of view, our findings do not contraindicate the spinal use of L-ASA in humans.

Analgesics↗
PubMed1983

The influence of dose, time of administration, body temperature and salicylate kinetics on the antithrombotic action of acetylsalicylic acid in male rats.

Acetylsalicylic acid (ASA), given i.v. to male rats 10 min before electrical injury to the carotid artery, was found to reduce rate and extent of thrombosis at 3.3 and 10.0 mg/kg but not at 1.7, 20 or 100 mg/kg, indicating a narrow, low-dose window for antithrombotic effect. ASA was more effective in rats in which body temperature was allowed to fall greater than 0.5 degrees C but protection was lost if injury was delayed 15 min or more after ASA administration. Serum salicylate studies did not support the view that loss of protection was due to competition between salicylate and ASA for cyclooxygenase-binding sites. ASA was also protective at 200 mg/kg i.v., possibly through non-specific toxic effects.

Animals↗
PubMed1983

Effects of acetylsalicylic acid on platelet aggregation before and during increase in dietary eicosapentaenoic acid.

The effect of acetylsalicylic acid (ASA) on platelet aggregation before and during a fish diet, already known to decrease the aggregability of platelets and to prolong the bleeding time, was studied in 10 healthy men. Two doses (3.5 and 10 mg/kg body weight) of ASA were given. Both doses equally decreased platelet aggregation to collagen and adenosine diphosphate (ADP). ASA, taken before the diet, diminished platelet aggregability to ADP by as much as did the diet alone. When ASA was administered during the diet, the effect on platelet aggregability to ADP was additive. Aggregation to collagen also decreased to the same extent as during the baseline period. The results, in conjunction with our earlier ones, indicate that the mechanism by which a fish diet delays primary haemostasis is different from the apparently similar effect of ASA. This raises the possibility of augmenting any antithrombotic effect of ASA by dietary means.

Adenosine Diphosphate↗
PubMed1980

[On the platelet aggregation inhibiting and analgesic activities of acetylsalicylic acid (author's transl)].

Acetylsalicylic acid (ASA)--now the most potent platelet-aggregation inhibitor--is being investigated in combination with glycine (Godamed; text preparation A) and microencapsulated (test preparation B) in view of the plasma total salicylate level and platelet aggregation inhibiting effect. The examination is conducted on 20 patients by the cross-over method. An increase of the plasma total salicylate level of test preparation A compared with test preparation B is highly significant up to 60 min after application of 1000 mg ASA respectively. As in shorter time a higher plasma total salicylate level is reached a significantly higher analgesic effect of the test preparation A may be expected. In certain indications, occurring with pain, as for instance arterial occlusive disease, thrombophlebitis, etc., this is absolutely desired. Additional application of analgetics is then often unnecessary. A differentiated use of ASA preparations as platelet-aggregation inhibitors is therefore required. To investigate the disaggregating effect of both ASA preparations the PAT-III test by Breddin was used. 2 h after the oral application of 1000 mg ASA a complete normalisation by both ASA preparations was reached, whereas before a significant higher platelet aggregation had been recognized. The somewhat faster reached effect of test preparation A is not significant and clinically not relevant. When in the acute phase as well as in the long-term treatment of the above mentioned indications an ASA-containing platelet-aggregation inhibitor is used, that preparation should get preference which is well tolerable and has the same platelet-disaggregating effect but with the higher analgesic effect.

Analgesics↗
PubMed1998

[Secondary prevention following cerebral ischemia: is monotherapy with acetylsalicylic acid still first choice?].

Acetylsalicylic acid (ASA) alone (at least 30 mg per day) in post-cerebral ischaemia patients reduces the relative risk of further vascular events by 13% compared with placebo. A meta-analysis of all studies shows that the combination of ASA with dipyridamole reduces the relative risk by 16% (95% confidence interval: 5-26%) compared with ASA alone, but confirmation by a major trial appears desirable, because of discrepant results of a recent trial and 4 previous ones. Clopidogrel might reduce the risk by 7% compared with ASA alone, but this drug is expected to be expensive. Anticoagulation therapy with an international normalized ratio (INR) of 2.0-4.0 is particularly efficacious for secondary prevention in patients with atrial fibrillation, but anticoagulation therapy with an INR of 3.0-4.5 is not safe in secondary prevention of cerebral ischaemia of presumed arterial origin. Finally, not all atherosclerotic vascular diseases are identical from the therapeutic point of view; the effect of treatment depends in part on the clinical manifestation form.

Anticoagulants↗
PubMed1998

Prevention of NNK-induced lung tumorigenesis in A/J mice by acetylsalicylic acid and NS-398.

Acetylsalicylic acid (ASA) is known to prevent cancer development, but its mechanism of action remains unclear. In this study, we compared the efficacies of this nonspecific cyclooxygenase (COX) inhibitor with N-[2-(cyclohexyloxy)-4-nitrophenyl]-methanesulfonamide (NS-398), a specific COX-2 inhibitor. COX-2-specific inhibitors are less toxic than ASA. Lung tumorigenesis was induced in A/J mice by the administration of the tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) in the drinking water for 7 weeks (weeks 0 to +7). Groups of 25 A/J mice were fed ASA (588, 294, 147, or 73 mg/kg diet) before and throughout the assay (weeks -2 to +23). ASA at a dose of 588 mg/kg diet was the most effective because it reduced lung tumor multiplicity by 53%. The preventive effect of ASA increased with the dose, being of 32, 30, and 44% for 73, 147, and 294 mg/kg diet, respectively. NNK increased plasma prostaglandin E2 (PGE2) basal levels by 413%, whereas ASA attenuated this elevation in a dose-response manner (r2 = 0.99). Plasma PGE2 levels in ASA + NNK-treated mice correlate with the logarithm of the number of tumors (r2 = 0.99). NS-398 inhibited lung tumor multiplicity by 34% and returned plasma PGE2 to basal levels observed in untreated mice. Among the NNK-exposed mice, ASA and NS-398 treatment decreased the mean of the lung tumor volumes. Incubation of 82-132 and LM2 murine lung tumor cells with ASA or NS-398 decreased cell proliferation by 50% at concentrations higher than 100 microM. Incubations of NNK with COX-1 and -2 produced both activation and detoxification products by alpha-carbon hydroxylation and N-oxydation pathways, respectively. Bioactivation of NNK was more extensive by COX-2 than COX-1. Anti-COX-1 and -2, arachidonic acid, ASA, and NS-398 inhibited NNK bioactivation by COX-1 and -2 from 22-49%. Our data suggest that NNK is bioactivated by COX-2 in lung tissues and that COX-2-specific inhibitors might be promising chemopreventive agents.

Animals↗
PubMed1975

Interaction of indomethacin and acetylsalicylic acid as shown by the serum concentrations of indomethacin and salicylate.

A clinical-pharmacological study was performed to determine the effect of acetylsalicylic acid upon the serum concentration of indomethacin. 14 rheumatic patients were given indomethacin orally (25 mg X 4 for 4 days) and concurrently acetylsalicylic acid 3.7 g orally (0.9 g X 3 and 1.0 g X 1 daily), and 21 rheumatic patients were given indomethacin rectally in the morning (100 mg X 1) and concurrently acetylsalicylic acid 3.7 g orally (0.9 g X 3 and 1.0 g X 1 daily). On comparison with treatment with oral or rectal indomethacin alone, it was found that peak serum concentrations of indomethacin were significantly reduced (1% level), the times of the peaks were not shifted, and the areas beneath the serum concentration curves of indomethacin were smaller, but significantly so only if compared with rectal administration. In 12 rheumatic patients given indomethacin by rectum in the evening (100 mg X 1) and concurrently acetylsalicylic acid 3.7 g (0.9 g X 3 and 1.0 g X 1 daily), the serum level of indomethacin on the following morning (after 11 h) did not differ from that found after rectal treatment. A statistically but not biologically significant difference was observed between the mean serum half-lives of indomethacin given orally and rectally. For unknown reasons, concurrent doses of acetylsalicylic acid and indomethacin made the mean serum half-life of indomethacin longer than after its oral administration, but shorter than when the same dose of indomethacin was given rectally. There was no difference between serum levels of salicylate after oral administration of acetylsalicylic acid alone or after a concurrent oral or rectal dose of indomethacin. The results have been related to those reported previously, with respect to the interaction between indomethacin and acetylsalicylic acid, the serum levels of indomethacin after oral and rectal dosing, and the serum half-life of indomethacin based upon a one- or two-compartment model. The clinical relevance of the study is discussed.

Administration, Oral↗
PubMed1993

Intrathecal acetylsalicylic acid and indomethacin are not analgesic for a supramaximal stimulus.

Intrathecal acetylsalicylic acid and indomethacin are analgesic for painful stimuli, and this has been demonstrated when the noxious stimuli are applied to normal and inflamed tissue. This study determined whether these drugs would alter the response to a supramaximal stimulus, e.g., tail-clamp. Rabbits were anesthetized with halothane and after arterial and venous cannulation, an intrathecal catheter was placed via a lumbar laminectomy. The minimum alveolar anesthetic concentration was then determined. Groups 1 (n = 8) and 2 (n = 6) received 0.5 mg/kg acetylsalicylic acid intrathecally and Group 3 (n = 7) 0.5 mg/kg indomethacin intrathecally. Group 4 (n = 8) did not undergo a laminectomy and received acetylsalicylic acid 25 mg/kg intraperitoneally. In addition, in Groups 2-4, before the surgical procedures, carrageenin 1 mg was injected into the tail to evoke an inflammatory response. Approximately 20 min after injection of the study drugs, minimum alveolar anesthetic concentration was determined again. In Groups 1-4, control minimum alveolar anesthetic concentration was 1.2 +/- 0.2%, 1.4 +/- 0.3%, 1.2 +/- 0.2%, and 1.5 +/- 0.1%, respectively; there was no statistically significant change in any group after injection of the study drugs. There were no temperature, hematocrit, or arterial blood pressure differences between groups or after injection of the study drugs. In this model intrathecal acetylsalicylic acid and indomethacin do not provide analgesia for a supramaximal stimulus.

Animals↗
PubMed1986

Effects of salicylic and acetylsalicylic acid alone and in combination on platelet aggregation and prostanoid synthesis in man.

The present study was designed to investigate the effects of salicylate on the antiplatelet action of acetylsalicylic acid as well as on in vivo prostanoid formation and platelet function in healthy volunteers. In the first study six female volunteers received 350 mg acetylsalicylic acid intravenously, with and without previous oral administration of sodium salicylate (1200 mg daily for 3 days). Urinary prostanoid excretion as well as platelet aggregation and thromboxane formation were measured before and during salicylate and after acetylsalicylic acid. In the second study seven female volunteers received sodium salicylate (52.6 mg kg-1) or acetylsalicylic acid (60.7 mg kg-1) for 8 days in a randomized cross-over protocol. Urinary prostanoid excretion, platelet aggregation and thromboxane formation as well as salicylate plasma concentrations were determined before, during and after administration of each drug. Sodium salicylate did not impair the complete suppression of arachidonic acid-induced platelet thromboxane formation and aggregation obtained by the single intravenous dose of acetylsalicylic acid in the first study. Sodium salicylate in the second study did not affect urinary excretion of prostaglandin E2, its major urinary metabolite (7 alpha-hydroxy-5,11-diketo-tetranor-prostane-1,16-dioic acid), and 2,3-dinor-6-keto-prostaglandin F1 alpha, the main urinary metabolite of epoprostenol (prostacyclin, PGI2). In contrast, acetylsalicylic acid significantly decreased excretion rates of these prostanoids by 64, 59 and 61%, respectively. In both studies platelet aggregation and thromboxane formation induced by collagen, thrombin or arachidonic acid were not significantly affected by salicylate administration, whereas acetylsalicylic acid inhibited platelet aggregation induced by all three agents as well as thrombin- and arachidonic acid induced thromboxane formation.(ABSTRACT TRUNCATED AT 250 WORDS)

6-Ketoprostaglandin F1 alpha↗
PubMed1991

Heparin and low molecular weight heparin but not hirudin stimulate platelet aggregation in whole blood from acetylsalicylic acid treated healthy volunteers.

The platelet aggregatory effect of heparin was investigated with whole blood aggregometry in blood from healthy volunteers with collagen as activator. Tests were performed before and 3 hours after 0.5 g acetylsalicylic acid given perorally. Three protocols were tested. In the first experiment and before acetylsalicylic acid low doses (2.5 and 5 IU/ml) of heparin and low molecular weight heparin (LMW-heparin) did not affect aggregation while higher doses (25 and 250 IU/ml) had an antiaggregatory effect (p less than 0.0001). After acetylsalicylic acid, and with the same amount of collagen as before acetylsalicylic acid, aggregation decreased by 82 +/- 4%. Both heparin and LMW-heparin increased the aggregation (p less than 0.05). In the second experiment the collagen dose was titrated to give a similar light to moderate degree of aggregation before as compared to after acetylsalicylic acid. Low doses of heparin (p less than 0.01) but not hirudin increased the aggregation to the same degree before and after acetylsalicylic acid. In the third experiment the RGDS peptide (ARG-GLY-ASP-SER), a blocker of GPIIb/IIIa platelet receptor dose dependently inhibited platelet aggregation by 93 +/- 17%. With added RGDS peptide heparin still increased aggregation (p less than 0.001). In conclusion, with whole blood aggregometry both heparin and LMW-heparin but not the specific thrombin inhibitor hirudin stimulated platelet aggregation before and after acetylsalicylic acid ingestion. The heparin aggregatory effect was not inhibited by the RGDS peptide implying platelet activation via non specific mechanisms. These heparin effects could be of clinical importance for the treatment of arterial thromboembolic disease.

Adult↗
PubMed1991

Effects of acetylsalicylic acid on renal function in patients with chronic heart failure.

PURPOSE: We conducted a double-blind, placebo-controlled trial to determine whether the administration of acetylsalicylic acid has adverse effects on renal function in patients with moderate chronic congestive heart failure with and without stimulation of the renin system. PATIENTS AND METHODS: Forty patients were randomly assigned to one of the following four groups: Group 1, low sodium diet and placebo; Group 2, low sodium diet and acetylsalicylic acid; Group 3, normal sodium diet and placebo; or Group 4, normal sodium diet and acetylsalicylic acid. Patients were studied over 8 days. After Day 5, patients in Groups 2 and 4 received acetylsalicylic acid (500 mg three times a day). The low sodium diet consisted of 13.6 mmol of sodium per day and the normal sodium diet consisted of 136 mmol of sodium per day. RESULTS: The low sodium diet resulted in a highly significant increase in the plasma renin (2p = 0.0001), aldosterone (2p = 0.0006), and urinary prostaglandin E2 (2p = 0.01) concentrations and the renal potassium excretion (2p = 0.0009), whereas renal sodium excretion was significantly reduced (2p = 0.0001). Severe sodium depletion led to a reduction of the glomerular filtration rate (2p = 0.007), which was independent from cyclooxygenase inhibition. In patients on the low sodium diet, acetylsalicylic acid reduced the elevated urinary prostaglandin E2 levels to normal values without changing the renal sodium excretion rate. In patients with a normal sodium intake, acetylsalicylic acid significantly reduced the renal sodium excretion rate by 29% (2p = 0.04). CONCLUSION: We conclude that severe sodium depletion has adverse effects on kidney function in patients with heart failure due to a reduction in the glomerular filtration rate. Administration of acetylsalicylic acid in doses that reduce the synthesis of renal prostaglandin E2 significantly reduces renal sodium excretion.

Aspirin↗
PubMed1999

[A pharmaceutical of the century will be 100. A historical vignette on the introduction of acetylsalicylic acid to the market in 1899].

This article describes the historic roots of acetylsalicylic acid (ASA) from the first experiments at 1800 until the introduction into the pharmaceutical market in 1899. In 1869, Hermann Kolbe enlightened the chemical structure of salicylic acid, which was used at that time as an analgetic and antipyretic drug. Because of the side effects, for example the irritation of the stomach, analytical chemists and pharmacologists searched for chemical modifications. In August 1897 Felix Hoffmann (1868-1946) was successful in acetylizing the salicylic acid to acetylsalicylic acid (ASA). Between 1897 and 1899 Kurt Witthauer (1865-1911) collected clinical data and experiences on the efficiency of ASA as an analgetic and antipyretic drug. In 1899 ASA was introduced into the pharmaceutical market as Aspirin and became soon one of the most successful drugs of its time. The indication exceeds analgesia in the mean time and to prophylaxis of myocardial ischaemia or cerebral stroke, among others.

English Abstract↗
PubMedDate not supplied

[Effect of combined administration of acetylsalicylic acid and antioxidants on cellular and plasma hemostasis].

It was found that upsovit (acetylsalicylic acid, 330 mg; ascorbic acid, 200 mg), composition 1 (acetylsalicylic acid, 330 mg; ascorbic acid, 200 mg; hypoxen, 50 mg), and composition 2 (acetylsalicylic acid, 330 mg; ascorbic acid, 200 mg; hypoxen, 100 mg) inhibit thrombocyte aggregation in vitro. Hypoxen per se induces the aggregation of thrombocytes, but inhibited the ADP aggregation. Intravenous injections of upsovit in rabbits did not influence the ADP aggregation, but inhibited the collagen aggregation, while composition 2 inhibited the aggregation processes of both types. Besides, the intravenous injections of upsovit decreased the thromboplastin time and the activated partial thromboplastin time (APTT) and reduced the protein C activity, while influencing neither the heparin cofactor activity of antithrombin III nor the level of fibrinogen and its degradation products. In contrast, composition II did not change the thromboplastin time, APTT, and the protein C activity, but increased the heparin cofactor activity.

Animals↗
PubMed1990

Effects of acetylsalicylic acid and paracetamol alone and in combination on prostanoid synthesis in man.

1. The present study was designed to investigate the effects of acetylsalicylic acid and paracetamol given separately and in combination on total body and renal PGE2 synthesis in healthy volunteers. 2. In a randomized four-way cross-over study eleven female volunteers received for two consecutive days 3 g day-1 acetylsalicylic acid or 3 g day-1 paracetamol or a combination of 1.5 g day-1 acetylsalicylic acid and 1.5 g day-1 paracetamol, or 1.5 g day-1 acetylsalicylic acid separated by washout phases of at least 5 days. Urinary excretion of the major urinary metabolite of PGE2 (PGE-MUM), PGE2 and creatinine clearance were measured before and on day 2 of each treatment period. Compliance was tested by measuring metabolites of the two drugs in urine. 3. Paracetamol did not reduce urinary excretion of PGE2 whereas both dosages of acetylsalicylic acid caused a significant reduction. 4. The combination of both drugs did not reduce PGE2 excretion more than acetylsalicylic acid alone. 5. All four drug schedules reduced urinary excretion of PGE-MUM significantly.

Acetaminophen↗
PubMed1980

Mild analgesics as an alternative to ergotamine in migraine. A comparative trial with acetylsalicylic acid, ergotamine tartrate, and a dextropropoxyphene compound.

The effect of ergotamine tartrate was compared with that of acetylsalicylic acid and a dextropropoxyphene compound (Doleron novum) on 525 acute migraine attacks in a double-blind crossover study of 25 adult female patients. Ergotamine tartrate and the dextropropoxyphene compound were equally effective and significantly superior to acetylsalicylic acid in preventing the attacks entirely. If the attacks were only partially prevented, the dextropropoxyphene compound was significantly superior to acetylsalicylic acid in making the attacks shorter and milder, while ergotamine tartrate did not differ significantly from acetylsalicylic acid or the dextropropoxyphene compound. The incidence of nausea and vomiting was lowest during treatment with the dextropropoxyphene compound. In the patients' overall preference, the dextropropoxyphene compound and ergotamine tartrate were significantly superior to acetyl-salicylic acid. In acute migraine the combination of dextropropoxyphene, a centrally acting analgesic, with acetylsalicylic acid and phenazone gives an alternative to ergotamine tartrate that is equally effective and causes less nausea and vomiting.

Adult↗
PubMed2002

Zolmitriptan versus a combination of acetylsalicylic acid and metoclopramide in the acute oral treatment of migraine: a double-blind, randomised, three-attack study.

This multicentre, randomised, double-blind study compared oral zolmitriptan 2.5 mg with a combination of oral acetylsalicylic acid 900 mg and metoclopramide 10 mg as acute anti-migraine therapy for 3 migraine attacks. In total, 666 patients took at least one dose of study medication (326 took zolmitriptan and 340 took acetylsalicylic acid plus metoclopramide). The percentage of patients with a 2-hour headache response after the first dose for all 3 attacks (the primary end point) was 33.4% with zolmitriptan and 32.9% with acetylsalicylic acid plus metoclopramide [odds ratio 1.06, 95% confidence interval (CI) 0.77-1.47; p = 0.7228]. For the majority of secondary end points, the two treatments demonstrated comparable efficacy. However, post hoc analysis showed that significantly more patients receiving zolmitriptan were free of pain 2 h after the first dose in all 3 attacks compared with patients receiving acetylsalicylic acid plus metoclopramide (10.7 vs. 5.3%; odds ratio 2.19, 95% CI 1.23-4.03; p = 0.0095). In addition, post hoc analysis showed that the overall 2-hour pain-free response rate was consistently higher with zolmitriptan (34.6%) than with acetylsalicylic acid plus metoclopramide (27.9%) (odds ratio 1.40, 95% CI 1.09-1.78; p = 0.007). Both treatments reduced migraine-associated nausea, vomiting, phonophobia and photophobia. There were no important inter-group differences with respect to the onset of meaningful migraine relief, the frequency of headache recurrence, the usage or efficacy of a second dose of medication or the use of escape medication. However, at the last attack, the proportion of patients who expressed overall satisfaction with the treatment was significantly higher in the zolmitriptan group, i.e. 83.7%, versus 75.0% with acetylsalicylic acid plus metoclopramide (p = 0.0346). Both agents were well tolerated. Adverse events were reported by 40.8% (133/326) of zolmitriptan-treated patients and 29.1% (99/340) of those treated with acetylsalicylic acid plus metoclopramide. The incidence of withdrawals due to adverse events was very low with both zolmitriptan (0.9%) and the combination regimen (1.5%); the latter percentage included 1 patient who withdrew from the study due to phlebitis, which was classified as a serious adverse event. This study showed that zolmitriptan is effective and well tolerated for the acute treatment of moderate to severe migraine. Zolmitriptan was at least as effective as acetylsalicylic acid plus metoclopramide in achieving a 2-hour headache response, but significantly more effective than the combination therapy for other end points, including the 2-hour pain-free response.

Acute Disease↗
PubMed1989

[Absolute bioavailability of a special sustained-release acetylsalicylic acid formulation].

Absolute Bioavailability of a Special Acetylsalicylic Acid Sustained Release Formulation. The absolute bioavailability of an acetylsalicylic acid (ASA) sustained release formulation (Contrheuma retard), containing 300 mg ASA as initial dose and 350 mg in a retard formulation, was determined in comparison to a standard ASA solution for intravenous administration in a two-treatment, two-period cross-over trial with 6 healthy male volunteers by comparing the areas under the plasma-fluctuation-time curves of the primary metabolite. In addition, it was examined by comparison of the mean times after administration of both formulations, whether the test formulation meets the requirements of a sustained release formulation. The investigations led to the following results: The absolute bioavailability of the test formulation was 95%. The statistical comparison of the areas under the concentration-time courses allowed no decision (neither for equivalence nor difference). The maximal concentration of SA after intravenous administration of the standard formulation was reached after 0.4 h on an average and amounted to 62 micrograms/ml. After oral administration of the test formulation, a mean concentration maximum of 28 micrograms/ml was calculated, which had been reached after about 2 h. The differences are statistically significant. The mean time for SA was 6 h after the standard formulation, whereas after administration of the test compound, a mean of 11.5 h was calculated. 24 h following administration, the concentration of SA was 1.3 micrograms/ml after intravenous administration of the standard formulation and 5.5 micrograms/ml after administration of the test formulation. These differences, too, are statistically significant. From the comparison of the mean time for SA, a retard factor of 1.9 was calculated.

Adult↗
PubMed1997

[Changes in thyroid function in rats after administration of methylene blue and interactions with estrogens and acetylsalicylic acid].

We have studied the thyroxine and triiodothyronine concentrations in male rats--the control, groups treated separately with estradiol benzoate, acetylsalicylic acid and methylene blue and with combinations of these substances. We have found out that the treatment with acetylsalicylic acid significantly lowers the thyroxine and triiodothyronine serum concentrations. The estradiol benzoate as well as methylene blue inhibited the drop in the serum thyroxine level when administered simultaneously with acetylsalicylic acid. The serum triiodothyronine decrease after acetylsalicylic acid treatment was inhibited by methylene blue and estradiol benzoate only in one of our two experiments. The simultaneous treatment with estradiol benzoate, acetylsalicylic acid and methylene blue did not change the triiodothyronine concentration comparing to control group and decreased the thyroxine serum concentration.

Animals↗