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PubMed2001

Analysis of trials evaluating combinations of acetylsalicylic acid and dipyridamole in the secondary prevention of stroke.

BACKGROUND: Stroke is one of the leading causes of morbidity and mortality in the United States. Patients who suffer a cerebrovascular event are at high risk of a recurrence, and secondary prevention is crucial to reducing the burden of cerebrovascular disease. Acetylsalicylic acid (ASA, aspirin) is an established method of stroke prophylaxis. OBJECTIVE: This review investigates whether the addition of dipyridamole to ASA further reduces the risk of stroke recurrence. METHODS: To identify clinical trials of the use of combinations of ASA and dipyridamole in the prevention of recurrent stroke in patients who have suffered a first stroke or transient ischemic attack, the English-language literature was searched from 1966 through May 2001 using the MEDLINE, International Pharmaceutical Abstracts, EMBASE, and BIOSIS databases. The search terms used were dipyridamole, aspirin, acetylsalicylic acid, ischemic stroke, and cerebrovascular disorders. CONCLUSIONS: Of the 5 published studies, 3 earlier studies detected no differences in outcome when dipyridamole was added to ASA therapy for stroke prophylaxis. Two more recent trials found that the addition of dipyridamole to ASA therapy provided further reduction in the risk of secondary cerebrovascular events compared with placebo and with ASA alone. Further studies are needed to confirm long-term benefit.

Aged↗
PubMed1994

Use of desmopressin acetate to reduce blood transfusion requirements during cardiac surgery in patients with acetylsalicylic-acid-induced platelet dysfunction.

OBJECTIVE: To determine whether desmopressin acetate (DDAVP) has the ability to reduce blood loss in patients with a known bleeding tendency. DESIGN: A randomized, double-blind, placebo controlled study. SETTING: A university teaching hospital. PATIENTS: Men under the age of 70 years who had taken acetylsalicylic acid within 7 days of scheduled coronary artery bypass surgery. Patients with an abnormal hematologic profile or a history of bleeding or who were receiving heparin or undergoing repeat coronary bypass surgery were excluded. Forty-four patients were randomized with restriction in blocks of 10; 20 received DDAVP and 24 received a placebo. MAIN OUTCOME MEASURES: Blood loss and blood transfusion requirements. RESULTS: Patients treated with DDAVP lost significantly (p < 0.01) less blood than those receiving a placebo (1543 mL versus 2376 mL respectively). Nineteen patients had a blood loss of more than 2000 mL; 15 of these were in the placebo group. Significantly (p < 0.02) fewer patients receiving DDAVP required blood transfusion (9 versus 18). CONCLUSIONS: DDAVP reduces blood loss during cardiac bypass surgery in patients who have taken acetylsalicylic acid within 7 days before operation.

Aspirin↗
PubMed2004

Dose-dependent immunomodulatory effects of acetylsalicylic acid and indomethacin in human whole blood: potential role of cyclooxygenase-2 inhibition.

The aim of the study was to characterize the in vitro effect of non-steroidal anti-inflammatory drugs (NSAIDs) on the production of pro-inflammatory cytokines in a human whole blood assay. Whole blood samples were pre-incubated with acetylsalicylic acid, indomethacin, selective cyclooxygenase (COX)-1 inhibitor (SC-560), COX-2 inhibitor (NS-398) or prostaglandin E2 (PGE2) before stimulation with lipopolysaccharide (LPS). Pro-inflammatory and anti-inflammatory cytokines were determined directly at the cell level with the help of flow cytometry and/or in the plasma supernatant with the help of ELISA. High doses of acetylsalicylic acid were needed to inhibit pro-inflammatory cytokine production. In contrast, low-to-moderate doses induced a modestly enhanced production of pro-inflammatory cytokines. Moreover, indomethacin was demonstrated to increase the expression of interleukin-6 (IL-6) and tumour necrosis factor-alpha (TNF-alpha) in a dose-dependent fashion. Upon addition of PGE2, however, LPS-induced IL-6 and TNF-alpha production was suppressed regardless of indomethacin presence. Interestingly, selective COX-2 inhibition (NS-398), but not selective COX-1 inhibition (SC-560), exerted a stimulatory effect on the expression of pro-inflammatory cytokines. These data emphasize that the immunomodulating effects of NSAIDs in whole blood are dose-dependent. Furthermore, the induction of pro-inflammatory cytokine expression by NSAIDs is potentially mediated by COX-2 inhibition. Although NSAIDs are successfully used in clinical practice for their net anti-inflammatory properties, our observations may contribute to the understanding of side effects induced by NSAIDs and selective COX-2 inhibitors.

Adjuvants, Immunologic↗
PubMed2002

Anthropometric data and acetylsalicylic acid pharmacokinetics.

The relationship between anthropometric data and pharmacokinetic characteristics of acetylsalicylic acid (ASA) after administration of a single oral dose of 500 mg ASA, an oral and intravenous dose of 500 mg D,L-lysine-mono-acetylsalicylate (Lys-ASA) and an oral dose of 1,000 mg Lys-ASA were evaluated. Individual data from an open, randomized crossover trial in 13 healthy volunteers (age 18-50 years, 6 female, 7 male, height 158-189 cm, weight 45-118 kg) were re-analyzed using a non-compartmental approach. The influence of body weight, height, body surface area and age on pharmacokinetic characteristics (Cmax, Tmax, AUClast, MRTlast, t 1/2, Cl, Vd) was assessed using the multiple regression method and pairwise multiple correlations were calculated. Multiple regression analysis showed significant multiple correlation coefficients of approximately 0.86 for Cmax (500 mg Lys-ASA i.v., 1,000 mg Lys-ASA per os and 500 mg ASA per os), Cl and AUClast (1,000 mg Lys-ASA per os). Standardized regression values (beta) reflected a major contribution for height, weight and body surface area, but age was not a relevant factor. Pairwise comparisons confirmed negative correlations between anthropometric characteristics and Cmax, AUClast and MRTlast and positive correlations between anthropometric data, Cl and Vd. In conclusion, apart from Tmax and t 1/2, all pharmacokinetic characteristics were influenced by body weight, height and body surface area. Whereas repeated administration of high doses in patients with low body weights may give rise to toxic effects, acute single dose administration would not lead to significant under-dosing in tall or stout patients.

Adult↗
PubMed1984

Drug interaction in middle molecule analysis, with special reference to acetylsalicylic acid.

Concerning the middle molecules in uremia and other diseases, the potential artifact that can impede an accurate quantitation of middle molecules and that is related to the absorption of a very commonly used drug, namely aspirin, is discussed. Peak 7c and peak b 4-2 are two different middle molecules separated by gel permeation chromatography followed by anion-exchange chromatography. Oral ingestion of acetylsalicylic acid modifies the chromatographic pattern of the middle molecule fraction in normal subjects and uremic patients. Peak 7c is increased in the urine of healthy subjects, whereas this is not the case for peak b 4-2: With the b 4-2 technique, ingestion of acetylsalicylic acid produces a higher peak b 5. This is consistent with the previous demonstration that peak 7c was eluted as peak b 5. Structural analogies between salicylate metabolites and orthohydroxyhippuric acid beta-glucuronate (i.e., the main component of peak 7c) could explain this drug-related artifact.

Aspirin↗
PubMed1975

Management of thrombo-embolism after aortic valve replacement with the Björk-Shiley tilting disc valve. Medicamental prevention with dicumarol in comparison with dipyridamole - acetylsalicylic acid. Surgical treatment of prosthetic thrombosis.

Dicumarol anticoagulation poved very effective in the prevention of thromboembolic complications after aortic valve replacement with the Björk-Shiley tilting disc valve. We have, however, encountered six late deaths because of massive cerebral hemorrhage, which represent 3% of the patients who were maintained on dicumarol medication at that time. This unacceptable mortality prompted us to introduce two programmes, one without anticoagulation and another one with dipyridamole-acetylsalicylic acid. Furthermore, dicumarol was terminated in patients with haemorrhagic episodes, instable anticoagulation, pregnancy, and in those reguiring surgery. The results were disappointing, however, and the majority of the patients involved were therefore put on dicumarol medication. Eleven of the 64 consecutive patients taking dipyridamole - acetylsalicylic acid had thrombo-embolic episodes during a mean follow-up period of 9 months...

Adult↗
PubMed1977

Effects of morphine and acetylsalicylic acid on kinin forming enzyme in rat paw.

Coaxial perfusion was carried out in the rat paw; pinching the instep of the foot and electrical stimulation of the sciatic nerve caused an increase in the release of a bradykinin-like substance and kinin forming enzyme into the perfusate. Release of the latter was noted with pinching even independently of the release of the bradykinin-like substance. Acetylsalicylic acid (200 mg/kg i.p.) inhibited the release of kinin forming enzyme due to pinching or to sciatic nerve stimulation, while morphine (5 mg/kg i.m.) inhibited only the release of the enzyme due to sciatic nerve stimulation. Our results suggest that production of localized pain may be largely due to the activity of the released kinin forming enzyme and the bradykinin-like substance. In addition, the mechanism of inhibition by morphine on release of kinin forming enzyme appears to differ from that of acetylsalicylic acid.

Animals↗
PubMed1993

Cyclooxygenase inhibitors acetylsalicylic acid and indomethacin do not affect capsaicin-induced neurogenic inflammation in human skin.

Neurogenic inflammation is evoked by neuropeptides released from primary afferent terminals and, presumably, by other secondarily released inflammatory mediators. This study examines whether prostaglandins might participate in the development of neurogenic inflammation in humans and whether cyclooxygenase inhibitors have any anti-inflammatory effect on this type of inflammation. In healthy volunteers, neurogenic inflammation was elicited by epicutaneously applied capsaicin (1%), after systemic pretreatment with acetylsalicylic acid, or topically applied indomethacin compared to pretreatment with saline or vehicle, respectively. The extent of neurogenic inflammation was quantified by planimetry of visible flare size and recording the increase of superficial cutaneous blood flow (SCBF) with a laser Doppler flowmeter. Capsaicin-induced flare sizes and outside SCBF (both representing neurogenically evoked inflammation) were unaffected by acetylsalicylic acid or indomethacin. Only the capsaicin-induced increase of inside SCBF was attenuated by local pretreatment with indomethacin, reflecting the participation of prostaglandins in the inflammatory response of those areas which were in direct contact with capsaicin.

Adult↗
PubMed1984

Effects of the anti-inflammatory agents indomethacin, metiamide and acetylsalicylic acid on the induction of hyperplasia in hamster cheek-pouch epithelium and ear epidermis.

Previous studies have shown that agents such as indomethacin and hydrocortisone act to reduce the level of epidermal hyperplasia produced by various chemical, but little information is available about the effects of such anti-inflammatory agents on the induction of hyperplasia in oral mucosa. Hamster cheek-pouch epithelium and ear epidermis were treated with indomethacin, metiamide and acetylsalicylic acid prior to treatment with turpentine, podophyllin or TPA. The levels of hyperplasia induced were monitored by rates of epithelial glycolysis, protein synthesis and mitosis. The response of the metabolic assays to epinephrine was also examined. Alone, turpentine, podophyllin and TPA each caused a 3-5 fold increase in the metabolic assays and loss of the normal tissue response to epinephrine. Tissues pretreated with indomethacin showed significant reductions in the levels of hyperplasia produced and they retained a normal response to epinephrine. No reduction in hyperplasia was observed following pretreatment with acetylsalicylic acid, an alternative inhibitor or prostaglandin synthesis or with metiamide, a histamine blocker. The results indicate that the production of epithelial hyperplasia by turpentine, podophyllin and TPA can be inhibited by indomethacin.

Animals↗
PubMed1979

Effects of acetylsalicylic acid, sulfinpyrazone and dipyridamole on platelet adhesion and aggregation in flowing native and anticoagulated blood.

The interaction of rabbit platelets with subendothelium of rabbit aorta was investigated under controlled blood flow conditions. Platelet adhesion and thrombus formation were compared after perfusion of native blood and of blood anticoagulated with citrate, heparin or heparin plus citrate. 15 mM citrate in plasma caused significant reduction of aggregation, thrombus volume and thrombus height; adhesion was concomitantly increased. Heparin (500 U/kg) had no significant effect on adhesion and thrombus dimensions. Treatment of rabbits with acetylsalicylic acid or sulfinpyrazone caused a significant reduction of thrombus volume and thrombus height in the presence of citrate. However, no significant effects were observed in native or heparinized blood. It is concluded that low citrate concentrations: (1) inhibit thrombus growth; (2) enhance thrombus breakdown; (3) therefore increase adhesion, and (4) strongly enhance a possible inhibitory effect of acetylsalicylic acid and sulfinpyrazone on thrombus growth.

Animals↗
PubMed1985

Influence of intravenous acetylsalicylic acid and sodium salicylate on human renal function and lithium clearance.

The influence of intravenous acetylsalicylic acid (ASA; D,L-lysine-mono-acetylsalicylate), equimolar doses of sodium salicylate (SA) and placebo (P) on renal function has been studied in 6 healthy female volunteers, in 150 mmol sodium balance, and in lithium (Li) steady state with a plasma Li between 0.6 and 0.8 mmol/l. Following a bolus injection of 0.5 g ASA, 0.444 g SA or P (50 ml saline) given over 10 min and a subsequent continuous infusion of 1.5 g ASA, 1.332 SA or P (150 ml saline) over 170 min, urine was collected for 3 h as well as 6 plasma samples at 30-min intervals. Plasma ASA levels were between 13.8 and 22.1 micrograms/ml and for SA they were 20.8 to 82.6 microgram/ml during ASA infusion, and between 22.5 and 108.9 microgram/ml for SA during SA infusion. Neither ASA nor SA caused a significant change in urine volume, in the renal clearances of Na, K, free water, osmolality, creatinine, inulin and p-aminohippurate (PAH) or in plasma Li level. Renal Li clearance was slightly reduced by SA, from 37.8 to 29.4 ml/min (p less than 0.05). Since renal prostaglandin (PG) synthesis (urinary PGE2 excretion) was 60.6% suppressed by ASA and was not affected by SA, the decrease in Li clearance cannot be related to inhibition of cyclooxygenase in the kidney.

Adult↗
PubMed1984

Antiinflammatory properties of a hydroperoxide compound, structurally related to acetylsalicylic acid.

3-Hydroperoxy-3-methylphthalide (3-HMP), a structural analog of acetylsalicylic acid (ASA), was found to have some antiinflammatory properties which are distinct from those of ASA. 3-HMP inhibits human platelet aggregation and ATP release in response to low concentrations of collagen but is less effective than ASA. 3-HMP inhibits prostaglandin and thromboxane production from exogenous [14C]arachidonic acid by human platelet lysates in vitro and does so at lower concentrations than ASA (3-HMP IC50 = 10 microM; ASA IC50 = 50 microM). 3-HMP is also more effective than ASA as an inhibitor of prostacyclin-like activity production by rings of rabbit aorta. Human polymorphonuclear (PMN) leukocyte [14C]arachidonic acid metabolism is inhibited by 3-HMP but not ASA. In urethane-anesthetized rats, 3-HMP (10 mg/kg intravenously) is effective in inhibiting PMN leukocyte accumulation in response to intrapleural carrageenan administration whereas ASA is ineffective (100 mg/kg intravenously). This hydroperoxy analog of ASA has antiinflammatory activity which may result from a combination of the ASA-like and hydroperoxide-related pharmacological properties.

Animals↗
PubMed2004

Comparison of fluorimetric, voltammetric and biosensor methods for the determination of total antioxidant capacity of drug products containing acetylsalicylic acid.

Antioxidant capacity of several drug specialities containing as mean component acetylsalicylic acid were experimentally evaluated using an enzymatic electrode, recently developed by the present authors, based on superoxide dismutase (SOD) enzyme. The precision of this method of analysis was found to be good (for drug samples RSD < or = 5%). The results were also compared with those ones by a traditional spectrofluorimetric method and by two other methods, respectively, based on cyclic and pulsed voltammetry, recently trialled by the present authors.

Antioxidants↗
PubMed2006

Acetylsalicylic acid exhibits anticlastogenic effects on cultured human lymphocytes exposed to doxorubicin.

Acetylsalicylic acid (ASA) is a non-steroidal anti-inflammatory drug (NSAID) with many pharmacological properties, such as anti-inflammatory, antipyretic and analgesic. Many studies have suggested the possible efficiency of ASA and other NSAIDs in preventing cancer. ASA could also have antimutagenic and antioxidant properties. The aim of this study was to investigate the possible clastogenic and anticlastogenic effects of different concentrations of ASA on doxorubicin-induced chromosomal aberrations in human lymphocytes. Human blood samples were obtained from six healthy, non-smoking volunteers; and the chromosomal aberration assay was carried out using conventional techniques. The parameters analyzed were mitotic index, total number of chromosomal aberrations and percentage of aberrant metaphases. The concentrations of ASA (25, 50 or 100 microg/mL) tested in combination with DXR (0.2 microg/mL) were established on the basis of the results of the mitotic index. The treatment with ASA alone was neither cytotoxic nor clastogenic (p>0.01). In lymphocyte cultures treated with different combinations of ASA and DXR, a significant decrease in the total number of chromosome aberrations was observed compared with DXR alone (p<0.01). This protective effect of ASA on DXR-induced chromosomal damage was obtained for all combinations, and it was most evident when ASA was at 25.0 microg/mL. In our experiments, ASA may have acted as an antioxidant and inhibited the chromosomal damage induced by the free radicals generated by DXR. The identification of compounds that could counteract the free radicals produced by doxorubicin could be of possible benefits against the potential harmful effects of anthracyclines. The results of this study show that there is a relevant need for more investigations in order to elucidate the mechanisms underlying the anticlastogenic effect of ASA.

Antimutagenic Agents↗
PubMed1988

Relief of pain and trismus in patients treated with naproxen or acetylsalicylic acid after tonsillectomy.

The pain-relieving efficacy of naproxen and acetylsalicylic acid (ASA) in tonsillectomized patients was compared in a double blind parallel clinical trial comprising 83 patients, among whom 42 were treated with naproxen and 41 with ASA. The patients were treated post-operatively for two days with either naproxen suppositories 500 mg. twice, or ASA effervescent tablets 1000 mg. three times, daily. The therapeutic gain was evaluated by recording the intensity of pain, reduced ability to open the mouth (trismus), consumption of supplementary analgesic (parcetamol), and pain-related sleep disturbances. The statistical analysis of the results revealed no differences in pain intensity, consumption of additional analgesics or pain-related sleep disturbances in the two treatment groups. A considerable degree of trismus was demonstrated in most of the tonsillectomized patients. This reduced ability to open the mouth was gradually overcome in the naproxen group while it remained unchanged in the ASA group, however, no statistical significant difference could be demonstrated. Additionally, no significant positive correlation between pain intensity and trismus was proven. The pain-relieving effect, however, was unsatisfactory in both the naproxen and the ASA group, and clinical controlled trial studies of alternative analgetics in tonsillectomized patients are still to be encouraged.

Adolescent↗
PubMed1995

Desmopressin effect on acetylsalicylic acid impaired platelet function.

The mechanism of DDAVP's shortening of acetylsalicylic acid (ASA) prolonged bleeding times was investigated. Sixteen healthy subjects received two dosages of ASA (100 mg) in 12 hours. Twenty four hours after the first ASA application and again after 32 hours DDAVP was administered intravenously (0.4 micrograms/kg). The trial was terminated after 48 hrs. In between, blood samples were drawn and analyzed for the in vivo bleeding time (Simplate time), in vitro bleeding test (IVBT, Thrombostat 4000), von Willebrand factor antigen (vWf:Ag), Ristocetin cofactor activity (vWf R:Co), plasma beta-thromboglobulin (beta-TG), platelet ATP/ADP, platelet aggregation (collagen, ADP, arachidonic acid), and plasma and platelet thromboxane levels. Simplate time (BT) and IVBT showed an excellent inverse correlation with vWf R:Co (r2 BT = 0.97 and r2 IVBT = 0.99, respectively) during the time when DDAVP was administered, suggesting the involvement of plasma vWF in DDAVP's shortening of the bleeding time. The involvement of plasma thromboxane in this mechanism could be excluded. In addition, DDAVP hampered platelet aggregation tests, possibly due to the inhibition of the release reaction (reduced beta-TG in plasma) by a direct interaction with platelets.

Adult↗
PubMed1976

Inhibition of platelet aggregation by acetylsalicylic acid and other inhibitors.

Effects on platelet aggregation were examined of acetylsalicylic acid (ASA), indomethacin and a number of other agents including dipyridamole, phenylbutazone and sulfinpyrazone under standardized conditions. The Born turbidometric method of measuring platelet aggregation was used with collagen as the stimulus for aggregation. ASA and indomethacin were shown to be among the most potent inhibitors of aggregation, being active at minimal effective concentrations of 1-3 mug/ml using a 10 min time of pre-incubation with the platelet-rich plasma (degree of aggregation inhibition was time dependent). Most of the other agents tested were also active in vitro and both prostaglandin E1 and adenosine were more potent than ASA or indomethacin. However, these agents were shown not to exert significant inhibitory effects when administered orally to rats (dose 10 and 30 mg/kg). ASA proved to be effective in doses as low as 3 mg/kg, and indomethacin in doses as low as 1 mg/kg orally. The inhibitory effects of ASA on aggregation remained for several days after a single oral dose, whereas the effects of indomethacin disappeared within 24 h.

Administration, Oral↗