Proceedings: Arterial thromboembolism and prosthetic heart valves. Effects of acetylsalicylic acid.
Explore the source record for details and available documents.
SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Aggrenox, launched in Belgium by Boehringer Ingelheim, is a fixed-dose combination of extended-release dipyridamole (200 mg) and aspirin (25 mg), two antiplatelet agents with different and complementary mechanisms of action. It is recommended, twice daily, in the protection against secondary stroke and transient ischaemic attacks. The placebo-controlled European study ESPS 2 (European Stroke Prevention Study 2) demonstrated that the administration of this combination was twice as effective as either agent alone in the secondary prevention of stroke in patients with prior stroke or transient ischaemic attack.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
After a century of therapeutic use of acetyl salicylic acid (ASA), the different mechanisms involved leading to the therapeutic activity and to the various clinical reactions (even life threatening) observed in patients sensitive to ASA or in general to the non steroidal anti-inflammatory drugs (NSAID's) are still to be discovered or confirmed. During the last century a lot of scientific results have been published in favour of a wide panel of mechanism including an humoral (IgE and/or IgG) or a cellular (lymphocytes) immune reaction, inhibition of the cyclooxygenases, a cellular activation (mast cells, basophils, eosinophils and platelets), a competition at the serum albumin level and an activation of the complement cascade. In general the same actors than in the anaphylactic reaction are found (mediators, cellular activation and amplification systems). It is clear today that these reactions for which an accurate diagnosis is mandatory cannot be explained by a single mechanism, which is the case of a lot of other allergens.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Caffeine is suspected to initiate the abuse of caffeine-containing analgesics. To clarify this matter the study investigated the effects of aspirin alone and in combination with caffeine on mood and cardiovascular parameters before, during, and after pain induction through mechanical stimulation. 96 healthy middle-aged women--all habitual coffee drinkers--were randomly designed to receive 0 or 500 mg aspirin together with 0, 50, or 100 mg caffeine administered in a double-blind design. Aspirin did not change ratings of mood scales. Caffeine decreased scores on negative mood scales, especially on the anxiety/sadness scale. The combination of aspirin and caffeine failed to increase any score on scales measuring positive moods. Only a few interactions are noticed. The results do not support the suggestion that caffeine increases the potential for abuse of aspirin.
Explore the source record for details and available documents.
Into the Heidenhain pouches of 3 dogs 30 ml of 0.1N HCl was instilled and removed at 30-minute intervals for 6 hours. During the 3rd and 4th periods the acid instillate contained 4.5 mg/ml or 12.4 mM of ASA, indomethacin or fenoprofen. All 3 agents affected the functional integrity of the mucosal barrier, but the characteristics of their actions were different. The H+ concentration was decreased by ASA and fenoprofen and increased by indomethacin when the instillate contained drug. All 3 drugs increased the net flux of Na+, K+, Ca++ and Mg++. Following initial augmentation of instillate volume and H+ concentration, indomethacin caused sustained back diffusion of acid from lumen to mucosa; this was accompanied by mucosal bleeding. Peak effects of ASA on the net flux of ions occurred during or immediately after drug infusion and were greater than those of indomethacin and fenoprofen. Fenoprofen at 12.5 nM had no effect on concentrations of Ca++ and Mg++ while both were significantly increased by equal molar dose of ASA or indomethacin. In onset of action indomethacin was slow but once disruption of functional integrity started, it continued for hours showing no signs of returning to normal condition. In this sense, the total disruptive action of an equal weight or molar dose of indomethacin was greater than that of ASA or fenoprofen. At pH 1, the absorption of ASA from the Heidenhain pouch was greater than that of indomethacin and fenoprofen; their respective concentrations in the plasma were 53.9, 14.2 and 13.7 mumol.
Explore the source record for details and available documents.