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The effects of centrally injected prostaglandins (PGE1 and PGF2 alpha), arachidonic acid and lysine acetylsalicylate were examined on the seizure activity and temperature changes produced by pentylentetrazole (PTZ) and also on maximal electroshock (MES) seizures. PGE1 antagonised both PTZ and MES seizures whilst PGF2 alpha had the reverse effect. In addition both PGs alone produced hyperthermia but attenuated PTZ hypothermia. Arachidonic acid protected against PTZ--but potentiated MES--seizures whilst lysine acetylsalicylate augmented the effects of both convulsive stimuli. Lysine acetylsalicylate and arachidonic acid alone were transiently hyperthermic and also antagonised PTZ hypothermia though the total net effect may have been due to a functional antagonism. It is suggested from these findings that PGE1 has anticonvulsant effects whilst PGF2 alpha promotes seizures neither of these properties correlating with thermoregulatory actions.
The interaction of phenol (PHE), salicylic acid (SA) and o-acetylsalicylic acid (ASA) with bilayers of 1,2-dipalmitoyl-sn-glycero-3-phosphocholine (DPPC) was investigated by infrared spectrometry. The temperature of the main gel to liquid crystal phase transition of DPPC is markedly depressed in the presence of the three guest molecules. The temperature depression depends on the nature and concentration of the additives. The temperature of the pretransition is also affected by these guest molecules and the depression in temperature is even more pronounced than that of the main transition temperature. Possible modes of interaction of these guest molecules with the lipid bilayers are discussed.
UNLABELLED: Acetylsalicylic acid inhibits aggregation of blood platelets through affecting arachidon acid metabolism--a precursor of thromboxan which is a strong platelet aggregation inhibitor. A standard method for measurement of aggregation activity blockade (in percents) of platelet rich plasma is turbidimetric aggregomethry based on spectrophotometric principle. According to results of recent studies administration of acetylsalicylic acid is one of the basic pillars of prevention of thrombotic complications in atherosclerotic arterial disease. Acetylsalicylic acid doses differ from study to study. An aim of our work was to measure speed of two different doses of acetylsalicylic acid. RESULTS: Level of aggregation activity blockade in samples of platelet rich plasma was measured by aggregometry in 26 healthy volunteers after administration of four inductors of thrombocyte aggregation (arachidon acid, adenosindiphosphate, collagen, and ristocetin). The samples were taken before administration and 120, 240, and 360 minutes after single peroral administration of 100 or 400 mg of acetylsalicylic acid. Samples of plasma were analysed immediately after sampling. Before drug administration there was no aggregation activity in 27.7% of the sample after arachidon acid administration, 28.3% after ADP administration, 21.5% after collagen administration and 25.3% after ristocetin administration. After administration of 400 mg of acetylsalicylic acid and administration of arachidon acid as an inductor 89.9% of the aggregation activity of the sample was blocked after 120 minutes, 89.6% after 240 minutes, and 90.6% after 360 minutes. After administration of adenosindiphosphate as an inductor 71.7% of the aggregation activity of the sample was blocked after 120 minutes, 68.3% after 240 minutes, and 69.9% after 360 minutes. And, after administration of ristocetin as an inductor 64% of the aggregation activity of the sample was blocked after 120 minutes, 66.4% after 240 minutes, and 54% after 360 minutes. Blockade of aggregation activity after collagen administration was not statistically significant. After administration of 100 mg of acetylsalicylic acid and administration of arachidon acid 83.8% of the aggregation activity of the sample was blocked after 120 minutes, 89.2% after 240 minutes, and 89.6% after 360 minutes. After adenosindiphosphate administration statistically significant blockade of aggregation activity was achieved after 360 minutes in the 56.7% of the sample. Also after collagen administration 42.5% of aggregation activity of the sample was blocked significantly after 360 minutes while ristocetin has not proved to influence aggregation in a statistically significant manner. CONCLUSION: Both doses of acetylsalicylic acid influenced aggregation activity of platelets in a statistically significant manner as soon as after 120 minutes following their peroral administration. However, they had different ability to influence platelets response to alternative ways of activation--by adenosindiphosphate, collagen, and ristocetin. 400 mg dose blocked these ways while 100 mg dose was efficient in blocking these ways after 360 minutes and in case of ristocetin--an inductor used to monitor platelet adhesion ability--100 mg dose has not led to statistically significant blockade at all.
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The interaction between acetylsalicylic acid (aspirin) and membrane was studied by NMR spectra. (1) NMR spectra showed acetylsalicylic acid did not insert into membrane; (2) 1H NMR spectrum recorded by spin-echo pulse sequence showed protons of the aromatic ring interacted with membrane; (3) the change of spin-lattice relaxation (T1) of 31P was ascribed to the association of acetylsalicylic acid to the polar head of lecithin; (4) the self-diffusion coefficient measured by pulsed field gradients NMR showed the mobility of acetylsalicylic acid was restricted by membrane and that acetylsalicylic acid changed membrane viscosity. Based on the results, the relationship between the interaction and the mechanism of the wide pharmacological functions of acetylsalicylic acid is discussed.
A double-blind study comparing the efficacy and safety of diflunisal (Unisal), a new derivative of salicylic acid, and acetylsalicylic acid (Aspirin) was conducted in the rheumatology clinics of the Cantonal Hospital Beau-Séjour, Geneva, and the Triemli City Hospital, Zurich. A total of 38 patients with established osteoarthritis of the hip and/or knee were studied for 12 weeks. The daily dose of diflunisal was 500-750 mg and that of acetylsalicylic acid 2000-3000 mg. After 12 weeks diflunisal was judged superior to Aspirin by both patients and investigators. Among the most important clinical symptoms evaluated were pain and limitation of motion. Side effects, particularly gastro-intestinal symptoms, of sufficient severity to cause discontinuation of therapy were more frequent in the acetylsalicylic acid-treated patients than in the group receiving diflunisal.
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The influence of ascorbic acid (CAS 50-81-7), acetylsalicylic acid (CAS 50-78-2) and ibuprofen (CAS 15687-27-1) on macrophages of C57BL/6 mice was investigated in vitro. It has been shown that ascorbic acid or acetylsalicylic acid alone did not stimulate or inhibit the production of interleukin-6, whereas a combination of both substances caused a significant stimulation. The viral replication in L929 fibroblasts was not affected by ascorbate and/or acetylsalicylic acid. In addition, the tumor-necrosis factor (TNF) synthesis of peritoneal macrophages was neither stimulated nor inhibited by both substances, alone or in combination. The oxygen radical production, however, was definitely inhibited by ascorbic acid, the effect of acetylsalicylic acid was far less marked, but at the high concentrations the inhibition was clearly discernible. Ibuprofen, a propionic acid derivate, was able to reduce the replication of vesicular stomatitis virus in L929 fibroblast cells. At the highest concentration of ibuprofen, 100 micrograms/ml, 34% of the fibroblast were able to survive. This protective effect declined as the ibuprofen concentration decreased. Ibuprofen could not stimulate peritoneal macrophages to secrete TNF, whereas the oxygen radical production was significantly reduced. In addition, ibuprofen activated mouse macrophages to produce interleukin-6 in a dose dependent way. The results of the in vitro experiments presented clearly show that ascorbic acid, acetylsalicylic acid in ibuprofen influenced the unspecific immune system.
Acetylsalicylic acid (CAS 50-78-2) (1000 mg orally) was investigated in a non-inflammatory experimental pain model in healthy male volunteers, selected for maximal homogeneity. Phasic pain was induced by intracutaneously applied electrical pulses of constant current. The nociceptive responses measured were, the pain ratings, the cerebral potentials and the EEG delta power in response to the stimuli. In addition, spontaneous EEG, auditory evoked potentials and reaction times were evaluated to determine effects upon the vigilance system. The study was performed in a placebo-controlled, double-blind repeated measures design. Blood samples were taken to monitor the plasma concentrations of the active agents. Acetylsalicylic acid produced clear analgesic effects in all pain relevant target variables. The effects increased with post-medication time, becoming significantly different from placebo 90 min after medication (p less than 0.01). At this time point the pain ratings were reduced by 4%, the pain related cerebral potentials by 15%, and the stimulus induced delta power of the EEG by 20%. These findings suggest a central action of acetylsalicylic acid by attenuation of experimentally induced nociceptive activity. No influences could be observed upon auditory evoked potentials, spontaneous EEG and reaction times. In other words, acetylsalicylic acid did not change vigilance by unspecific alterations of the CNS. The plasma concentration of acetylsalicylic acid reached mean values of 2.5 +/- 2.4 micrograms/ml within 25 min after oral medication, which remained constant during the entire post-medication period of 105 min. In contrast, the concentration of the metabolite salicylic acid increased steadily reaching mean values of 32.0 +/- 16.8 micrograms/ml at the end of the investigated period.(ABSTRACT TRUNCATED AT 250 WORDS)
The effect of acetylsalicylic acid on endothelial prostaglandin synthesis was measured in the presence of exogenous and endogenous substrates. In both types of measurement, a rate of inhibition was found similar to that observed for acetylsalicylic acid inhibition of cyclooxygenase activity in platelets. After withdrawal of acetylsalicylic acid, a rapid restoration of cyclooxygenase activity was observed when exogenous [1-14C]arachidonate was used as a substrate (50% of initial activity at 5 h). However, when endogenous substrate, released after phospholipase activation induced by thrombin treatment of the cells, was used to test cyclooxygenase activity, only partial restoration of enzymic activity was observed (30% after 48 h). Phospholipase activity, measured by the release of free fatty acids, was not inhibited by acetylsalicylic acid. Measurement of turnover times by incubating the cells with cycloheximide revealed a short turnover time for the enzymic activity tested with exogenous [1-14C]arachidonate (2.3 h) and a relatively long turnover time for the cyclooxygenase activity tested with endogenous substrate released after thrombin treatment of the cells (54 h). These results suggest that at least two pools of cycloxygenase are involved in endothelial prostaglandin synthesis.
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The interaction of acetylsalicylic acid with alcohol dehydrogenase was investigated. Horse liver alcohol dehydrogenase bound to a p-hydroxyacetophenone affinity column was eluted by acetylsalicylic acid. In vitro enzymatic activity of alcohol dehydrogenase in the presence of ethanol as a substrate was significantly increased by incubation with acetylsalicylic acid. These results suggest that acetylsalicylic acid has an affinity with alcohol dehydrogenase and enhances its activity.
The mutual effects of acetylsalicylic acid and paracetamol used in combination were studied in rats and mice. The antiexudative effects of acetylsalicylic acid in the edema tests on the hind paw of the rat, the antipyretic activity against yeast-fever of the rat and the analgesic effect on the inflamed hind paw of the rat was potentiated by paracetamol given simultaneously. The biosynthesis of prostaglandins in vitro by an enzyme preparation from bovine seminal vesicles was inhibited by acetylsalicylic acid and paracetamol in additive synergistic mode. The hepatotoxicity of paracetamol in mice measured by an increase of GOT in serum is antagonized by acetylsalicylic acid in dose-dependent manner. The suppression of the hepatotoxicity of paracetamol by acetylsalicylic acid in mice is not the consequence of interaction during absorption. The 3H-content of the liver following an oral dose of 3H-paracetamol is not influenced by acetylsalicylic acid given in combination with paracetamol. The mechanism of interactions between acetylsalicylic acid and paracetamol is discussed.
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