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The glycoregulation of 17 type II diabetics was observed to improve by administering 1 g of acetylsalicylic acid three times per day, during a one-year study. The subjects did not lose weight during the experimental period, but the insulin daily requirement of 7 patients did decrease by 60%.
Optimum conditions for a simultaneous determination of propyphenazone, paracetamol, guaiacol glycerol ether, caffeine and acetylsalicylic acid were described for preparations with analgesic-antipyretic activity, which don't allow a direct determination of the active principle because of interference phenomena. Using an external standard for calibration the determination was carried out by adsorption measurement (reflectance detection) in situ. Beside the determination of the drug content the method can be used to identify substances according to their RT and RF-values as well as by on-plate spectra taken.
The effects of short-term oral treatments with prostaglandin (PG) synthesis inhibitors, acetylsalicylic acid (ASA), or diclofenac (DCF), on basal and stimulated growth hormone (GH) and prolactin (PRL) secretion were studied in 23 healthy volunteers. Before and after 4 days on ASA (3.2 g daily) or DCF (75 mg daily), subjects were given cimetidine or metoclopramide to evaluate PRL reserve. Arginine infusion test (for GH and PRL response) was performed only in ASA-treated subjects. Arginine-induced GH and PRL release was abolished and enhanced, respectively, by ASA pre-treatment. PRL response to cimetidine was greater than that observed in basal conditions when ASA was given, but remained unchanged after DCF administration. Neither ASA nor DCF was capable of modifying the PRL response to metoclopramide. Basal GH and PRL levels were not influenced by ASA or DCF. In conclusion, some PG may play an important role in the regulation of GH and PRL secretion, and some PG inhibitors (like ASA) may significantly interfere with some dynamic tests for pituitary reserve.
The effect of controlled long-term oral trial with 2 g/die of acetylsalicylic acid (ASA) in addition to diet in 14 patients suffering from impaired glucose tolerance (according to WHO criteria) was compared to diet alone plus placebo (PL). All patients were randomly assigned to ASA or PL, and then submitted to cross-over scheduling procedure (30 + 30 days). Plasma glucose levels observed after an oral glucose tolerance test (OGTT, 100 g) became normal in patients receiving ASA for 30 days (p less than 0.01 at x2 analysis). No change of abnormal OGTT data was observed when patients were treated with PL. Insulin secretin after OGTT and after i.v. glucose tolerance test (IVGTT, 5 g) was unmodified by ASA. Basal glucose levels and plasma glucose disappearance rate after IVGTT also remained unchanged after ASA. Only two subjects had to stop ASA treatment because of gastric discomfort. The oral administration of 2 g of ASA might possibly interfere with intestinal glucose absorption. The well known influence of ASA on prostaglandin synthesis and on insulin secretion could not be relevant in our own pharmacological approach.
We studied the effects of two non-steroidal anti-inflammatory analgesics (NSAIAs), acetylsalicylic acid (ASA) and acetaminophen, on sleep patterns in rats with adjuvant-induced arthritis. We found that in the normal rat both NSAIAs reduced non-rapid eye movement (NREM) sleep. In arthritic rats ASA and acetaminophen had opposite effects on sleep. ASA increased wakefulness and decreased all sleep stages and acetaminophen decreased wakefulness and increased NREM sleep and paradoxical sleep during the light hours (the hours of maximal sleep in the normal rat). When the effects of severity of arthritis were factored out, both drugs still had large and significant effects on sleep and wakefulness. Thus, two prostaglandin synthetase inhibitors showed differential effects on sleep and wakefulness in the normal rat and in rats experiencing chronic pain. Although ASA is important in the treatment of pain in rheumatic diseases, it may contribute to abnormal sleep patterns.
We investigated whether the measurement of N-ethylmaleimide stimulated malondialdehyde (MDA) formation by blood platelets from normal subjects is equally sensitive to acetylsalicylic acid intake as are platelet aggregation studies. MDA production and platelet aggregation by collagen and arachidonate were assayed in ten healthy volunteers before and up to ten days after a single oral dose of 500 mg aspirin. Discordant results of the two tests were seen in several subjects 4 to 6 days after aspirin intake. In three cases with still suppressed MDA values on day 4, collagen or arachidonate induced aggregation was normalized. However, on day 6, when MDA was normalized in all subjects, the aggregation response to arachidonate was still pathologic in 5 of the ten volunteers. In case of a patient with abnormal aggregation response to arachidonate and/or collagen, therefore, a normal MDA value does not permit to exclude aspirin as the cause of the platelet dysfunction.
We evaluated the effect of four weeks treatment with 90 mg and 1500 mg of acetylsalicylic acid (ASA), 990 mg of ASA together with 225 mg of dipyridamole and 225 mg of dipyridamole daily on the production of thromboxane A2 (TxA2) by platelets of atherosclerotic subjects. All doses of ASA studied inhibited 99% or more of TxA2 production from the third day to the end of the treatment, whereas dipyridamole did not have any effect. After the treatment, TxA2 production recovered in two weeks. Our results argue against the clinical relevance of the recent suggestions that salicylate accumulating during prolonged treatment with ASA could reduce the effect of the parent drug on the synthesis of TxA2 by platelets. Our data also dispute the inhibition of TxA2 synthesis as an antithrombotic mechanism of dipyridamole.
A reversed-phase high-performance liquid chromatography (HPLC) method has been developed for the simultaneous assay of acetylsalicylic acid (I) and salicylic acid (II) in film-coated aspirin tablets. As little as 0.1% II (relative to I) can be quantitatively determined. Using a 5-microns octadecylsilane column with water-acetonitrile-phosphoric acid (76:24:0.5) as the mobile phase enabled the chromatographic separation to be completed in 4 min. Due to the slow rate of decomposition of I to II in the extraction solvent, acetonitrile-methanol-phosphoric acid (92:8:0.5), the analysis of many samples was routinely performed by means of automated HPLC equipment. Other compounds (non-aspirin salicylates, caffeine and acetaminophen) were also separated by the chromatographic system.
Phototherapy of newborn infants with hyperbilirubinemia was shown to result in an increase in hematocrit values and in the activity of the erythrocyte enzyme acetylsalicylic acid esterase. The elevation of the enzyme activity also could be produced in light-treated rabbits and in vitro after illumination of blood from adult volunteers. The binding of bilirubin to serum albumin and of salicylate to plasma proteins did not alter, nor did the concentrations of albumin or total proteins in plasma. It is concluded that light does not increase the unbound fraction of bilirubin in blood.
1. Using canine testis-spermatic nerve preparations in vitro, we studied the effects of acetylsalicylic acid (ASA), an inhibitor of cyclooxygenase, on the polymodal receptor response to heat stimulation itself and on the sensitizing effects on the heat and bradykinin responses induced by strong heat stimulation (55 degrees C for 30 s). 2. Greater heat responses tended to be strongly suppressed by ASA (550 microM), with a significant correlation observed between the response magnitude and the magnitude of the suppression (r = 0.88 for the response at 45 degrees C; r = 0.83 for the response at 48 degrees C). The change in the heat response at 48 degrees C from 1.18 +/- 0.19 to 0.62 +/- 0.11 imp/s was statistically significant (n = 21, P < 0.01). 3. After stimulation at 55 degrees C in the presence of ASA, resting discharges at 34 degrees C appeared in only 2 of the 21 units tested. The responses at 45 and 48 degrees C, however, were significantly potentiated after this stimulation (those at 45 degrees C from 0.12 +/- 0.05 to 2.19 +/- 0.51 imp/s, mean +/- SE; those at 48 degrees C from 0.62 +/- 0.11 to 2.42 +/- 0.49 imp/s; P < 0.01, n = 21 for both). Sensitization was observed up to 50 min after stimulation at 55 degrees C.(ABSTRACT TRUNCATED AT 250 WORDS)
In an acute migraine clinic, patients were all treated with metoclopramide 10 mg i.m. and diazepam 5 mg p.o. In addition, 435 received acetylsalicylic acid 1,000 mg and 254 paracetamol (acetaminophen) 1,000 mg p.o. A computer analysis revealed the two groups of patients to be not statistically significantly different. In fact they were almost identical with respect to a large number of clinical parameters. The treatment results in the two groups were identical. The present study indicates that the two drugs are equipotent in the treatment of the acute migraine attack.
Procollagen-induced platelet aggregation, platelet retention (Hellem II), and platelet factor 3 availability (PF-3) were determinded in a group of healthy volunteers,acetylsalicylic acid (ASA) treated patients and in uraemic patients. ASA ingestion did not influence platelet retention and PF-3 availability. Uraemic patients had apronounced decrease in platelet aggregation and retention and PF-3 availability revealed inconsistent alterations. The relevance of the tests and the benefit of an ASA treatment for prophylaxis of thrombosis in Climino fistulae are discussed.
In a double-blind clinical trial a new, non-steroidal anti-inflammatory agent with analgesic properties, Fenbufen, was compared to acetylsalicylic acid (ASA) and placebo. Six hundred (600) out-patients, following surgical removal of an impacted lower wisdom tooth, were divided into three groups and randomly given either Fenbufen (500 mg capsules), ASA (750 mg capsules), or placebo. One capsule was taken immediately after the surgical procedure, followed by another capsule every 6 hours. The duration of treatment was 24 hours. Thus, a total of 4 capsules were taken. Self-evaluation forms were provided to the patients and were returned to the investigators the following day. The results were statistically analyzed. Both Fenbufen and ASA were statistically superior (p less than or equal to 0.01) to placebo in relieving pain. A comparison of the Fenbufen and ASA groups demonstrated a statistically significant (p less than or equal to 0.05) superiority for Fenbufen in relieving pain. Also sleep was less disturbed in the Fenbufen group. Side-effects reported were few, minor in character, and fewer in number in the Fenbufen group.
The objective of the study was to determine the effect on energy intake and appetite of acetylsalicylic acid (ASA), commonly used by the elderly to treat arthritis. In a double blind cross-over study, 23 free-living osteoarthritic patients 60 years of age or older were treated for two-weeks intervals with a mean daily ASA intake of 2.44 and 1.29 grams, respectively. Twenty healthy persons similar in age, taking no medication, and matched in sociocultural characteristics were included as a control group. Appetite was measured directly, using a visual analogue scale, and indirectly by calculating energy intake from three-day food records. Varying the dose of ASA was without effect on appetite and food energy intake; however, as appetite was rated lower by the medicated osteoarthritic than by the healthy group, although the energy intakes were not significantly different, the former should be considered as potentially at nutritional risk.
This study was carried out in order to examine the effect of increasing doses of intravenously administered lysine-acetylsalicylic acid (ASA) on renal function in dogs. The first purpose was to examine the acute effects on renal water and solute output. The second purpose was to correlate the para-aminohippuric (PAH) clearance measurements with measurement of renal PAH extraction and renal blood flow (RBF). After 7 mg/kg ASA (20-80 microgram SA/ml plasma) a decrease in sodium excretion was observed in all dogs. With increasing ASA doses, the urine sodium excretion declined to 23% of the control period excretion. Tubular reabsorption of free water increased 10%. A significant and dose-related decrease in PAH clearance was observed in all dogs, from 108.7 ml/kg ASA to 58.8 ml/min after 200 mg/kg ASA. The creatine clearance was unchanged. PAH extraction fell in all dogs, RBF (measured by flowmeter decreased 21% at the highest plasma SA levels, as compared with 46% decrease in PAH clearance. ASA seems to inhibit tubular transport of PAH. Inhibition of prostaglandin synthesis by ASA offers one explanation of the effects of RBF and sodium excretion.
After reference to the results of investigations reported in literature with regard to the effects of ingestion of acetylsalicylic acid on the blood biochemism in normal and pathological conditions, the Authors illustrate the results of their research on patients with chronic obstructive arteriopathy or with post-phlebitic syndrome of the lower limbs. An accurate evaluation was made of the variations induced in some important blood coagulation parameters by the said drug, which was found to cause a clear increase in fibrinolytic activity and which is moreover endowed with marked antithrombophilic therapeutic capacity.
Combined use of sulfalen and sulfadimethoxine with benzylpenicillin and ampicillin resulted in increased binding of sulfalen to serum proteins of man. Acetylsalicylic acid promoted a decrease in the sulfanilamide binding to the serum proteins. The observed changes in the sulfanilamide binding to proteins of human blood serum were due to increased or decreased affinity of the drugs to the protein molecules.
Magnesium sulfate given orally in a hypertonic or isotonic solution did not alter the absorption of therapeutic doses of acetylsalicylic acid or lithium carbonate, despite a purgative effect in 10 volunteers. The concentration of magnesium in serum remained unchanged during the experiments.