Influence Of Acetylsalicylic Acid Research Articles

Aspirin Stimulates the Osteogenic Differentiation of Human Adipose Tissue-Derived Stem Cells In Vitro.

This study investigates the impact of acetylsalicylic acid (ASA), also known as aspirin, on adipose tissue-derived stem cells (ASCs), aiming to elucidate its dose-dependent effects on morphology, viability, proliferation, and osteogenic differentiation. Isolated and characterized human ASCs were exposed to 0 µM, 100 µM, 200 µM, 400 µM, 800 µM, 1000 µM, 10,000 µM, and 16,000 µM of ASA in vitro. Cell morphology, viability, and proliferation were evaluated with fluorescent live/dead staining, alamarBlue viability reagent, and CyQUANT® cell proliferation assay, respectively. Osteogenic differentiation under stimulation with 400 µM or 1000 µM of ASA was assessed with alizarin red staining and qPCR of selected osteogenic differentiation markers (RUNX2, SPP1, ALPL, BGLAP) over a 3- and 21-day-period. ASA doses ≤ 1000 µM showed no significant impact on cell viability and proliferation. Live/dead staining revealed a visible reduction in viable cell confluency for ASA concentrations ≥ 1000 µM. Doses of 10,000 µM and 16,000 µM of ASA exhibited a strong cytotoxic and anti-proliferative effect in ASCs. Alizarin red staining revealed enhanced calcium accretion under the influence of ASA, which was macro- and microscopically visible and significant for 1000 µM of ASA (p = 0.0092) in quantification if compared to osteogenic differentiation without ASA addition over a 21-day-period. This enhancement correlated with a more pronounced upregulation of osteogenic markers under ASA exposure (ns). Our results indicate a stimulatory effect of 1000 µM of ASA on the osteogenic differentiation of ASCs. Further research is needed to elucidate the precise molecular mechanisms underlying this effect; however, this discovery suggests promising opportunities for enhancing bone tissue engineering with ASCs as cell source.

Acetylsalicylic Acid Administered in Patients with Type 2 Diabetes Mellitus and Its Effect on the Antioxidant Enzyme System

Type 2 diabetes mellitus and its complications are associated with oxidative stress and the depletion of antioxidant defenses. The influence of acetylsalicylic acid on reversing the decrease in antioxidants, insulin resistance, glucose homeostasis, and inflammatory cascade can help prevent diabetes complications. Purpose: The aim of the study was to evaluate the effect of acetylsalicylic acid on the antioxidant enzymatic system in patients with diabetes. Methods: A randomized, double-blind, placebo-controlled clinical trial was carried out in 21 patients of both sexes with Type 2 diabetes for less than five years at the time of diagnosis, without pharmacological treatment, and randomly selected. Acetylsalicylic acid (300 mg) was administered orally for three months to the study group (n = 11) compared to the placebo control group (n = 10). Before and after the intervention, anthropometric and metabolic measurements were taken, fasting plasma glucose, glycated hemoglobin A1c, lipid profile panel, glutathione peroxidase, superoxide dismutase, catalase, and antioxidant capacity/activity were determined; values are presented as mean ± standard deviation. Intra- and intergroup differences were tested by Wilcoxon signed rank and Mann-Whitney U test, respectively; p-value ≤ 0.05 was considered statistically significant. Results: The acetylsalicylic acid group showed a decrease in weight (85.6 ± 19.3 vs. 84.1 ± 19.0 kg p = 0.01), cholesterol (205.9 ± 16.6 vs. 186.0 ± 23.2 mg/dL p = 0.02), and glycated hemoglobin A1c (7.8% ± 0.9% vs. 7.0% ± 0.7% p = 0.02). The placebo group exhibited reduction in weight (76.1 ± 14.9 vs. 74.9 ± 15.0 kg p = 0.04), glycated hemoglobin A1c (6.9% ± 0.6% vs. 6.2% ± 0.4% p = 0.004), and total antioxidant capacity (4.1 ± 0.5 vs. 4.8 ± 0.3 mmol/L p = 0.002). Conclusion: The administration of acetylsalicylic acid did not modify the antioxidant enzyme system.

The influence of acetylsalicylic acid and alcohol on absorption kinetics of hen´s egg white in a human passive cutaneous anaphylaxis model.

BackgroundDespite the well-known fact that acetylsalicylic acid (ASA) can induce anaphylaxis in patients susceptible to wheat-dependent exercise-induced anaphylaxis, few studies have sought to investigate the effects of cofactors on type-1 food allergy and none with ASA and hen’s egg and hen’s egg and alcohol combined.Methods and resultsWe applied the experimental model of ‘passive cutaneous anaphylaxis’ in humans to study whether the absorption kinetics of egg white is altered while being treated with ASA or under the influence of alcohol. Donor sera from four egg allergic patients with specific immunoglobulin E (s-IgE) to ovalbumin (0.1–8.87–19.5–170 kUA/L) were injected intracutaneously into the forearm of 12 healthy volunteers who were then challenged separately to: 1) egg white 2) egg white + ASA and 3) egg white + alcohol. ‘Time to wheal’ and ‘wheal size’ were compared among the three experiments.We saw that ‘time to wheal’ with both ASA (P = 0.001) and alcohol (P = 0.019) added as cofactor significantly decreased compared with baseline.ConclusionIn this passive cutaneous anaphylaxis model, ASA and alcohol affected both reaction time and size of reactions elicited after egg ingestion. This suggests that patients with egg allergy could have faster and more severe reactions during ASA treatment or under alcohol influence.

Физиологические механизмы действия салицилатов на сердечно-сосудистую систему

In modern literature, there is an increased interest in studying the biological and therapeutic effects of salicylates. Extensive clinical trials have demonstrated the effectiveness of acetylsalicylic acid (ASA) and its complex compounds in the treatment and prevention of ischemic heart disease, chronic heart failure, hypertension, and others, which makes it possible to assess the breadth of beneficial effects of ASA on the functioning of the cardiovascular system (CVS) and to state lack of other equivalent medicines in the coming years. The essential direction remains the expansion and enhancement of the known therapeutic activity (antipyretic, analgesic, anti-inflammatory, antioxidant, antidepressant, anti-migraine, anxiolytic, etc.) against the background of reducing and/or eliminating side effects since ASA occupies a leading position among all non-steroidal anti-inflammatory drugs in terms of volumes and one of the first places for the number of side effects. A promising solution to this problem is the creation of complex compounds of salicylates, since the formation of new coordination compounds based on them may lead to the emergence of new useful biological properties, as well as the strengthening of physiological effects characteristic of ASA, which will help to solve the problem of reducing side effects, resistance to aspirin therapy and increasing the therapeutic potential of the initial compound to obtain effective new-generation drugs. The article summarizes extensive information about the physiological and molecular mechanisms of action of ASA and its derivatives on CVS in health and disease, including on various physiological and biochemical links of the body's homeostasis: vasoregulatory function of the vascular endothelium, vascular-platelet hemostasis; fibrinolysis; processes of free radical oxidation and antioxidant protection; cyclooxygenase and lipoxygenase pathways of arachidonic acid oxidation; molecular markers of inflammation processes (prostaglandins; pro- and anti-inflammatory cytokines; anti-inflammatory lipid mediators). We analyzed and described the literature data and our own experimental studies of salicylates' effects on central hemodynamics and tissue microcirculation. We concluded that it is promising to study quantitative and qualitative changes in microcirculatory processes under the influence of ASA and its derivatives, which will clarify the mechanisms of these compounds' biological action on the CVS.

Acetylsalicylic acid (Aspirin®) and liver regeneration: experimental study in rats.

to evaluate the influence of acetylsalicylic acid (ASA) on cell proliferation after partial hepatectomy in rats. 40 male Wistar rats were separated into four groups of ten rats each. Groups 1 and 2 (controls): undergoing 30% partial hepatectomy and, after one day (group 1) and seven days (group 2), to euthanasia; daily administration of 0.9% saline solution (1mL per 200g of body weight). Groups 3 and 4 (experimental): undergoing 30% partial hepatectomy and, after one day (group 3) and seven days (group 4), to euthanasia; daily administration of ASA (40mg/mL, 1mL per 200g of body weight). The absolute number of cells stained with PCNA was counted in photomicrographs, in five fields, and it was calculated the mean of positive cells per animal and per group. the final mean of PCNA+ cells per group was: in group 1, 17.57 ± 6.77; in group 2, 19.31 ± 5.30; in group 3, 27.46 ± 11.55; and, in group 4, 12.40 ± 5.23. There was no significant difference at the two evaluation times in the control group (p=0.491), but there was in the experimental group (p=0.020), with a lower number of PCNA+ cells on the seventh day. The comparison between the two groups, on the first day, showed more PCNA+ cells in the livers of the animals that received ASA (p=0.047), and on the seventh day the number was lower in the experimental group (p=0.007). ASA induced greater hepatocyte proliferation.

The influence of acetylsalicylic acid in bone regeneration: systematic review and meta‐analysis

The influence of acetylsalicylic acid in bone regeneration: systematic review and meta‐analysis

Aspirin Administration Affects Neurochemical Characterization of Substance P-Like Immunoreactive (SP-LI) Nodose Ganglia Neurons Supplying the Porcine Stomach.

Background Acetylsalicylic acid (ASA) is a commonly used anti-inflammatory, antipyretic, and analgesic drug, which has many side effects on the gastric mucosal layer. Despite this, knowledge concerning the influence of ASA on neuronal cells supplying the stomach is very scanty. Methods This investigation was performed on ten immature gilts of the Large White Polish race divided into two groups (five animals in each): a control group and animals which were treated with ASA. The retrograde neuronal tracer Fast Blue (FB) was injected into the prepyloric region of the stomach in all animals. ASA was then given orally to the experimental (ASA) group of gilts from the seventh day after FB injection to the 27th day of the experiment. After this period, all animals were euthanized. Immediately after euthanasia, nodose ganglia (NG) were collected and subjected to a standard double-labelling immunofluorescence technique using antibodies directed toward substance P (SP) and other selected neuronal factors, such as galanin (GAL), neuronal isoform of nitric oxide synthase (nNOS), vasoactive intestinal polypeptide (VIP), and calcitonin gene-related peptide (CGRP). Key Results. The obtained results show that SP-LI neurons located in NG supplying the porcine stomach were also immunoreactive to all the above-mentioned neuronal factors. Moreover, ASA administration caused an increase in the degree of colocalization of SP with other neuronal active substances, and the most visible changes concerned the number of neurons simultaneously immunoreactive to SP and CGRP. Conclusions and Inferences. These observations indicate that the population of SP-LI neurons supplying the stomach is not homogeneous and may undergo changes after ASA administration. These changes are probably connected with inflammatory processes and/or neuroprotective reactions although their exact mechanisms remain unknown.

Влияние фармацевтических препаратов на скорость деградации полилактогликолидных матриксов

Исследовано влияние ацетилсалициловой кислоты, ибупрофена, 6-метилурацила и хондроитин сульфата, импрегнированных в полилактогликолидные матриксы различного химического состава и молекулярной массы c помощью сверхкритического диоксида углерода, на процессы деградации матриксов в растворе фосфатно-соленого буфера pH 7,4 и определены константы скоростей этих процессов. Показано, что включение в полилактогликолидный матрикс ацетилсалициловой кислоты и ибупрофена значительно увеличивает скорость гидролиза полимерной основы, в то время как присутствие метилурацила и хондроитин сульфата их практически не меняют.

Influence of acetylsalicylic acid and low-molecular weight heparins on the formation of renal hematoma after shock wave lithotripsy.

To investigate the risk of renal hematoma (RHT) after shock wave lithotripsy (SWL) among patients on acetylsalicylic acid (ASA) or low-molecular-weight heparin (LMWH). Retrospective analysis of 434 patients treated with SWL for nephrolithiasis and ureterolithiasis of the proximal ureter. Primary endpoint was detection of RHT by ultrasound the day after SWL. Secondary outcome variables included transfusion of erythrocyte concentrate(s), interventions, hospital readmission or death due to RHT within 30days of SWL. Binary logistic regression analysis was used including a post hoc one-way analysis. Of 434 patients, 33 (7.6%) and 67 (15.4%) patients were medicated with ASA and LMWH, respectively. RHT was detected in 20 of 434 (4.6%) patients. Of those, 3 (20%) were on ASA, 6 (35%) were on LMWH, 1 (5%) was on ASA and LMWH, and 10 (50%) had no anticoagulation. Univariate analysis showed a statistically significant higher risk for RHT among patients on ASA (p=0.04) and LWMH (p=0.02) with an untreated urinary tract infection (UTI) (p=0.008) and history of cardiovascular disease (p=0.028). On multivariate analysis, ASA medication, untreated UTI (OR 4.4, 95% CI 1.31-14.75, p=0.016 and OR 5.79, 95% CI 1.65-20.32, p=0.03) and a therapeutic dose of LMWH (OR 10.4, 95% CI 1.74-62.27, p=0.01) were independent predictors for RHT. Before SWL, a patient risk profile should be evaluated. If feasible, LMWH in therapeutic dosing should be avoided, and ASA should be discontinued. UTI should be treated before SWL in any case. http://www.clinicaltrials.gov ; Identifier NCT02875717.

Influence of acetylsalicylic acid (Aspirin) on cutaneous microcirculation

The protective effect of acetylsalicylic acid (aspirin) in primary and secondary prophylaxis of cardiovascular events is attributed to the inhibition of platelet cyclooxygenase (COX). However, a recent animal study found a vasodilating and blood pressure lowering effect of aspirin independent of COX, but mediated by inhibition of the RhoA/Rho kinase signaling pathway. Prospective, randomized, double-blind, placebo-controlled cross-over study. In each instance 5 healthy volunteers received either aspirin 500 mg/d or placebo for 7 days. Capillary red blood cell velocity (vRBC) at rest and after postischemic hyperemia was determined on day 1 and 7 by means of nailfold capillary microscopy. In the aspirin group after 7 days a significant increase of vRBC was found at rest and during hyperemia. In the placebo group vRBC did not change. The finding was confirmed by the cross-over design of the study. Aspirin at a dosage of 500 mg/d has an impact on vasoregulation in the microcirculation. At present, the underlying mode of action in humans is unknown.

Inhibition of human platelet aggregation by amides and ester of salicylic acid with platelet-activating factor analogs.

The influence of acetyl salicylic acid (ASA) derivatives with platelet-activating factor (PAF) lipid analogs on PAF-induced human platelet aggregation has been studied. It was found that the ASA amide with an ethanolamine plasmalogen PAF analog (1-0-alk-1'-enyl-2-acetyl-sn-glycero-3-phospho-(N-2'-acetoxybenzoyl)ethanolamine) and the ASA ester with a choline plasmalogen PAF analog (1-0-alk-1'-enyl-2-(2'-acetoxybenzoyl)-sn-glycero-3-phosphocholine) at concentrations of 10-7-10-6 M effectively inhibit PAF-induced aggregation of human platelets. In contrast to these compounds, the ASA amide with an alkyl PAF analog (1-0-alkyl-2-acetyl-sn-glycero-3-phospho-(N-2'-acetoxybenzoyl)ethanolamine) did not inhibit PAF-induced platelet aggregation. As possible mechanisms of action of the studied compounds, the blockade of PAF-receptor and cyclooxygenase inhibition are proposed.

Influence of acetylsalicylic acid on oxidation of native and glycated low-density lipoprotein

It is generally accepted that oxidation of low-density lipoproteins (LDL) is a causal factor in the development of atherosclerosis. Non-enzymatic glycosylation of LDL, i.e.“glycation”, plays a central role in late complications of diabetes mellitus and may initiate and/or accelerate the oxidation process. Therefore, the inhibition of this processes is of major therapeutic relevance. The influence of acetylsalicylic acid (ASA) on the oxidation of native and glycated LDL was studied in vitro. LDL (0.25 mg protein ml ) was oxidatively modified with 5.0 μM CuSO 4. Only at “supratherapeutical” ASA concentrations in the range 0.06–2.0 mg ml we found a significant concentration-dependent inhibition of LDL oxidation both for native and glycated LDL, which was from 0.2 mg ml upwards significantly more marked for native LDL than for glycated LDL. The maximal inhibitory effect occurred at 2.0 mg ml with 89.6% inhibition of LDL-oxidation for native LDL and 64.4% for glycated LDL. At 0.2 mg ml ASA the respective inhibitory values were 38.5% and 31.0%. For glycated LDL the ASA doses of maximal- and approximately 50%-inhibition, as found for native LDL, were chosen to investigate the inhibitory effect on 2,4,8 and 24 hours oxidation of glycated LDL to monitor the time-dependency of inhibition by ASA. This revealed that ASA only delayed, not permanently inhibited LDL oxidation.

Influence of acetylsalicylic acid on development of radiation-induced nephropathy

Purpose : Previous studies have demonstrated that long-term treatment with acetylsalicylic acid (ASA) can significantly reduce the renal functional impairment that develops after high doses of irradiation. The effect is hypothesized to be mediated by selective inhibition of thromboxane A 2 synthesis and inhibition of platelet aggregation. The present study was undertaken to investigate this phenomenon further using more clinically relevant fractionated and re-irradiation schedules. Methods and materials : Groups of mice were given bilateral renal irradiation with a series of four or 20 daily fractions of X-rays, or 10 daily fractions with a single dose of re-irradiation (0-10Gy) after 27 weeks. Half the mice received ASA in drinking water (2.4 g.l -1) from 1 week before the start of irradiation and continuously throughout the follow-up period. Renal function was assessed by clearance of [ 51 Cr]EDTA, about every 4 weeks for up to 80 weeks after the start of treatment. Histological damage in representative groups of mice was also assessed. Results : Oral administration of ASA caused inhibition of thromboxane A2 synthesis (to < 36% of controls) and a strong inhibition of platelet aggregation in whole mouse blood (ex vivo) . Prolonged treatment with ASA also resulted in a small, non-significant reduction of radiation-induced renal functional damage. No reduction in histological damage was seen in the ASA treated mice. Conclusion : Long-term oral administration of ASA gave only a modest, non-significant reduction of renal radiation injury after clinically relevant fractionated irradiation schedules.

Better increase in fibrin gel porosity by low dose than intermediate dose acetylsalicylic acid.

To investigate the influence on plasma fibrin gel structure of low and intermediate doses of acetylsalicylic acid in healthy individuals. The influence of acetylsalicylic acid on thrombin formation, fibrinolytic capacity and plasminogen inhibitor-1 in plasma was also investigated. Nineteen subjects were treated with 75 mg and 11 with 320 mg acetylsalicylic acid daily; eight subjects received both doses. Fibrin gel structure was determined by a permeability technique yielding a porosity constant (Ks), and the thromboxane metabolite 11-dehydro-thromboxane B2 (TxM) was determined by an ELISA. Acetylsalicylic acid increased fibrin porosity by 65% at 75 mg (P<0.001, n=19), whereas lower increases were found at 320 mg (+22%, P<0.05, n=11). One week after withdrawal Ks had essentially returned to baseline (ns). Urinary thromboxane metabolites were suppressed during treatment (-61%, P<0.001 at 75 mg, n=19; -46%, P<0.01 at 320 mg, n=11). The intra-individual comparison showed similar results (Ks +92%, TxM -62% at 75 mg; Ks +5%, TxM -52% at 320 mg). Fibrinolytic capacity, plasminogen inhibitor-1 levels and thrombin generation (in platelet-poor citrated plasma) were not influenced. Low dose acetylsalicylic acid causes the greatest increase in fibrin gel porosity; this may well be of therapeutic importance.

Risk of haemorrhage from transurethral prostatectomy in acetylsalicylic acid and NSAID-treated patients.

Postoperative bleeding in patients who regularly ingest acetylsalicylic acid (ASA) has been reported after several types of surgery. However, data on the influence of ASA on the risk of haemorrhage from transurethral prostatectomy (TUR-P) have been conflicting. We have studied retrospectively the unselected clinical records of all patients undergoing TUR-P in the Department of Urology at Hvidovre Hospital (during 1992-1994) with special focus on the use of ASA and non-steroidal anti-inflammatory drugs (NSAIDs). In total, 457 records were examined: 99 patients on ASA/NSAID received 42 units of blood, while 358 patients free from such medication received 68 units of blood, a significantly smaller amount (p = 0.0390). We conclude that ASA and NSAIDs increase the risk of bleeding during and after TUR-P, and we recommend the withdrawal of these drugs for one week before TUR-P.

The influence of ethylene on in vitro rooting of GF 677 (Prunus persica × Prunus amygdalus) hybrid peach rootstock

Treatments differing from each other for the type of tube closure (i.e., cotton plug for free gas exchange, airtight rubber cap, and rubber cap with ethysorb) and/or rooting culture medium (i.e., enriched or not by 25 to 100 µM acetylsalicylic acid) were compared for their effects on gaseous composition of the culture atmosphere and microcutting rooting of the GF 677 (Prunus persica × Prunus amygdalus) hybrid. Rubber capping, which leads to rapid ethylene accumulation inside tubes, strongly reduced rooting time and in some cases enhanced final rooting percentage over that of cotton plugs. Ethysorb almost completely absorbed ethylene produced by shoots, which showed lower rooting percentages within 9 d than microcuttings cultured in the absence of ethysorb. In contrast, no significant difference in rooting was found between the two treatments after 14 d. Carbon dioxide concentration was similar in all treatments within 5 to 9 d and seemed to be ineffective for rooting. The influence of acetylsalicylic acid on rooting was unclear. Root number and length were not significantly influenced by the treatments. These results demonstrate that the use of airtight closures, leading to rapid ethylene accumulation, can reduce time of rooting expression for GF 677 microcuttings. However, free gas exchange towards the end of the rooting period (from Day 9 to Day 14) is advisable to prevent leaf yellowing. No significant difference in plantlet survival and growth after transfer ex vitro was found among treatments.

Influence of acetylsalicylic acid and metabolites on DU-145 prostatic cancer cell proliferation.

Conflicting reports have been published on the anti-tumour activities of acetylsalicylic acid in various cancers. Therefore, the effect of acetylsalicylic acid and its major metabolites has been studied on human prostatic carcinoma DU-145 cells. Investigations concentrated on the influence of acetylsalicylic acid, salicylic acid and salicyluric acid, on cell proliferation, DNA- and protein synthesis of DU-145 cells. DNA and protein synthesis determinations were done in vitro by [3H]thymidine and [3H]glycine incorporation, respectively. No effect on cell plating efficiency was observed, however proliferation studies showed that acetylsalicylic acid and salicylic acid inhibited cell growth (10 mM, 100% inhibition). No significant effect on cell proliferation was ascertained with salicyluric acid. Both DNA and protein synthesis were 40% inhibited by 0.1 mM acetylsalicylic acid. This study demonstrates that acetylsalicylic acid exhibits a significant influence on cell growth of prostatic DU-145 cells. These preliminary results may contribute to a better understanding of the anti-tumour capabilities of acetylsalicylic acid.

Influence of acetylsalicylic acid on a Listeria monocytogenes infection.

The influence of acetylsalicylic acid (ASA, CAS 50-78-2) on the Listeria monocytogenes infection in balb/c mice was investigated. One day prior to lethal or sublethal infection, balb/c mice were treated intravenously with therapeutic concentrations of ASA alone or ASA in combination with murine recombinant interferon gamma, a lymphokine produced by T-helper cells. Three days post-infection, parasite burdens of spleen and liver were determined by the colony-forming unit assay. It was shown that the prophylactic application of ASA in a concentration of 5 mg/kg body weight resulted in a more than 10-fold reduction of viable Listeria monocytogenes in spleen and liver of balb/c mice. In addition, the combination of a suboptimal dosage of interferon gamma with ASA resulted in a significantly higher survival rate compared to the untreated controls.

Acetylsalicylic acid has no effects on various isolated immune cells in vitro.

In addition to the well known biological effects of acetylsalicylic acid (ASA), its stimulating effect on the immune system has recently been described. In the present study, therefore, the influence of ASA on isolated leucocytes was investigated in vitro. Various concentrations of ASA, representing therapeutic concentrations, had neither an inhibitory nor a stimulating influence on the cytotoxicity of CD16-positive cells. The phytohaemagglutinin-induced proliferation of lymphocytes and the phagocytosis activity of monocytes and neutrophilic granulocytes was similarly unaffected. These results would indicate that the immunostimulating effects already described for ASA cannot be examined in isolated leucocytes in vitro and should be attributed to an interaction of various effector cells in vivo.

Antiplatelet therapy following carotid bifurcation endarterectomy. Evaluation of a controlled clinical trial. Prognostic significance of histologic plaque examination on behalf of survival

To determine whether antiplatelet therapy following carotid bifurcation endarterectomy influences postoperative survival and whether signs of progression in the plaques harvested at the time of surgery might be a prognostic indicator, a controlled clinical trial was undertaken. During 1982 to 1985, 66 patients were recruited, operated on (carotid endarterectomy) and assigned, using the method of adaptive randomisation to the therapy group (n = 32) receiving 1.0 g acetylsalicylic acid (ASA) per day, starting day two prior to surgery, or to the control group (n = 34), which remained without antiplatelet medication. The plaques harvested at the time of surgery were processed using standard histopathological methods and examined "blindly" by light microscopy for signs of arterio-sclerotic progression. The final endpoint was patient survival. The last assessment of the participants survival status was done by June 1989. During follow-up, 20 patients died, six in the treatment group and 14 in the untreated group, the difference being statistically significant (P less than 0.013 Breslow, P less than 0.029 Mantel). In 27 instances the histo-pathological examination showed signs of progression. In this subgroup ASA yielded a significant prolongation of patient survival (P less than 0.017 Breslow, P less than 0.048 Mantel). In the remaining patients no signs of cellular infiltration were evident and no influence of ASA on patient survival was demonstrable (P less than 0.503 Breslow, P less than 0.390 Mantel).