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PubMed1999

Comparison of the effects of acetylsalicylic acid, ticlopidine and cilostazol on primary hemostasis using a quantitative bleeding time test apparatus.

We examined and compared the effects of aspirin (ASA), ticlopidine (TP) and cilostazol (CS) on bleeding time (BT) in 10 healthy adult male subjects using a newly developed quantitative bleeding time (QBT) test apparatus capable of simultaneously measuring total blood loss (Tv), maximum bleeding rate (Rmax), and bleeding pattern in addition to BT. All 3 drugs inhibited platelet aggregation response to ADP, collagen, epinephrine and arachidonic acid (p < 0.05), but not to ristocetin. Following oral administration of ASA (330 mg/day) or TP (300 mg/day) for 3 days, BT was significantly prolonged (mean BT increased from 359.3 to 646.0 s, p < 0.001, and from 323.3 to 528. 7 s, p < 0.01, respectively) and Tv was significantly increased (from 14.5 to 30.2 microl, p < 0.05, and from 12.5 to 19.2 microl, p < 0.01, respectively). Aspirin also increased Rmax (from 0.118 to 0. 159 microl/s, p < 0.05). The prolonged bleeding patterns after administration of ASA and TP were both type III, which has been reported to be less likely to lead to bleeding accidents. In contrast, none of these QBT parameters were altered by CS administration.

Adult↗
PubMed1999

Endotoxin-induced activation of the coagulation cascade in humans: effect of acetylsalicylic acid and acetaminophen.

During Gram-negative septic shock, lipopolysaccharide (LPS, endotoxin) induces tissue factor (TF) expression. TF expression is mediated by nuclear factor kappaB and amplified by activated platelets. TF forms a highly procoagulant complex with activated coagulation factor VII (FVIIa). Hence, we hypothesized that aspirin, which inhibits LPS-induced, nuclear factor kappaB-dependent TF expression in vitro and platelet activation in vivo, may suppress LPS-induced coagulation in humans. Therefore, we studied the effects of aspirin on systemic coagulation activation in the established and controlled setting of the human LPS model. Thirty healthy volunteers were challenged with LPS (4 ng/kg IV) after intake of either placebo or aspirin (1000 mg). Acetaminophen (1000 mg) was given to a third group to control for potential effects of antipyresis. Neither aspirin nor acetaminophen inhibited LPS-induced coagulation. However, LPS increased the percentage of circulating TF(+) monocytes by 2-fold. This increase was associated with a decrease in FVIIa levels, which reached a minimum of 50% 24 hours after LPS infusion. Furthermore, LPS-induced thrombin generation increased plasma levels of circulating polymerized, but not cross-linked, fibrin (ie, thrombus precursor protein), whereas levels of soluble fibrin were unaffected. In summary, a single 1000-mg dose of aspirin did not decrease LPS-induced coagulation. However, our study showed, for the first time, that LPS increases TF(+) monocytes, substantially decreases FVIIa levels, and enhances plasma levels of thrombus precursor protein, which may be a useful marker of fibrin formation in humans.

Acetaminophen↗
PubMedDate not supplied

Effect of acetylsalicylic acid on pulmonary arteriosclerosis induced by a one-year Dirofilaria immitis infection.

The ability of aspirin to block arteriosclerosis that developed in response to chronic, low-level injury to pulmonary arteries was evaluated in 21 dogs during their 1-year infection with Dirofilaria immitis. Three groups, with seven dogs in each group, were studied before and after sustained injury produced by the transplantation of 28 adult Dirofilaria immitis into each dog. Group A received no treatment and served as controls; Group B received no treatment for 6 months and then received 7 mg/kg of aspirin daily) for 6 months; Group C received 7 mg/kg of aspirin daily for the entire year. The pulmonary arterial response was evaluated by hemodynamic and arteriographic studies at 6 and 12 months and by scanning electron microscopy at the end of the 12-month study. All groups developed a similar, mild pulmonary hypertension. The arteriographic changes of dilation and flow obstruction were worse in Groups A and B than in Group C at 6 months, and at 12 months both Groups B and C were less obstructed than Group A. Scanning electron microscopy revealed large, complex myointimal proliferations in Group A, whereas the two aspirin-treated groups had smaller, less complex lesions that covered a much smaller surface area. We concluded that: 1) aspirin markedly reduced the microscopic and macroscopic arteriosclerosis in Groups B and C; 2) aspirin in Group B not only arrested further development but also permitted resolution of arteriosclerosis while the arteries were still being injured.

Angiography↗
PubMed1999

Acetylsalicylic acid reduces vegetation bacterial density, hematogenous bacterial dissemination, and frequency of embolic events in experimental Staphylococcus aureus endocarditis through antiplatelet and antibacterial effects.

BACKGROUND: Platelets are integral to cardiac vegetations that evolve in infectious endocarditis. It has been postulated that the antiplatelet aggregation effect of aspirin (ASA) might diminish vegetation evolution and embolic rates. METHODS AND RESULTS: Rabbits with Staphylococcus aureus endocarditis were given either no ASA (controls) or ASA at 4, 8, or 12 mg. kg-1. d-1 IV for 3 days beginning 1 day after infection. Vegetation weights and serial echocardiographic vegetation size, vegetation and kidney bacterial densities, and extent of renal embolization were evaluated. In addition, the effect of ASA on early S aureus adherence to sterile vegetations was assessed. In vitro, bacterial adherence to platelets, fibrin matrices, or fibrin-platelet matrices was quantified with either platelets exposed to ASA or S aureus preexposed to salicylic acid (SAL). ASA at 8 mg. kg-1. d-1 (but not at 4 or 12 mg. kg-1. d-1) was associated with substantial decreases in vegetation weight (P<0.05), echocardiographic vegetation growth (P<0.001), vegetation (P<0.05) and renal bacterial densities and renal embolic lesions (P<0.05) versus controls. Diminished aggregation resulted when platelets were preexposed to ASA or when S aureus was preexposed to SAL (P<0.05). S aureus adherence to sterile vegetations (P<0.05) or to platelets in suspension (P<0.05), fibrin matrices (P<0.05), or fibrin-platelet matrices (P<0.05) was significantly reduced when bacteria were preexposed to SAL. CONCLUSIONS: ASA reduces several principal indicators of severity and metastatic events in experimental S aureus endocarditis. These benefits involve ASA effects on both the platelet and the microbe.

Animals↗
PubMed1977

Effects of repeated ingestion of large quantities of acetylsalicylic acid on membranous bone growth and dentin apposition in young monkeys.

Four daily doses of ASA were administered by mouth to young growing monkeys which received six injections of lead acetate every seven days as an intravital stain to indicate sites of bone and dentin mineralization. Microscopic evaluation of the inhibitory effects on membranous bone growth and dentin apposition was made. Four doses of ASA at 325 mg/kg inhibited membranous bone growth as well as the remodeling of the Haversian canal systems for about 16-18 days, with incomplete recovery during the experimental period. No comparable effect on dentinogenesis was observed. This preliminary study indicates that four doses of ASA at this level caused a toxic effect directly on membranous bone growth but not on dentin apposition.

Administration, Oral↗
PubMed1994

Influence of protein malnutrition on teratogenicity of acetylsalicylic acid in rats.

The effect of protein malnutrition (PM) on the embryotoxicity and teratogenicity of aspirin in rats has been studied. Protein malnourishment was produced from Days 7 to 21 of gestation by limiting the casein content of the diet to 5% in comparison to 20% for the normal animals. Six dose levels of aspirin (50-175 mg kg-1) were administered p.o. from Days 8 to 11 of pregnancy. Aspirin from 75 mg kg-1 d-1 induced growth retardation, embryolethality and teratogenicity, as shown by external, skeletal and visceral malformations. All these effects were potentiated by protein malnutrition.

Abnormalities, Drug-Induced↗
PubMed2004

Influence of acetylsalicylic acid (aspirin) on biofilm production by Candida species.

Candida spp. are important causative agents of infections associated with biofilm formation. Management of biofilm-related infections is extremely difficult and therefore new therapeutic solutions are needed. This study for the first time explored the possible effect of aspirin on Candida spp. Biofilm-producing capacity. Two strains of C. guilliermondii, and one strain per species of C. kefyr, C. glabrata, C. albicans, and C. parapsilosis were included in the study. The antifungal property of aspirin was tested by the broth microdilution method, while effect of aspirin on biofilm formation was determined by the microtiter-plate test. The minimal inhibitory concentrations of aspirin obtained ranged from 2.17 to 8.67 mM and minimal fungicidal concentrations were from 4.33 to 8.67 mM. The concentrations of aspirin which induced statistically significant decrease in biofilm formation ranged from 0.43 mM to 1.73 mM of aspirin, depending on the tested yeast strain. Therefore, the significant effects of aspirin on growth and biofilm formation of Candida spp. were achieved only with suprapharmacological concentrations of the drug. The influence of the inoculum size on the effect of aspirin on biofilm formation was determined for C. albicans only and a significant decrease was observed also at suprapharmacological concentrations of aspirin, irrespective of the inoculum size. The results obtained in the present study show aspirin to be a drug with the potential to affect and suppress biofilm formation by Candida spp., and provide support for further investigation.

Anti-Inflammatory Agents, Non-Steroidal↗