Aspirin and Bleeding-Time

Rajah, S M; Penny, Alan F.; Kester, R. C.

doi:10.1016/s0140-6736(78)91846-9

Cited by 49 publications

(6 citation statements)

References 2 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In the present study, we examined and compared the effects of 3 antiplatelet drugs, ASA, TP and CS, on BT in 10 healthy adult male subjects using our new QBT test apparatus [10]. Administration of ASA (330 mg/day) significantly prolonged BT, corresponding to the findings of other reports [12][13][14][15], and administration of TP (300 mg/day) also prolonged BT; it has been reported to have a similar effect [16][17][18]. Although the effect of TP seems to be weaker than that of ASA, at a normal TP dose of 300 mg/d the difference between the 2 drugs was not statistically significant in our study.…”

Section: Discussionsupporting

confidence: 71%

Comparison of the Effects of Acetylsalicylic Acid, Ticlopidine and Cilostazol on Primary Hemostasis Using a Quantitative Bleeding Time Test Apparatus

Tamai

Takami²,

Nakahata³

et al. 1999

Pathophysiol Haemos Thromb

View full text Add to dashboard Cite

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 μl, p < 0.05, and from 12.5 to 19.2 μl, p < 0.01, respectively). Aspirin also increased Rmax (from 0.118 to 0.159 μl/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.

show abstract

Section: Discussionsupporting

confidence: 71%

Comparison of the Effects of Acetylsalicylic Acid, Ticlopidine and Cilostazol on Primary Hemostasis Using a Quantitative Bleeding Time Test Apparatus

Tamai

Takami²,

Nakahata³

et al. 1999

Pathophysiol Haemos Thromb

View full text Add to dashboard Cite

show abstract

“…b) In our patient series, 324 mg aspirin/day do not prolong bleeding time more than 50 mg/day. This is somewhat at variance from what seen by Rajah et &1., who observed a progressive lenghtening of bleeding time for doses up to 1 g (27). However, it should be pointed out that single doses of aspirin were used in that study, and that prolonged administration, such as ours, could conceivably result in a peak effect with much lower doses.…”

Section: Effects Of Treatments On Txb2 Generationmentioning

confidence: 57%

Equal Antiplatelet Effects of Aspirin 50 or 324 mg/Day in Patients After Acute Myocardial Infarction

et al. 1985

View full text Add to dashboard Cite

SummaryThis study explores the effects on some hematological parameters of a low-dose aspirin regimen (50 mg/day) versus a conventional aspirin treatment with reported antithrombotic efficacy (324 mg/day), in patients with acute myocardial infarction. Fifteen patients were randomized into 3 equal groups receiving 50 mg or 324 mg aspirin or placebo, daily for 21 days. Compared with placebo, bleeding time was significantly and similarly prolonged with both aspirin doses (+ 71 ± 22% and + 69 ± 20%, mean ± S.D.). Aspirin 50 mg/day suppressed arachidonate-induced platelet aggregation and secondary phase aggregation after ADP and adrenaline. Collagen aggregation was inhibited by 44 ± 15%. In no case were differences in the antiplatelet effects of the two doses observed. The effects of 50 mg/day persisted without attenuation during the observation period. Platelet thromboxane B2 generation during arachidonate-induced aggregation was inhibited by 95 ± 2 and 99 ± 1% compared to placebo group after 50 and 324 mg/day, respectively (P between doses <0.05). No change was observed with any treatment in coagulation time, prothrombin time or plasma thromboplastin time. Thus, in patients with acute myocardial infarction, the antiplatelet effects of aspirin 50 mg/day are stable over time and superimposable on those of 324 mg/day. The antithrombotic efficacy of aspirin 50 mg/day remains to be tested clinically.

show abstract

“…This dose-dependent effect has been attributed to the low dose affecting only platelets and allowing prostacyclin production to continue, while both systems are inhibited by high-dose aspirin. These results have been confirmed in human volunteers by some workers (O'Grady & Moncada, 1978;Rajah, Penny & Kester, 1978) but not by others (Godal, Eika, Dybdahl, Daae & Larsen, 1979). This discrepancy may be due to the fact that the volunteers in the study by O'Grady & were in a younger agegroup than those in the study by Godal et al (1979).…”

Section: Aspirin Haemostasis and Thrombosismentioning

confidence: 65%

Eighth Gaddum Memorial Lecture University of London Institute of Education December 1980: Biological Importance of Prostacyclin

Moncada¹

1982

British J Pharmacology

266

View full text Add to dashboard Cite

Aspirin and Bleeding-Time

Cited by 49 publications

References 2 publications

Comparison of the Effects of Acetylsalicylic Acid, Ticlopidine and Cilostazol on Primary Hemostasis Using a Quantitative Bleeding Time Test Apparatus

Comparison of the Effects of Acetylsalicylic Acid, Ticlopidine and Cilostazol on Primary Hemostasis Using a Quantitative Bleeding Time Test Apparatus

Equal Antiplatelet Effects of Aspirin 50 or 324 mg/Day in Patients After Acute Myocardial Infarction

Eighth Gaddum Memorial Lecture University of London Institute of Education December 1980: Biological Importance of Prostacyclin

Contact Info

Product

Resources

About