Inhibition And Recovery Of Prostacycun And Thromboxane A After Low-Dose Aspirin

1981 ◽  
Author(s):  
F E Preston ◽  
C A Jackson ◽  
M Greaves ◽  
C J Stoddard
Keyword(s):  
Low Dose ◽  
Thromboxane A2 ◽  
Selective Inhibition ◽  
Inhibitory Effect ◽  
Prostaglandin Synthesis ◽  
Inhibitory Effects ◽  
Dose Aspirin ◽  
Low Dose Aspirin ◽  
Prostacyclin Synthesis ◽  
Platelet Thromboxane

We have compared the inhibitory effects of low-dose aspirin (ASA) on prostaglandin synthesis by vessel walls and platelets. Two groups of volunteers have been studied. Vein biopsies were obtained from five subjects before and at various intervals after 300 or 150 mg ASA. A further group of volunteers received aspirin 40 mg daily. In this group the second vein biopsy was taken three days after commencement of the drug. Prostacyclin synthesis was assessed by a radioimmunoassay (RIA) for 6-keto PGF1α. Platelet thromboxane A2 production was examined by RIA for thromboxane B2 (TXB2) 81-100 per cent inhibition of PgI2 synthesis was apparent 2 hours after 300 or 150 mg ASA. 86 per cent inhibition was still evident at 8 hrs. Simultaneously complete inhibition of platelet TXA2 production persisted more than 24 hrs. At this dose of ASA there is no difference in the initial inhibitory effect of aspirin on platelet and vessel wall cyclooxygenase. Also, in males the prolongation of the bleeding times following ASA does not appear to be the consequence of selective inhibition of TXA2. ASA 40 mg daily produced a cumulative inhibitory effect on TXA2 synthesis. Its effect PgI2 synthesis will be compared with that obtained after a single 300 mg dose ASA.

Rapid and Selective Inhibition of Platelet Aggregation and Thromboxane Formation by Intravenous Low Dose Aspirin in Man

1993 ◽  
Vol 84 (5) ◽  
pp. 517-524 ◽  
Author(s):  
Rainer H. Böger ◽  
Stefanie M. Bode-Böger ◽  
Frank M. Gutzki ◽  
Dimitrios Tsikas ◽  
Hans-P. Weskott ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Low Dose ◽  
Thromboxane A2 ◽  
Systemic Circulation ◽  
High Dose ◽  
Dose Aspirin ◽  
Major Urinary Metabolite ◽  
Low Dose Aspirin ◽  
High Dose Aspirin ◽  
Platelet Thromboxane

1. One of the major problems in the clinical use of low dose aspirin for the prevention of vascular occlusion is that it takes about 3–5 days to become effective, a time too long for patients with unstable angina or coronary thrombolysis. Intravenous aspirin may be expected to exert a more rapid effect, but its influence on endothelial prostacyclin synthesis is uncertain. 2. In a single-blind, randomized, prospective study, we compared the effects of a single intravenous low dose (50 mg) or high dose (500 mg) of aspirin or placebo infused over a 60 min period on platelet aggregation, platelet thromboxane A2 production and whole-body prostanoid synthesis in 10 healthy male subjects by gas chromatography-tandem mass spectrometry. 3. Before the study, blood flow rates in the basilic and subclavian veins were determined by sonographic colour velocity imaging; the infusion rate for low dose aspirin was calculated to avoid biologically effective plasma levels of aspirin in the systemic circulation. 4. Platelet aggregation induced by 1 mmol/l arachidonic acid was similarly inhibited by >85% within 30 min after the start of the infusion of high dose or low dose aspirin, respectively, and remained suppressed for 24 h. Platelet thromboxane A2 release declined gradually after low dose aspirin, reaching a minimum of 93% inhibition after 60 min. High dose aspirin suppressed platelet thromboxane A2 release to below the detection limit after 10 min. 5. Urinary excretion of the major urinary metabolite of thromboxane A2 (2,3-dinor-thromboxane B2) was equally suppressed by both dosages of aspirin [no significant difference between high dose (−83.2%) and low dose (−67.4%)]. The urinary excretion of the major urinary metabolite of prostacyclin (2,3-dinor-6-keto-prostaglandin F1α) and of prostaglandin E2 was also markedly decreased, by 79.2% and 63.5%, respectively, by high dose aspirin, whereas low dose aspirin suppressed 2,3-dinor-6-keto-prostaglandin F1α excretion significantly less (−30.3%; P <0.02), and had no inhibitory effect at all on prostaglandin E2 excretion, indicating that after intravenous low dose aspirin no biologically active acetylsalicylate was present in the systemic circulation. 6. These data show that intravenous low dose aspirin can inhibit platelet aggregation and thromboxane B2 synthesis within less than 2 h while sparing systemic cyclo-oxygenase activity. Partial inhibition of prostacyclin formation seems to be an unavoidable consequence of effective inhibition of platelet cyclooxygenase by aspirin.

scholarly journals Effects of low-dose aspirin on the osseointegration process in rats

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Ana Carolina Lupepsa ◽  
Paula Vargas-Sanchez ◽  
Marcella Goetz Moro ◽  
Leomar Emanuel Almeida Mecca ◽  
Marcela Claudino ◽  
...  
Keyword(s):  
Low Dose ◽  
Inhibitory Effect ◽  
Control Group ◽  
Implant Placement ◽  
Dose Aspirin ◽  
Low Dose Aspirin ◽  
Male Wistar Rats ◽  
Bone To Implant Contact ◽  
Bone Deposition

Abstract Background Several drugs are capable of promoting changes in bone metabolism. The aim of this study was to evaluate the effect of long-term low-dose aspirin (LDA) therapy on implant osseointegration. Methods Male Wistar rats were divided into 4 groups (n = 8/group) according to oral gavage solution received prior (42 days) to the implant surgery on the tibia. The control group was treated with saline solution for 7 (CG-7) and 28 (CG-28) days. The use of low-dose aspirin was performed in AG groups (6.75 mg/kg of aspirin) for 7 (AG-7) and 28 (AG-28) days. After experimental periods, histomorphometric evaluation of bone-to-implant contact (BIC) and the bone area between threads (BABT) was performed. Results Reduced BIC values were detected in AG-7 (62.8% ± 17.1) group compared to AG-28 (91.9% ± 5.4), CG-7 (82.7% ± 15.2), and CG-28 (89.9% ± 9.7). BABT evaluation revealed lower values in AG-7 (70.9% ± 15.2) compared to AG-28 (95.4% ± 3.7) and CG-28 (87.1% ± 10.2) groups. Conclusions The treatment with low doses of aspirin promoted a discrete inhibitory effect in the early stages (7 days) of repair after implant placement, specifically in the bone deposition. However, these effects were not detected in the late stages (28 days), considering BIC and BABT parameters.

Selective inhibition of thromboxane-related platelet function by low-dose aspirin in patients after myocardial infarction

1985 ◽  
Vol 55 (5) ◽  
pp. 589-590 ◽  
Author(s):  
Raffaele De Caterina ◽  
Daniela Giannessi ◽  
Walter Bernini ◽  
Paolo Gazzetti ◽  
Claudio Michelassi ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Platelet Function ◽  
Low Dose ◽  
Selective Inhibition ◽  
Dose Aspirin ◽  
Low Dose Aspirin
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