LOW DOSE ASPIRIN INHIBITS PLATELET AGGREGATION AS WELL AS HIGH DOSE

InPharma ◽  
1980 ◽  
Vol 245 (1) ◽  
pp. 13-13
Keyword(s):  
Platelet Aggregation ◽  
Low Dose ◽  
High Dose ◽  
Dose Aspirin ◽  
Low Dose Aspirin

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 Dose-dependent roles of aspirin and other non-steroidal anti-inflammatory drugs in abnormal bone remodeling and skeletal regeneration

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Yong Xie ◽  
Meng Pan ◽  
Yanpan Gao ◽  
Licheng Zhang ◽  
Wei Ge ◽  
...  
Keyword(s):  
Bone Formation ◽  
Bone Remodeling ◽  
Low Dose ◽  
High Dose ◽  
Dose Aspirin ◽  
Low Dose Aspirin ◽  
Inflammatory Drugs ◽  
Anti Inflammatory ◽  
Dose Dependent ◽  
High Dose Aspirin

AbstractThe failure of remodeling process that constantly regenerates effete, aged bone is highly associated with bone nonunion and degenerative bone diseases. Numerous studies have demonstrated that aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs) activate cytokines and mediators on osteoclasts, osteoblasts and their constituent progenitor cells located around the remodeling area. These cells contribute to a complex metabolic scenario, resulting in degradative or synthetic functions for bone mineral tissues. The spatiotemporal effects of aspirin and NSAIDs in the bone remodeling are controversial according the specific therapeutic doses used for different clinical conditions. Herein, we review in vitro, in vivo, and clinical studies on the dose-dependent roles of aspirin and NSAIDs in bone remodeling. Our results show that low-dose aspirin (< 100 μg/mL), which is widely recommended for prevention of thrombosis, is very likely to be benefit for maintaining bone mass and qualities by activation of osteoblastic bone formation and inhibition of osteoclast activities via cyclooxygenase-independent manner. While, the roles of high-dose aspirin (150–300 μg/mL) and other NSAIDs in bone self-regeneration and fracture-healing process are difficult to elucidate owing to their dual effects on osteoclast activity and bone formation of osteoblast. In conclusion, this study highlighted the potential clinical applications of low-dose aspirin in abnormal bone remodeling as well as the risks of high-dose aspirin and other NSAIDs for relieving pain and anti-inflammation in fractures and orthopedic operations.

scholarly journals What dose of aspirin should be used in the initial treatment of Kawasaki disease? A meta-analysis

Rheumatology ◽  
2020 ◽  
Vol 59 (8) ◽  
pp. 1826-1833
Author(s):  
Xinyi Jia ◽  
Xiao Du ◽  
Shuxian Bie ◽  
Xiaobing Li ◽  
Yunguang Bao ◽  
...  
Keyword(s):  
Kawasaki Disease ◽  
Random Effects ◽  
Initial Treatment ◽  
Low Dose ◽  
Cochrane Library ◽  
High Dose ◽  
Random Effects Model ◽  
Dose Aspirin ◽  
Low Dose Aspirin ◽  
High Dose Aspirin

Abstract Objective The use of IVIG plus high- or low-dose aspirin for the initial treatment of Kawasaki disease remains controversial. The aim of this study was to evaluate the efficacy of IVIG plus high-dose aspirin compared with IVIG plus low-dose aspirin in the treatment of Kawasaki disease. Methods Studies related to aspirin therapy for Kawasaki disease were selected by searching the databases of Medline (PubMed), Embase and the Cochrane Library before March 2019. Statistical analyses were performed by using a Review Manager Software package and STATA v.15.1. Results Eight retrospective cohort studies, characterizing 12 176 patients, were analysed. Overall, no significant difference was found in the incidence of coronary artery abnormalities between the high- and low-dose aspirin groups [relative risk (RR) 1.15; 95% CI: 0.93, 1.43; P = 0.19; random-effects model]. The patients treated with high-dose aspirin had slightly faster resolution of fever [mean difference (MD) −0.30; 95% CI: −0.58, −0.02; P = 0.04; random-effects model]. but the rates of IVIG resistance (RR, 1.26; 95% CI: 0.55, 2.92; P = 0.59; random-effects model) and days in hospital (MD, 0.22; 95% CI: −0.93, 1.37; P = 0.71; random-effects model) were similar between the two groups. Conclusion Low-dose aspirin plus IVIG might be as effective as high-dose aspirin plus IVIG for the initial treatment of Kawasaki disease. Considering that high-dose aspirin may cause more adverse reactions than low-dose aspirin, low-dose aspirin plus IVIG should be recommended as the first-line therapy in the initial treatment of Kawasaki disease.

Modification of the Outcome of Coronary Thrombo-Embolism by Low and High-Dose Aspirin

1979 ◽  
Author(s):  
S. Moore ◽  
L.W. Belbeck ◽  
S.A. Pineau
Keyword(s):  
Low Dose ◽  
Myocardial Damage ◽  
High Dose ◽  
Aluminum Wire ◽  
Ischaemic Damage ◽  
Dose Aspirin ◽  
Low Dose Aspirin ◽  
Group 3 ◽  
High Dose Aspirin ◽  
Heart Foundation

Previous work in this laboratory has shown that an occlusive thrombus (O.T.) induced. the left anterior descending coronary artery (L.A.D.) of dogs, by the placement of a segment of magnesium-aluminum wire (M.A.W.) in the lumen of the artery, is associated with the development of full thickness infarct (F.T.I.). Incomplete (mural) thrombus is associated with focal areas of ischaemic damage, mainly sub-endocardial, in the myocardium of the antero-lateral left ventricle. A 1.0 cm. length of M.A.W., shaped in the form of a tennis racquet, was placed by cardiac catheterization in the proximal L.A.D. of 30 mongrel dogs. Ten dogs received low dose aspirin (L.D.A.); (14 or 29 mgm/Kg daily in a single dose). Ten dogs received high dose aspirin (H.D.A.); (100 mgm/Kg daily in divided doses). Treatment was begun one day before operation and continued until death or killing. Ten control dogs received no drug. All control dogs died within 3 days of operation. Five had O.T. and F.T.I. The remainder showed focal ischaemic myocardial damage. None of the L.D.A. group died. At autopsy 3 or 4 days after operation, none had O.T. or F.T.I. In the H.D.A. group 3 died; 4 had O.T. and F.T.I. Thus L.D.A. provided significant protection from death, O.T., and F.T.I. H.D.A. provided some (P <0.005) but less protection from death but did not significantly affect the incidence of O.T. or F.T.I. Supported by Ontario Heart Foundation Grant T15-7.

Effects of low-dose aspirin on in vitro platelet aggregation in the early minutes after ingestion in normal subjects

1994 ◽  
Vol 74 (7) ◽  
pp. 720-723 ◽  
Author(s):  
Salim F. Dabaghi ◽  
Suraj G. Kamat ◽  
John Payne ◽  
Gary F. Marks ◽  
Robert Roberts ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Low Dose ◽  
Normal Subjects ◽  
Dose Aspirin ◽  
Low Dose Aspirin

Comparison of High-Dose With Low-Dose Aspirin in Patients With Mechanical Heart Valve Replacement Treated With Oral Anticoagulant

Circulation ◽  
1996 ◽  
Vol 94 (9) ◽  
pp. 2113-2116 ◽  
Author(s):  
Rau´l Altman ◽  
Jorge Rouvier ◽  
Enrique Gurfinkel ◽  
Alejandra Scazziota ◽  
Alexander G.G. Turpie
Keyword(s):  
Valve Replacement ◽  
Heart Valve ◽  
Oral Anticoagulant ◽  
Low Dose ◽  
Mechanical Heart Valve ◽  
Heart Valve Replacement ◽  
High Dose ◽  
Dose Aspirin ◽  
Low Dose Aspirin

Effects of Combining Aspirin with Non-Steroidal Anti-Inflammatory Drugs or COX-2 Inhibitors on Shear-Induced Platelet Aggregation.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 1853-1853
Author(s):  
Angela Bergeron ◽  
Carol Sun ◽  
Jennifer Wood ◽  
Jo Ellen Schweinle ◽  
Frank L. Lanza ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Naproxen Sodium ◽  
Low Dose ◽  
Closure Time ◽  
Dose Aspirin ◽  
Low Dose Aspirin ◽  
Inflammatory Drugs ◽  
The Mean ◽  
Cox 2 ◽  
Cox 2 Inhibitors

Abstract Aspirin has been widely used as a cardiac protective drug, often with hemostasis inhibition and bleeding risks. This concern becomes even more significant when it is used in combination with non-steroidal anti-inflammatory drugs (NSAIDs) or COX-2 inhibitors, both of which may have independent effects on platelets. To study how hemostasis may be affected by these drugs, we conducted a multiple-dose, single-blind, parallel-group study to determine the effects of aspirin combined with over-the-counter NSAIDs or COX-2 inhibitors on shear-induced platelet aggregation (SIPA). For this study, 87 healthy individuals (age 40 to 75) who met inclusion and exclusion criteria were recruited. All subjects received 81 mg of aspirin (non-enteric coated and chewable) daily for eight days. In addition, beginning 2 hours after low-dose aspirin, the subjects also received one of the following drugs: acetaminophen (4 doses of 1000 mg daily), ibuprofen (3 doses of 400 mg daily), naproxen sodium (440 mg morning and 220 mg evening), additional aspirin (4 doses of 650 mg daily), celecoxib (2 doses of 200 mg daily) and rofecoxib (1 dose of 25 mg daily). The second drugs were given 2 hrs after initial aspirin intake. The control group received only 81 mg of aspirin. Blood was drawn before the treatment and at 24 hr and 7 days (before any medications on Day 8) after the initial drug intake. Shear-induced platelet aggregation (SIPA) on a collagen matrix with either ADP or epinephrine was measured in citrated whole blood using a platelet function analyzer. The aggregation was defined as closure time (sec) under a constant shear rate of 1500 −s, a level of pathological high shear stress. We found that the closure time with the collagen/ADP cartridge was not affected by any of the treatments (83 – 108 sec). In contrast, SIPA with the collagen/epinephrine cartridge showed a time-dependent inhibition by 81 mg of aspirin with the mean closure times being 118, 138, and 222 sec before drug administration, 24 hr and 7 day after treatments, respectively. The course of low-dose aspirin inhibition of SIPA was not changed by acetaminophen, celecoxib, or rofecoxib. In contrast, the mean closure time at 24 hr after the treatment was 249 and 264 sec for samples from individuals on a combined treatment of low-dose aspirin with either naproxen sodium or a high dose of aspirin (2600 mg), significantly longer than those of other treatment groups (P< 0.001). It has been demonstrated that SIPA, which is primarily initiated by the GP Ib-VWF interaction, is insensitive to aspirin. Our results suggest that aspirin inhibits SIPA induced in the presence of collagen and epinephrine, but not collagen and ADP. Furthermore, this effect was significantly enhanced by either naproxen sodium or a higher dose of aspirin (2600 mg), suggesting that the simultaneous intake of low-dose aspirin and either analgesic doses of aspirin or naproxen may enhance the risk of aspirin-induced bleeding tendency.

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