Endogenous Inhibitory Mechanisms and the Regulation of Platelet Function

2011 ◽  
pp. 341-366 ◽  
Author(s):  
Chris I. Jones ◽  
Natasha E. Barrett ◽  
Leonardo A. Moraes ◽  
Jonathan M. Gibbins ◽  
Denise E. Jackson
Keyword(s):  
Platelet Function ◽  
Inhibitory Mechanisms

scholarly journals Receptor-mediated inhibitory mechanisms and the regulation of platelet function

2015 ◽  
Vol 58 (12) ◽  
pp. 1299-1301
Author(s):  
ZhiPeng Cheng ◽  
JunLing Liu
Keyword(s):  
Platelet Function ◽  
Inhibitory Mechanisms

Evaluation of platelet dense granules for determining storage pool deficiencies by HVEM image and quantitative analysis

1996 ◽  
Vol 54 ◽  
pp. 770-771
Author(s):  
W.T. Gunning ◽  
J.N. Turner ◽  
K. Buttle ◽  
E.P. Calomeni ◽  
N.A. Lachant ◽  
...  
Keyword(s):  
Quantitative Analysis ◽  
Platelet Function ◽  
Electron Microscopic ◽  
Von Willebrand's Disease ◽  
Dense Granules ◽  
Storage Pool ◽  
Prolonged Bleeding ◽  
Microscopic Evaluation ◽  
Storage Pools ◽  
Electron Lucent

There are a variety of conditions which have been associated with prolonged bleeding times. If other etiologies including von Willebrand's disease have been ruled out, a platelet function disorder must be considered. The best, if not only, technique to make this diagnosis is the electron microscopic evaluation of whole air dried platelets. Bull first described the presence of dense granules in whole platelets in 1968 and the technique has been utilized extensively The electron dense or delta granules are easily distinguished from the larger more numerous alpha granules which are electron lucent. The significance of the dense granules is that they are known to be “storage pools” of serotonin, calcium, adenosine di- and triphosphate, and pyrophosphate. Prolonged bleeding times may be directly related to an insufficiency of these substances. The diagnosis of a storage pool deficiency is made when either the storage content of the dense granules is abnormal or their number is diminished. We observe normal platelets to have 4-6 dense granules, which agrees with the literature.

Influence of platelet function on long-term LV performance in myocardial infarction treated with primary angioplasty

2008 ◽  
Vol 7 ◽  
pp. 126-126
Author(s):  
Z HUCZEK ◽  
K FILIPIAK ◽  
J KOCHMAN ◽  
R PIATKOWSKI ◽  
M ROIK ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Platelet Function ◽  
Primary Angioplasty

Uremic toxins and platelet function

1970 ◽  
Vol 126 (5) ◽  
pp. 823-826 ◽  
Author(s):  
H. I. Horowitz
Keyword(s):  
Platelet Function ◽  
Uremic Toxins

“Aspirin - resistance”? A few critical considerations on definition, terminology, diagnosis, clinical value, natural course of atherosclerotic disease, and therapeutic consequences

VASA ◽  
2011 ◽  
Vol 40 (6) ◽  
pp. 429-438 ◽  
Author(s):  
Berent ◽  
Sinzinger
Keyword(s):  
Platelet Function ◽  
Point Of Care ◽  
Aspirin Resistance ◽  
Point Of View ◽  
Evidence Based ◽  
Platelet Function Tests ◽  
Clinical Value ◽  
Vascular Events ◽  
Therapeutic Consequences ◽  
Function Tests

Based upon various platelet function tests and the fact that patients experience vascular events despite taking acetylsalicylic acid (ASA or aspirin), it has been suggested that patients may become resistant to the action of this pharmacological compound. However, the term “aspirin resistance” was created almost two decades ago but is still not defined. Platelet function tests are not standardized, providing conflicting information and cut-off values are arbitrarily set. Intertest comparison reveals low agreement. Even point of care tests have been introduced before appropriate validation. Inflammation may activate platelets, co-medication(s) may interfere significantly with aspirin action on platelets. Platelet function and Cox-inhibition are only some of the effects of aspirin on haemostatic regulation. One single test is not reliable to identify an altered response. Therefore, it may be more appropriate to speak about “treatment failure” to aspirin therapy than using the term “aspirin resistance”. There is no evidence based justification from either the laboratory or the clinical point of view for platelet function testing in patients taking aspirin as well as from an economic standpoint. Until evidence based data from controlled studies will be available the term “aspirin resistance” should not be further used. A more robust monitoring of factors resulting in cardiovascular events such as inflammation is recommended.

Effect of Heparin on Platelet Function

1975 ◽  
Vol 33 (01) ◽  
pp. 063-065 ◽  
Author(s):  
Marjorie B Zucker
Keyword(s):  
Platelet Function

Does Increased Platelet Release Normalize During Anti-Hypertensive Treatment?

1987 ◽  
Vol 58 (03) ◽  
pp. 834-838
Author(s):  
Knut Lande ◽  
Sverre Erik Kjeldsen ◽  
Ivar Eide ◽  
Paul Leren ◽  
Knut Gjesdal
Keyword(s):  
Platelet Function ◽  
Adrenergic Receptor ◽  
Blood Platelet ◽  
Placebo Treatment ◽  
Sampling Procedure ◽  
Β Blocker ◽  
Platelet Release ◽  
Hypertensive Drug ◽  
Second Period ◽  
Release Product

SummaryBlood platelet function was evaluated in 10 men, all 50 years old, with untreated, mild hypertension. Each patient was examined four times: At the beginning of the study, after 5 weeks on placebo treatment, after the following 5 weeks on propranolol 160 mg daily, and finally after a second period of 5 weeks on placebo. At baseline the plasma level of the platelet release product (β-thromboglobulin (BTG) was 41.6 (30.5-57.0) μg/l (median and 95% confidence interval). During the first placebo period BTG was normalized to 21.0 (14.1-25.9) μg/l. While systolic blood pressure and heart rate fell during β-adrenergic receptor blockade, BTG remained unchanged throughout the rest of the observation periods. Platelet size increased significantly during treatment with β-blocker. The present study indicates that the normalization of elevated platelet function which previously has been reported to occur during anti-hypertensive drug therapy, may be explained by patient adaptation to the blood sampling procedure.

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