ANTI-PLATELET ACTIVITY OF BETA-ADRENERGIC ANTAGONISTS: INHIBITION OF THROMBOXANE SYNTHESIS AND PLATELET AGGREGATION IN PATIENTS RECEIVING LONG-TERM PROPRANOLOL TREATMENT
References (16)
- et al.
Protective effect of propranolol in threatened myocardial infarction
Lancet
(1978) - et al.
Effect of propranolol on platelet function
Blood
(1977) The physiology and pharmacology of alpha- and beta-blockade
Cardiovasc Med
(1981)- et al.
Reduction by propranolol of myocardial necrosis following temporary coronary artery occlusion in dogs
Circ Res
(1973) - Wb Campbell, Ks Callahan, Ar Johnson, PD. Hirsh, Mechanism of the antiplatelet activity of the β-adrenergic...
- et al.
Thromboxanes: a new group of biologically active compounds derived from prostaglandin endoperoxides
Proc Natl Acad Sci U.S.A.
(1975) Aggregation of blood platelets by adenosine diphosphate and its reversal
Nature
(1962)
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2003, American Heart JournalCitation Excerpt :β-Blockers have antiplatelet effects that should reduce platelet aggregation and deposition on the arterial wall.23-25 They also decrease platelet production and release of thromboxane A2.9,26 β-Blockers lower heart rate, reducing mean blood velocity and shear stress on the arterial wall, reducing adverse remodeling resulting from intimal hyperplasia.23,27,28
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2003, American Journal of CardiologyCitation Excerpt :Beta blockers reduce myocardial oxygen demand,17 improve infarct zone motion, and reduce noninfarct zone motion,18 contributing to reduced infarct size and improved regional myocardial function. In experimental studies, β blockers redistribute blood flow to ischemic subendocardial regions19,20; further, β blockers inhibit platelet aggregation and thromboxane synthesis in vitro and in vivo.21,22 These properties could explain the higher incidence of spontaneous recanalization in β patients in our study, as well as their lower incidence of death from reinfarction, shock, or heart failure.
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