Epinephrine platelets

Prolonged use of nitroprusside may lead to hypothyroidism because of interference with the iodine uptake of the thyroid (147 ). Nitroprusside is both in vivo and in vitro a potent inhibitor of platelet function. In the presence of nitroprusside, platelets show blockage of ADP and serotonin release and inhibition of aggregation in response to ADP, collagen and epinephrine. Platelets from patients receiving nitroprusside also... 

Platelet Inhibition Ginger extract has been found to inhibit platelet aggregation induced by arachidonic acid, epinephrine, ADP, and collagen (Srivastava 1984). The extract s ability to inhibit cyclooxygenase activity and thromboxane levels correlated well with inhibition of platelet aggregation (Srivastava 1984 Mustafa et al. 1993). The type of preparation used also affects platelet inhibition, because roasted and charcoal of ginger were effective, while ether extracts of raw and dried ginger were not (Wu et al. 1993). 

Platelets can be activated by a variety of agents including the physiologic agonists ADP, thromboxane A2, epinephrine, collagen, and thrombin. Platelet activation is generally associated with a change in platelet shape (except for epinephrine-induced platelet activation) from discs to spiny spheres with pseudopodia. Platelet pseudopod formation is dependent on actin polymerization in the activated platelets. The interaction of actin filaments with myosin, mediated by calcium (9), facilitates platelet contractile activity (e.g., clot retraction). 

Similar to findings in animal models of early-life stress, elevated 24-hour urinary NE, epinephrine (E), and dopamine (DA) excretion as well as decreased platelet adrenergic receptors have been measured in abused children with PTSD (Perry, 1994 DeBellis et al., 1999a). Abused children with PTSD also exhibit... 

MAOIs act by mitigating the actions of monoamine oxidase in the neuron and increasing monoamine content. There are two forms of monoamine oxidase. MAO-A is present in both dopamine and norepinephrine neurons and is found primarily in the brain, gut, placenta, and liver its primary substrates are norepinephrine, epinephrine, and serotonin. MAO-B is found primarily in serotonergic and histaminergic neurons and is distributed in the brain, liver, and platelets. MAO-B acts primarily on tyramine, phenylethylamine, and benzylamine. Both MAO-A and -B metabolize tryptamine and dopamine. 

Binding to aggregin is required for epinephrine-induced platelet aggregation to take place. In turn, epinephrine increases the affinity of ADP for its receptor. Thrombin stimulates platelet aggregation independent of ADP, but by raising the level of calcium in the cytoplasm, it activates platelet calpain, which in turn cleaves aggregin (Figure 4.1). 

The mildness of this defect is supported by the fact that very modest hemostatic defects are noted in patients with diseases involving deficiencies of platelet COX and thromboxane synthase—eg, these patients have no history of increased or decreased bleeding. Blockade of either of these two enzymes inhibits secondary aggregation of platelets induced by ADP, by low concentrations of thrombin and collagen, or by epinephrine. Thus, these platelet enzymes are not necessary for platelet function but may amplify an aggregating stimulus. 

BennetJS, Vilaire G. Exposure of platelet fibrinogen receptors by ADPand epinephrine. J Clin Invest 1979 64(5) 1393-1401. 

Many platelet agonists, such as ADF) TXA2, epinephrine, serotonin, and thrombin, interact with specific transmembrane receptors that are coupled to G-proteins, initiating several signaling pathways that lead to PLC activation ending in platelets shape change and granule secretion (Fig. 4). 

Epinephrine activates platelets through the a-adrenergic receptor coupled to a G-protein receptor, It is proposed that this agonist shares with ADP the P2Y 2 receptor signaling (16). 

Abbreviations-. AA, arachidonic acid AMI, acute myocardial infarction AR, aspirin resistance ASA, aspirin CABG, coronary artery bypass graft surgery CAD, coronary artery disease CK-MB, creatinine kinase-MB CVA, cerebrovascular accident EPI, epinephrine HS, healthy subjects LTA, light transmittance aggregometry mm, millimolar PAR, platelet activity ratio PCI, percutaneous coronary intervention PR, platelet reactivity RPFA, rapid platelet function analyzer TXA2, thromboxane A2. 

Folts JD, Rowe GG (1988) Epinephrine reverses aspirin inhibition of in vivo platelet thrombus formation in stenosed dog coronary arteries. Thromb Res 50 507-516... 

Mice are viable, fertile, appear normal do not suffer spontaneous bleeding or thrombosis have normal tail bleeding time. Platelets fail to aggregate irreversibly to ADP, collagen, or U 46619. Arterial and venous thrombosis is inhibited and mice are protected from fatal thromboembolism after injection of collagen plus epinephrine (Angelillo-Scherrer et al. 2001). 

Impaired platelet aggregation to epinephrine resistance to fatal thromboembolism exaggerated response to cocaine, reduced effect of morphine and antidepressant drugs (Yang et al. 2000). 

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