Jon M. Gerrard

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Alpha-adrenergic agonists that promote platelet aggregation were found to reduce ferric heme to ferrous heme. Agents that bind iron in heme inhibited epinephrine-induced platelet aggregation. It is proposed that epinephrine first binds to its receptor and then reduces an adjacent heme group to transmit its agonist stimulus.
Unactivated platelets contain about 69% G actin and less than 10% of the contractile proteins in a cytoskeletal core resistant to extraction with 1% Triton X-100. Activation by thrombin leads, within 1 min, to the formation of pseudopodia and contractile gels, accompanied by the reduction of the G-actin content to about 22% and the development of(More)
We explored the retraction or contraction of platelet-fibrin clots under isometric conditions. In the presence of micromolar calcium clots of normal platelet-rich plasma developed tension at an initial rate of 0.1 to 0.2 g/min per cm2 (initial cross-sectional area). Electron microscopy of clots fixed after attaining a force of 1.6 g/cm2 revealed platelets(More)
Inhibition of human platelet aggregation by N,N-diethyl-2-[4-(phenylmethyl)phenoxy]ethanamine-HCl (DPPE), a novel antagonist of histamine binding, suggested that histamine might serve a critical role in cell function. Phorbol-12-myristate-13-acetate (PMA) or collagen was found to increase platelet histamine content in parallel with promotion of aggregation.(More)
Concanavalin A (Con A) has been used to activate platelets, inducing a specific interaction between the glycoprotein IIb-IIIa complex and the cytoskeleton of the activated platelet. In agreement with this, we have shown that Con A activates human platelets, initiating phosphorylation, secretion, and cytoskeletal formation. Con A and cytochalasin B were used(More)
Washed platelets activated by alpha-thrombin, gamma-thrombin, thrombocytin or the ionophore A23187 (ref. 3) lose their disk shape, produce pseudopodia and become cohesive. This cohesiveness is accompanied by the expression of an endogeneous haemagglutinin which, although apparently bound to the platelet membrane, is dependent on cell secretion. The(More)
To evaluate the effect of 1-deamino-8-D-arginine vasopressin (DDAVP) in various bleeding disorders, 10 micrograms/m2 DDAVP was administered to subjects with von Willebrand disease (13), platelet function defects (12), von Willebrand disease and platelet defects together (8), or isolated prolongation of the bleeding time (5). DDAVP shortened the bleeding(More)