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The hemostatic system in children undergoing intensive plasma exchange.
TLDR
There is increased potential for thrombosis in patients undergoing intensive plasmapheresis, despite the depletion of coagulation factors, according to the ability of the synthetic mechanisms in children to replenish hemostatic factors rapidly.
Platelet‐activating factor is a weak platelet agonist: Evidence from normal human platelets and platelets with congenital secretion defects
TLDR
The studies indicate that PAF is a weak platelet agonist, which is dependent on secreted ADP and thromboxane A2 synthesis, and occurs by mechanisms common to a number of agonists.
Differential requirements for platelet aggregation and inhibition of adenylate cyclase by epinephrine. Studies of a familial platelet alpha 2-adrenergic receptor defect
We describe a family whose members have impaired platelet aggregation and secretion responses to epinephrine with normal responses to adenosine diphosphate and collagen. Platelet alpha 2-adrenergic
Inhibition of platelet function by contrast media: iopamidol and ioxaglate versus iothalamate. Work in progress.
TLDR
It is indicated that the newer agents inhibit platelet function less than iothalamate does, and that chelation of Ca2+ may not be the major mechanism of platelet inhibition by contrast agents.
Platelet secretion defect associated with impaired liberation of arachidonic acid and normal myosin light chain phosphorylation.
TLDR
Four patients with impaired platelet aggregation and 14C-serotonin secretion during stimulation with adenosine diphosphate, epinephrine, collagen, and platelet-activating factor are described, exemplify a congenital defect, other than deficiencies of cyclooxygenase and thromboxane synthetase, by which throm boxane production may be impaired in platelets.
Inhibition of thromboxane A2 synthesis in human platelets by coagulation factor Xa.
TLDR
The results indicate that factor Xa binding to platelets through factor Va not only stimulates thrombin formation but also has a countervailing effect by inhibiting TXA2 formation.
A major role of ADP in thromboxane transfer experiments: studies in patients with platelet secretion defects.
TLDR
It is found optimum dense granule secretion to be dependent on the presence of an intact cyclooxygenase pathway in the recipient platelets and on close cell contact, suggesting that thromboxane A2 may not be as strong an agonist (direct inducer of secretion) as generally considered.
Comparative antithrombotic activities of the phosphodiesterase inhibitors pelrinone (AY-26,768), AY-31,390 and milrinone.
TLDR
Pelrinone, milrinone to a greater extent, and AY-31,390 to the greatest extent were effective inhibitors of white thrombus formation in the in vivo rabbit arteriovenous shunt model and these agents would be expected to be efficacious therapeutic antithrombotics.
Differential requirements for platelet aggregation and inhibition of adenylate cyclase by epinephrine. Studies of a familial platelet alpha 2-adrenergic receptor defect.
TLDR
These patients with an inherited receptor defect provide evidence that fewer platelet alpha 2-adrenergic receptors are required for epinephrine-induced inhibition of adenylate cyclase than for aggregation.
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