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Showing papers on "Blood Platelet Disorders published in 1986"


Journal ArticleDOI
TL;DR: It is concluded that platelet aggregation can be studied conveniently with the impedance method in the more physiologic medium of WB, and an increased sensitivity of the WB system to some aggregating and anti-platelet agents is shown.
Abstract: Platelet aggregation studies generally are performed in platelet-rich plasma (PRP) by the turbidometric method. The authors compared this technic with the recently introduced impedance aggregometry in PRP and whole blood (WB). In healthy controls there was a good correlation between the two technics when aggregation was induced by ADP or collagen. As compared with PRP, platelets in WB were more sensitive to the aggregating effect of thrombin, ristocetin, and arachidonic acid. Platelet sensitivity to prostacyclin was increased in WB. The anti-platelet effect of a single oral dose of aspirin could be detected for a longer period in WB than in PRP. Platelet aggregation tests in WB from patients with platelet dysfunctions showed the same response pattern to different aggregating agents as in PRP. In contrast to turbidometry, the impedance method in PRP and WB enabled registration of platelet aggregation in a dose-de-pendent fashion in a sample from a patient with severe hyper-lipoproteinemia. It is concluded that platelet aggregation can be studied conveniently with the impedance method in the more physiologic medium of WB. Providing the same information as the well-established turbidometry, the time-sparing impedance method needs less citrated blood. Moreover, our results show an increased sensitivity of the WB system to some aggregating and anti-platelet agents.

123 citations


Journal ArticleDOI
01 Jun 1986-Blood
TL;DR: The data suggest that thrombin-mediated induction of canine platelet fibrinogen receptors may proceed by pathway(s) alternate to those shared by other platelet agonists, and/or that secreted granule constituents may act synergistically withThrombin to overcome inhibition of signal-response-coupled reactions mediating the interaction of fibr inogen with its receptor.

40 citations


Journal Article
TL;DR: It is demonstrated that in each of five independent mouse models the thrombopathy of SPD is due to a platelet progenitor cell defect correctable byBone marrow transplantation, suggesting that in severe cases human SPD may be amenable to treatment by bone marrow transplants.

15 citations



Journal ArticleDOI
TL;DR: The ultrastructure of the Platelet contacts with collagen fibrils (CF) as well as the course taken by CF on the platelet surface were studied on ultrathin sections of platelets and CF, indicating that the glycoproteins IIb/IIIa-complex plays a significant role in the plateel collagen interaction.

5 citations