Thromb Haemost 1977; 37(01): 017-028
DOI: 10.1055/s-0038-1649197
Original Article
Schattauer GmbH

Platelet Interaction with Collagen Fibrils in Flowing Blood

II. Impaired Adhesion-Aggregation in Bleeding Disorders. A Comparison with Subendothelium
Hans R. Baumgartner
1  Pharmaceutical Research Department F. Hoffmann-La Roche and Co., Ltd. CH-4002 Basel, Switzerland
2  Department of Medicine (Division of Hematology) Roosevelt Hospital and Columbia University College of Physicians and Surgeons, New York City, U.S.A.
,
Thomas B. Tschopp
1  Pharmaceutical Research Department F. Hoffmann-La Roche and Co., Ltd. CH-4002 Basel, Switzerland
2  Department of Medicine (Division of Hematology) Roosevelt Hospital and Columbia University College of Physicians and Surgeons, New York City, U.S.A.
,
Harvey J. Weiss
1  Pharmaceutical Research Department F. Hoffmann-La Roche and Co., Ltd. CH-4002 Basel, Switzerland
2  Department of Medicine (Division of Hematology) Roosevelt Hospital and Columbia University College of Physicians and Surgeons, New York City, U.S.A.
› Author Affiliations
Further Information

Publication History

Received 18 June 1976

Accepted 24 July 1976

Publication Date:
03 July 2018 (online)

Summary

Anticoagulated whole blood from patients and control subjects was circulated through an annular perfusion chamber in which the fibrillar collagen of α chymotrypsin-digested subendothelium and intact subendothelium were exposed. The blood flow conditions corresponded to those in arteries (830 sec–1 wall shear rate). Platelet surface interaction was measured mor-phometrically.

Decreased adhesion to fibrillar collagen associated with normal spreading and normal adhesion-induced formation of platelet thrombi was found with blood of patients with von Willebrand’s disease and the Bernard Soulier Syndrome, indicating a defect in the initial attachment reaction of platelets with collagen. Platelets of patients with thrombasthenia did normally adhere to the collagen fibrils and also lost their subcellular organelles during this reaction, but they totally failed to adhere to each other. In storage pool disease platelet thrombus formation was consistently inhibited whereas adhesion and spreading was inhibited in some patients and normal in others. In contrast adhesion was always normal after ingestion of aspirin which consistently caused a marked inhibition of platelet thrombi. These findings correspond – in essence – to those previously described on intact subendothelium. However, the observed defects are more pronounced on the fibrillar collagen than on intact subendothelium.