EFFECT OF SHEAR RATE ON PLATELET INTERACTION WITH SUBENDOTHELIUM IN CITRATED AND NATIVE BLOOD .1. SHEAR RATE-DEPENDENT DECREASE OF ADHESION IN VON WILLEBRANDS DISEASE AND BERNARD-SOULIER SYNDROME

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  • 1 January 1978
    • journal article
    • research article
    • Vol. 92  (5) , 750-764
Abstract
Previous studies demonstrated impaired adhesion of platelets to the subendothelium in von Willebrand''s disease. These studies were performed by circulating (in a closed system) citrated whole blood through a chamber containing everted segments of rabbit aorta from which the endothelium had been removed by balloon catheter. The average wall shear rate was 800 s-1 and the perfusion time was 10 min. In the present study the interaction of platelets with subendothelium in native (nonanticoagulated) blood was measured, using a recently described technique where the vessel segments are perfused with directly sampled venous blood. The system was open, i.e., the blood was not recirculated. Blood flow rates of 20, 40 and 50 ml/min were used, which correspond to calculated shear rates of 1300, 2600 and 3300 s-1 and perfusion times of 3, 2 and 2 min, respectively. For comparison, parallel studies at 1300 s-1 were also obtained with citrated blood. In normal subjects, at a shear rate of 1300 s-1, platelet adhesion was less in native blood than in citrated blood, but thrombus formation was greater. Platelet adhesion in 5 patients with von Willebrand''s disease was decreased in both citrated and native blood. The magnitude of the adhesion defect was strongly dependent on the shear rate. In citrated blood studied at a shear rate of 1300 s-1, adhesion was 75% less than in normal subjects, whereas in previous studies at 800 s-1 the reduction in adhesion was 29%. In native blood, adhesion in von Willebrand''s disease was normal at a shear rate of 1300 s-1, whereas 53% and 77% reductions in adhesion were obtained at shear rates of 2600 and 3300 s-1, respectively. The latter shear rates are within the range of those that exist in the microvasculature. At all shear rates studied, adhesion of platelets in native blood was also decreased in the Bernard-Soulier syndrome but was normal in hemophilia and afibrinogenemia. The findings with native blood provide further evidence that impaired adhesion of platelets to the vessel wall accounts for the hemostatic defect in von Willebrand''s disease. This adhesion defect was shear rate-dependent.