EXPOSURE OF BLOOD TO BIOMATERIAL SURFACES LIBERATES SUBSTANCES THAT ACTIVATE POLYMORPHONUCLEAR GRANULOCYTES

Human whole blood, anticoagulated or not, was exposed to hydrophilic g lass surfaces or methylated hydrophobic glass surfaces under saline co ver. Platelet-poor plasma or serum was prepared after 10 minutes of ex posure, measured in respect to complement activation, and transferred to a suspension of granulocytes, which acted as bioprobes. The granulo cytes were prepared from blood, anticoagulated with ethylenediaminetet raacetic acid, and evaluated regarding intracellular Ca2+ concentratio n (Calcium Green-1 fluorescence), integrin expression (CD-11b immunohi stochemistry), respiratory burst (chemiluminescence), and priming (inc rease in N-formyl-methionyl-leucyl-phenylalanine-induced respiratory b urst). The results indicate that humoral factors formed during the sur face exposure of blood were able to activate the probe granulocytes. T he exposure to hydrophilic surfaces led to a calcium transient three t imes the magnitude of that of hydrophobic surfaces. This response coul d be blocked by the presence of heparin during the blood-surface expos ure but was not affected by the addition of heparin to the probe granu locytes. Hirudin, a specific thrombin blocker, had no effect. The expo sure to hydrophobic surfaces led to complement activation in serum tha t induced priming and respiratory burst of the probe granulocytes. In conclusion, the study provides evidence that hydrophilic-hydrophobic s urface treatment significantly affects the immediate inflammatory resp onse of a blood-biomaterial interaction that is moderated by the prese nce of heparin.