Exposure of blood to biomaterial surfaces liberates substances that activate polymorphonuclear granulocytes.

Human whole blood, anticoagulated or not, was exposed to hydrophilic glass surfaces or methylated hydrophobic glass surfaces under saline cover. Platelet-poor plasma or serum was prepared after 10 minutes of exposure, measured in respect to complement activation, and transferred to a suspension of granulocytes, which acted as bioprobes. The granulocytes were prepared from blood, anticoagulated with ethylenediaminetetraacetic acid, and evaluated regarding intracellular Ca2+ concentration (Calcium Green-1 fluorescence), integrin expression (CD-11b immunohistochemistry), respiratory burst (chemiluminescence), and priming (increase in N-formyl-methionyl-leucyl-phenylalanine-induced respiratory burst). The results indicate that humoral factors formed during the surface exposure of blood were able to activate the probe granulocytes. The exposure to hydrophilic surfaces led to a calcium transient three times the magnitude of that of hydrophobic surfaces. This response could be blocked by the presence of heparin during the blood-surface exposure but was not affected by the addition of heparin to the probe granulocytes. Hirudin, a specific thrombin blocker, had no effect. The exposure to hydrophobic surfaces led to complement activation in serum that induced priming and respiratory burst of the probe granulocytes. In conclusion, the study provides evidence that hydrophilic-hydrophobic surface treatment significantly affects the immediate inflammatory response of a blood-biomaterial interaction that is moderated by the presence of heparin.