Alterations of fibronectin and reticuloendothelial phagocytic function during adaptation to experimental shock.

Fibronectin is a large molecular weight glycoprotein that participates in opsonization as well as in adhesive structural tissue support. The effect of repetitive low grade traumatic shock on circulating fibronectin, opsonic activity, and RES phagocytic function was studied in rats during the process of adaptation to trauma. Enhanced hepatic Kupffer cell phagocytic activity was observed in rats that were resistant to trauma. During the adaptation process, serum fibronectin levels, as measured by immunoassay, were altered markedly and manifested a pattern of acute deficiency early post-trauma followed by rebound and sustained elevation of fibronectin greatly in excess of control levels. At the time adaptation to trauma was achieved, the circulating fibronectin was within the normal range. In an in vitro system, livers from adapted rats exhibited increased phagocytic ability. The data suggest that Kupffer cell activation occurs during the development of adaptation to trauma and that increased hepatic RE activity accounts for the overall increase in RES clearance seen in the trauma-adapted animals. Since repetitive low grade trauma, which can lead to adaptation, will cause immunoreactive opsonic fibronectin levels to become substantially higher than normal throughout much of the duration of the adaptation protocol, it is possible that this excessive circulating fibronectin represents a means by which local conditioning of blood vessels to trauma may be achieved. Most likely, this would be due to incorporation of the circulating fibronectin into the insoluble tissue fibronectin pool, which has been recently shown to take place. The findings suggest that RES function and fibronectin may be factors influencing trauma tolerance.