INVITRO STUDIES ON PMN-INDEPENDENT ENDOTHELIAL-CELL DAMAGE IN TRAUMA - DECREASE OF PMN-ENDOTHELIAL CELL ADHERENCE BY FIBRINOGEN DEGRADATIONPRODUCTS AND DISTURBANCE OF ENDOTHELIAL-CELL MEMBRANE INTEGRITY BY TRAUMA SERUM
P. Vogel et al., INVITRO STUDIES ON PMN-INDEPENDENT ENDOTHELIAL-CELL DAMAGE IN TRAUMA - DECREASE OF PMN-ENDOTHELIAL CELL ADHERENCE BY FIBRINOGEN DEGRADATIONPRODUCTS AND DISTURBANCE OF ENDOTHELIAL-CELL MEMBRANE INTEGRITY BY TRAUMA SERUM, European surgical research, 25(2), 1993, pp. 83-90
Trauma favors the development of adult respiratory distress syndrome (
ARDS). Adherence of polymorphonuclear leukocytes (PMN) to endothelial
cells (EC) with subsequent EC damage by the respiratory burst products
and proteases of the PMN is thought to be one of the basic mechanisms
in the pathogenesis of ARDS. Recent studies have shown that there mig
ht also be PMN-independent mechanisms of EC damage. It would speak for
PMN-independent EC damage if in the state of risk for this damage fac
tors were found which decrease PMN activity or if EC damage appeared w
ithout PMN. Because in trauma and sepsis pathologic coagulation with h
igh levels of fibrinogen degradation products (FDP) is often diagnosed
, we investigated whether FDP-D and FDP-E might influence PMN adherenc
e to EC. We also investigated whether serum of traumatized patients mi
ght provoke EC damage in a PMN-independent system in vitro. To achieve
this we evaluated the viability of EC using a fluorescence staining m
ethod. We found that both FDP-D and FDP-E decreased PMN adherence to h
uman EC significantly (p < 0.01) at a concentration of 50 mug/ml. Furt
hermore we found that EC membrane integrity can be disturbed by serum
of trauma patients. These results suggest that in trauma also PMN-inde
pendent mechanisms are important for EC damage.