Early activation of humoral proteolytic systems in patients with multiple trauma

Dynamics of fibrinogen in acute phases of trauma

“…In severe trauma, especially blunt trauma, massively injured tissues accelerate thrombin generation [14][15][16][17]. This excessive thrombin generation not only induces fibrin formation, but also simultaneously promotes plasmin generation and the consumption of α 2 -plasmin inhibitor [36,41,61]. Low levels of the α 2 -plasmin inhibitor trigger the release of plasmin and induce hyperfibrino(geno)lysis.…”

Die klinische Wertigkeit biochemischer Faktoren beim Polytrauma

“…Risberg et al [187] berichteten von signifikanten Unterschieden bei einzelnen Faktoren der humoralen proteolytischen Kaskadensysteme (Prokallikrein, AT III, Plasminogen, a2-Plasmininhibitor, Cl INH, C3 und C4) sowohl bei Versterben/Überleben als auch bei der Entwicklung eines ARDS. Ihre Ergebnisse lassen jedoch wiederum keine prognostischen Schlußfolgerungen zu.…”

Oxygen Radicals Induce Pulmonary Vasoconstriction in Pigs without Activating Plasma Proteolytic Cascade Systems

“…Since both allopurinoi and catalase reduce this output we believe that oxygen radicals induced by hypo xanthine-xanthine oxidase exert their effects on the pulmonary circulation by enhancing prostanoid synthesis either in the vascular en dothelium or in circulating platelets or both. Plasma proteolytic systems are activated in shock and trauma [7]. as well as in endoloxinemia [6.…”

“…When activated, the contact factors plasma prekallikrein, Hageman factor (FXII) and fac tor XI are converted to serine proteases that are capable of activating the plasma comple ment, fibrinolytic, coagulation and the kallikrein-kinin systems [1][2][3][4][5], Activation of the proteolytic cascade systems of plasma is asso ciated with trauma, septicemia, adult respira tory distress syndrome as well as the neonatal respiratory distress syndrome [6][7][8][9][10][11][12][13][14], Pre-studies [20][21][22][23][24], Increased concentration of thromboxane At was also found in pulmonary venous plasma when the pulmonary circula tion was exposed to oxygen radical generating systems and this could explain the pulmonary vasoconstriction found in such experiments [15,18,19], In addition it is well known that endotoxincmia activates the plasma proteo lytic systems [6,8,9], Both oxygen radicals and endotoxins increase capillary permeabil ity and induce edema. Therefore, from a theo retical point of view, several possible linkages between plasma proteolytic systems as the plasma kallikrein-kinin and fibrinolytic sys tems and oxygen radicals may exist.…”