M Gerlach

Early detection of increased tumour necrosis factor alpha (TNFα) and soluble TNF receptor protein plasma levels after trauma reveals associations with the clinical course

Background: The inflammatory response after trauma includes tumour necrosis factor alpha (TNFα) as pro‐inflammatory cytokine. Furthermore, both soluble TNF receptor proteins (sTNF‐R1 and sTNF‐R2) were described to influence the post‐traumatic inflammatory response and organ dysfunction.

L-selectin in trauma patients: a marker for organ dysfunction and outcome?

Systemic inflammatory response syndrome (SIRS) and multiple organ dysfunction syndrome (MODS) are important factors affecting morbidity and mortality after trauma. Adhesion molecules, e.g. L‐selectin (CD62 L), play crucial roles in both conditions.

Reduction of platelet trapping in membrane oxygenators by transmembraneous application of gaseous nitric oxide.

Bleeding during extracorporeal circulation (ECC) is often induced and/or aggravated by thrombocytopenia due to platelet-trapping in hollow fiber membrane oxygenators (HFMO). Nitric oxide (NO) has platelet anti-aggregating and dis-aggregating properties. In a paired system we tested whether gaseous NO, added to the gas compartment of one of two parallel running heparin-bonded HFMO attenuated platelet-trapping. Platelet consumption was markedly reduced in the NO-treated HFMO. These data strongly indicate that the application of gaseous NO could prove a new therapeutical approach to reduce bleeding during ECC, serving as a new way of preventing platelet loss, thus reducing the need for high systemic heparinization.

Global and extended coagulation monitoring during extracorporeal lung assist with heparin-coated systems in ARDS patients.

Heparin-coated systems for extracorporeal lung-assist (ECLA) were developed to reduce hemorrhagic risk by lowering the systemic heparinization, monitored by global tests, e.g. activated coagulation time (ACT) and activated partial thromboplastin time (APTT). Since this strategy gives no insight into procoagulant states, five ARDS patients receiving ECLA with heparin-coated systems were investivated for changes in coagulation using both global and extended tests. During ECLA onset the APTT and ACT were within or near normal ranges, platelets decreased 76.5% within 48h, fibrinogen decreased 28.7%, thrombin-antithrombin-III complexes were elevated before ECLA (53 μg/L), but demonstrated an additional peak (238 μg/L), plasminogen-activator-inhibitor-1 increased 12-fold, and the C1-inhibitor dropped 14.1%. In conclusion, after the onset of ECLA from a previous prethrombotic state, the precoagulant, anticoagulant, fibrinolytic and complement systems were activated in a similar way to that reported for non-heparinized systems with high-dose heparin. This was however only monitored by an extended test panel which was unable to predict thromboembolic events during ECLA.

Nitric oxide: The different effects on platelet membrane receptor expression during activation

NITRIC OXIDE: THE DIFFERENT EFFECTS ON PLATELET MEMBRANE RECEPTOR EXPRESSION DURING ACTIVATION D.Keh, M.Gerlach, I.KiJrer, S.Seiler, T.Kerner, K.Falke, H.Gerlach From the Clinic of Anesthesiology and Intensive Care Medicine, Virchow Clinic, Humboldt University, BerLin-Germany Nitric oxide (NO) is known as a regulator of platelet function. Although NO-platelet interactions were intensively studied by several investigators, no data exist about NO-effects on platelet receptor changes during stimulation measured by flow cytometry. Two-co/our flow cytometry assays were performed using fluoresceine-isothiocyanate or phycoerythrine-conjugated monoclonal antibodies (MoAb) directed against: a) Giycoprotein(GP)lb (CD42b, v.Willebrand receptor) which is expressed by unstimulated platelets and downregulated by internalization and shedding after activation, b) GPIIbllla (CD41,fibrinogen receptor) which is upregulated after activation due to externalization of GPIIbllla