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Glycoprotein IIB/IIIA‐Inhibition and Microcirculatory Alterations During Experimental Endotoxemia—An Intravital Microscopic Study in the Rat

Objective: Endothelial damage during early endotoxemia has been shown to be leukocyte‐independent. Platelet‐activating factor (PAF) and serotonin‐receptor antagonism are known to reduce leukocyte‐independent macromolecular leakage significantly, thereby focusing the field of interest to the platelets. We hypothesized that inhibition of the GP IIb/IIIa receptor, using the unspecific GP IIb/IIIa inhibitor abciximab, would reduce leukocyte‐independent endothelial damage during early endotoxemia, and furthermore, that inhibition of the GP IIb/IIIa receptor with abciximab might improve microcirculatory disturbances, seen in a leukocyte‐dependent animal model during endotoxemia.