Continuous heparinization and circulating adhesion molecules in the critically ill

Endothelial activation and damage are common endpoints of a complex process that may result in multiple organ dysfunction syndrome (MODS). The influence of continuous intravenous heparinization on plasma levels of circulating adhesion molecules was studied in 28 trauma patients (injury severity score between 15 and 25 points) and 28 sepsis patients secondary to abdominal surgery. According to a prospective, randomized sequence the patients received either unfractionated heparin (aim: activated partial thromboplastin time (aPTT) approximately 2 x normal) (trauma-heparin (n = 14); sepsis-heparin (n = 14)) or not (trauma (n = 14); sepsis (n = 14)). Plasma levels of circulating soluble endothelial leukocyte adhesion molecule-1 (sELAM-1), vascular cell adhesion molecule-1 (sVCAM-1), intercellular adhesion molecule-1 (slCAM-1), and granule membrane protein-140 (sGMP-140) were serially measured from arterial blood samples for 5 days. Approximately 600 U/h of heparin were given to increase aPTT to approximately 60 s. Plasma levels of all adhesion molecules increased in all groups. This increase was significantly (p < .05) highest in both sepsis groups (sepsis: sELAM-1: from 50+/-11 to 84+/-19 ng/mL; slCAM-1: 410+/-68 to 700+/-95 ng/mL), but did not differ significantly between the treated and nontreated patients (sepsis-heparin: sELAM-1: from 60+/-131 to 88+/-20 ng/mL; slCAM-1: from 398+/-99 to 686+/-119 ng/mL). Trauma patients showed a less pronounced increase in all adhesion molecules without differences between the two subgroups. Only sGMP-140 increased significantly (p < .05) more in the trauma (from 102+/-20 to 169+/-16 ng/mL) than in the trauma-heparin group (from 109+/-19 to 132+/-17 ng/mL). It is summarized that continuous heparinization with approximately 600 U/h did not attenuate the rise in circulating adhesion molecules in sepsis and trauma patients. The study findings suggest that heparin in this dose regimen may be unlikely to influence endothelial inflammation or endothelial function in critically ill patients.