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 influen ce of continuous intravenous heparinization on plasma levels of circulating adhesion molecules was studied in 28 trauma patients (injury severity scor e between 15 and 25 points) and 28 sepsis patients secondary to abdominal s urgery. According to a prospective, randomized sequence the patients receiv ed either unfractionated heparin (aim: activated partial thromboplastin tim e (aPTT) approximately 2 x normal) (trauma-heparin (n = 14); sepsis-heparin tn = 14)) or not (trauma (n = 14); sepsis (n = 14)). Plasma levels of circ ulating soluble endothelial leukocyte adhesion molecule-1 (sELAM-1), vascul ar cell adhesion molecule-1 (sVCAM-1), intercellular adhesion molecule-1 (s ICAM-1), and granule membrane protein-140 (sGMP-140) were serially measured from arterial blood samples for 5 days. Approximately 600 U/h of heparin w ere given to increase aPTT to approximately 60 s. Plasma levels of all adhe sion 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; sICAM-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; sICAM-1: from 398 +/- 99 to 6 86 +/- 119 ng/mL). Trauma patients showed a less pronounced increase in all adhesion molecules without differences between the two subgroups. Only sGM P-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 1 32 +/- 17 ng/mL). It is summarized that continuous heparinization with appr oximately 600 U/h did not attenuate the rise in circulating adhesion molecu les 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.