Infection and resulting sepsis continue to be important causes of morbidity and mortality in surgical patients. Although much has been learned about the pathogens and the leukocyte responses to these pathogens, we are only beginning to understand the role of the host in these pathologies. The endothelium is a dynamic participant in cellular and organ function rather than a static barrier as it was once believed. Emerging evidence implicates the endothelium as a central effector in the inflammatory response. Through the expression of surface proteins and secretion of soluble mediators, the endothelium controls vascular tone and permeability, regulates coagulation and thrombosis, and directs the passage of leukocytes into areas of inflammation. Derangements in these normal functions may contribute significantly to a maladaptive inflammatory response leading to systemic inflammation and multiple organ failure.

Alterations in neutrophil L-selectin, not endothelial CAMs, are important in decreased neutrophil exudation. Reduced levels of neutrophil L-selectin associated with increased levels of serum L-selectin in patients with SIRS suggest premature intravascular shedding of neutrophil L-selectin. This would compromise the initial interaction between neutrophils and the endothelium, and, consequently, impede exudation.

Septic patients deliver fewer PMNs to secondary inflammatory sites. In addition, neutrophil exudation results in loss of the small priming effect for phagocytosis and bactericidal function induced by sepsis. Failure to produce a gradient to C5a and intravascular shedding of L-selectin may be responsible for this sepsis-induced reduction in neutrophil exudation to secondary inflammatory sites.

We postulate that the increased plasma levels of vWf and the decreased staining in the peripheral dermal plexus represent the generalized activation and degranulation of endothelium in vascular beds remote from the original inflammatory focus.