Hemorrhagic shock induces endothelial cell apoptosis, which is mediated by factors contained in mesenteric lymph.

Objective: Trauma-hemorrhagic shock is one of the leading causes of acute respiratory distress syndrome. This syndrome is associated with disruption of the alveolar barrier consisting of both epithelial and endothelial cells, which leads to a major increase in epithelial and microvascular permeability in the lungs. Although alveolar epithelial cell apoptosis has been documented as a contributing factor to this increase in permeability, it is unclear whether endothelial cell apoptosis occurs following trauma-hemorrhagic shock and, if so, the source of factors leading to this process.

A study of the biologic activity of trauma-hemorrhagic shock mesenteric lymph over time and the relative role of cytokines.

Background: Gut-derived factors in intestinal lymph have been recently shown to cause lung injury, activate neutrophils, and injure endothelial cells in rats subjected to hemorrhagic shock (T/HS). However, the time course of the appearance and disappearance of these factors in intestinal lymph is unclear. Thus the goal of this study was to characterize the biologic activity of T/HS lymph collected at various times during and after shock.

Trauma-hemorrhagic shock mesenteric lymph induces endothelial apoptosis that involves both caspase-dependent and caspase-independent mechanisms.

Objective: To determine the mechanism by which gut-derived factors present in mesenteric lymph from rats subjected to trauma-hemorrhagic shock (T/HS) induce endothelial cell death.

Summary Background Data: Intestinal ischemia after hemorrhagic shock results in gut barrier dysfunction and the subsequent production of biologically active and tissue injurious factors by the ischemic gut. These factors are carried in the mesenteric lymph and reach the systemic circulation via the mesenteric lymph, thereby ultimately resulting in distant organ injury.

Disruption of the actin cytoskeleton results in nuclear factor-kappaB activation and inflammatory mediator production in cultured human intestinal epithelial cells.

The cytoskeleton in eukaryotic cells is composed of two major filament systems, the microtubule system and the actin cytoskeleton. The microtubule system has recently emerged as an important regulator of NF-kappaB function. However, the role that the actin microfilament system plays in controlling NF-kappaB activation is incompletely understood.