Systemic Not Just Mesenteric Lymph Causes Neutrophil Priming After Hemorrhagic Shock

Abstract

Inflammatory mediators in postshock mesenteric lymph have been causally linked to systemic polymorphonuclear cells (PMNs) priming resulting in acute lung injury (ALI) and multiple organ failure. Earlier human and animal studies demonstrated ALI after lower limb ischemia/reperfusion (I/R) injury. As hemorrhagic shock (HS) is in essence a systemic I/R insult, we postulated that systemic lymph after HS would exhibit PMN priming and this was studied in vitro. Lymph was collected at intervals from the hind limb of dogs subjected to sham or HS and crystalloid resuscitation. Human PMNs isolated from heparinized blood of normal volunteers were incubated with buffer, sham lymph, or lymph after 120 minutes of shock or resuscitation. PMN priming was indexed by CD11b expression (mean fluorescence intensity), superoxide anion (O2(-)) generation (nanomoles/mg protein), and elastase release (%) after the addition of fMLP (1 micromol). PMNs with buffer served as control. PMN priming after exposure to either shock or postshock resuscitation lymph was noted by increased expression of CD11b, superoxide generation, and elastase release after exposure to fMLP. No priming effect was noted with sham lymph. Maximal bioactivity of shock or postresuscitation shock lymph was noted at 2 hours postresuscitation. Exposure with systemic lymph after HS resulted in PMN priming. These results question the unique properties attributed to post-HS lymph from the splanchnic bed in causing PMN priming and ALI after shock. The causal agent(s) for these effects are unclear.