Hypertonic saline resuscitation abrogates neutrophil priming by mesentericlymph

Objective: Neutrophil (PMN) priming after hemorrhagic shock is predictive o f the subsequent development of multiple organ failure, but the mechanism r emains unknown. Recently, we and others have demonstrated that mesenteric l ymph from shock animals resuscitated with lactated Ringer's solution (LR) i s not only a potent PMN priming agent but also causes lung injury. Work by others has shown that resuscitation with hypertonic saline (HTS) protects a nimals from lung injury after hemorrhagic shock. Therefore, we hypothesize that resuscitation with HTS will abolish PMN priming by postshock mesenteri c lymph. Methods: After mesenteric lymph duct catheterization, male rats underwent h emorrhagic shock (mean arterial pressure of 40 mm Hg for 90 minutes) and re suscitation with shed blood plus either LR (2x volume of shed blood) or 4 m L/kg of 7% HTS (isonatremic), Priming for superoxide by PMN was measured af ter fMLP (1 mu M) activation. Results: Shock significantly decreased mesenteric lymph flow from preshock levels in both groups, LR resuscitation produced significantly more mesente ric lymph than HTS resuscitation. Mesenteric lymph from LR animals primed P MN for superoxide production, whereas, HTS eliminated this priming. Conclusion: I-ITS not only decreases postshock mesenteric lymph production, it eliminates PMN priming by mesenteric lymph, suggesting a mechanism for the beneficial effects of HTS resuscitation.