• Tomohiko Masuno, Ernest E Moore, Aaron M Cheng, Eric L Sarin, and Anirban Banerjee.
• Department of Surgery, Denver Health Medical Center and University of Colorado Health Sciences Center, Denver, CO 80204, USA.
• Shock. 2006 Sep 1; 26 (3): 285-9.

AbstractMesenteric hypoperfusion due to circulatory shock is a key event in the pathogenesis of subsequent distant organ injury. Postshock mesenteric lymph (PSML) has been shown to contain proinflammatory mediators elaborated from the ischemic gut. We hypothesize that the relative bioactivity of PSML depends on the depth and duration of circulatory shock. To first determine the timing of PSML bioactivity, we subjected rats to hemorrhagic shock (30 mm Hg x 45 min) and then resuscitation with 50 vol% of shed blood and normal saline (4x shed blood) over 2 h. Mesenteric lymph was collected hourly up to 6 h after shock. Superoxide release was measured from human neutrophils (polymorphonuclear neutrophils [PMNs]) incubated with lymph fractions collected from each of the hourly time points. Rats were then subjected to four different shock variations: (1) 30 mm Hg x 45 min, (2) 30 mm Hg x 15 min, (3) 45 mm Hg x 45 min, and (4) 45 mm Hg x 15 min, and were resuscitated. PSML flow depends on depth of shock, but not duration of shock or resuscitation volume. Maximal PSML bioactivity, as measured by PMN priming for the respiratory burst, occurred during the third postshock hour, which correlated with peak lymph flow rate. PSML bioactivity was greatest with 30 mm Hg x 45 min, followed by 30 mm Hg x 15 min, 45 mm Hg x 45 min, and 45 mm Hg x 15 min. Hemorrhagic shock provokes the release of bioactive agents in PSML that is dependent on both depth and duration of shock.

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