NEUTROPHIL REGULATION OF SPLANCHNIC BLOOD-FLOW AFTER HEMORRHAGIC-SHOCK

Objective This study examines the hypothesis that neutrophils impair splanchnic blood flow during resuscitation from hemorrhage by inhibiting the release of the compensatory vasodilator PGI(2) from the bowel. Summary Background Data Resuscitation from hemorrhagic shock is associated with neutrophil infiltration into the intestine, reduced splanchnic perfusion, and reduced release of PGI(2) from the intestine. Methods Sprague-Dawley rats received either vinblastine (VIN) to deplete circulating neutrophils or normal saline (NS). These animals then underwent either hemorrhage and resuscitation (SK + R) or sham operation (SHAM). Superior mesenteric artery flow and splanchnic 6-keto PGF(1a) (metabolite of PGI(2)) release were measured. Results Superior mesenteric artery blood flow was significantly greater in VIN-treated animals sustaining SK + R than in those treated with NS (p < 0.05). Neutrophil depletion preserved 6-keto PGF(1a) release after SK + R, whereas 6-keto PGF(1a) release in the NS-treated, SK + R group was significantly reduced (p < 0.05). Conclusion These data are compatible with the hypothesis that neutrophils may influence splanchnic perfusion after SK + R by inhibiting splanchnic PGI(2) release.