Hemorrhagic shock (HS) with conventional resuscitation (CR) (HSCR) primes neurophils and modulates leukocyte (WBC)–endothelium interaction as part of an exaggerated systemic inflammatory response. We hypothesize that topical application of clinical peritoneal dialysis solutions (PD) modulates such interaction.

Intestinal intravital microscopy was used to measure WBC rolling in terminal ileum post capillary venules (V2 and V3) in sham-operated animals, and in animals that underwent fixed pressure hemorrhage (50% mean arterial pressure for 60 minutes), followed by conventional resuscitation with the return of the shed blood and 2 vol of saline. Number of rolling WBCs per thirty seconds in selected V2 and V3, bathed in either Kreb’s solution or a 2.5% clinical peritoneal dialysis solution (PD) was quantified. Diameters were measured for the in-flow arterioles (A1), and out-flow venules (V1), for calculation of local blood flow with optical Doppler velocimetry.

The PD solution significantly (P < .05, n = 11) attenuated WBC–endothelium interaction in sham-operated animals while no significant difference was elicited in HSCR (P > .05, n = 9 Kreb’s, n = 7 PD). In addition, the PD solution produced an instantaneous dilation at all levels of the intestinal arterioles in both sham and HSCR. While intestinal venular blood outflow was increased by the PD solution, venular diameters changed very little.

Superfusion of the gut with glucose-based peritoneal dialysis solutions decreases the concentration of rolling leukocytes along the venular vascular endothelium by a vasodilation-mediated increase in arteriolar inflow and venous outflow mechanism. Hemorrhagic shock and conventional resuscitation enhance the concentration of rolling leukocytes presumably by mechanisms related to upregulation of the adhesion molecules and the low-flow state. Hemorrhage and resuscitation-enhanced leukocytes rolling was not reversed by adjunctive DPR despite the associated marked increase in arterial inflow and venous outflow. The status of the endothelium and the level of leukocyte priming in low-flow states are stronger predictors of leukocyte–endothelium interaction than rheology factors.