Objective: To determine the effects of reinfusion of shed blood on the regional blood flow changes induced by hemorrhage and hemorrhage plus nociceptive nerve stimulation (injury) with special reference to the gut.
Design: Randomized controlled laboratory study.
Setting: Medical Research Council laboratory, university medical school.
Subjects: Four groups of anesthetized immature female Large-White pigs (15-27 kg): 30% hemorrhage, 30% hemorrhage plus afferent nerve stimulation, nerve stimulation alone, surgical controls.
Interventions: In addition to standard invasive hemodynamic monitoring, electromagnetic flow probes were placed around a branch of the superior mesenteric artery and the right femoral artery. Stimulating electrodes were placed on brachial nerves in both axillae. Animals underwent 30% hemorrhage over 30 mins. After a 30-min shock period, the shed blood was reinfused at 2 mL/kg/min.
Measurements and main results: Measurements/calculations of standard global hemodynamics, gut and femoral blood flows/vascular resistance, metabolism, arterial plasma lactate, portal venous endotoxin, interleukin-6, and tumor necrosis factor-alpha were made before and after hemorrhage, before and after reinfusion, and at 30-min intervals for 3 hrs. Blood and tissue samples were taken for the presence of translocated coliforms. Hemorrhage elicited the expected changes in global hemodynamics, metabolism, and gut and femoral blood flows. There was a partial hemodynamic recovery during the shock period. Nearly all hemodynamic and metabolic variables were rapidly restored by reinfusion. The response to hemorrhage was modified by nerve stimulation: Reductions in systemic hemodynamics and gut flow were greater, and there was no recovery during the shock phase. Cytokine and endotoxin concentrations increased significantly in all groups. There was no bacterial translocation.
Conclusions: When hemorrhage occurs in the presence of nerve stimulation (injury), the relative protection of the gut circulation is attenuated and this effect persists after the end of hemorrhage and reinfusion. However, there was no evidence that injury increased the hemorrhage/surgery-induced cytokine and endotoxin responses.