Dopexamine reverses colonic but not gastric mucosal perfusion defects in lethal endotoxin shock

Background. Whilst dopexamine appears to increase overall splanchnicblood flow in postoperative and septic patients, the effectson gastric mucosal perfusion are controversial and based onconcomitantly increasing mucosal to arterial PCO₂ gradients(PdCO₂). We hypothesized that dopexamine alters splanchnic bloodflow distribution and metabolism during experimental endotoxinshock and modifies the inflammatory response induced by endotoxin. Methods. In an experiment with anaesthetized normovolaemic,normoventilated pigs, 21 animals were randomized into: (i) subacutelethal endotoxin shock for 14 h (n=7 at baseline); (ii)endotoxin shock with dopexamine infusion (aiming to exceed baselinecardiac output, n=7); or (iii) controls (n=7). Regional bloodflow and metabolism were monitored. Results. Endotoxin produced a hypodynamic phase followed bya normo/hyperdynamic, hypotensive phase. Despite increasingsystemic blood flow in response to dopexamine, proportionalsplanchnic blood flow decreased during the hypodynamic phase.Dopexamine gradually decreased fractional coeliac trunk flow,while fractional superior mesenteric arterial flow increased.Dopexamine induced early arterial hyperlactataemia and augmentedthe gastric PdCO₂ gradient while colonic luminal lactate releaseand colonic PdCO₂ gradient were reversed. Dopexamine did notmodify the inflammatory response as evaluated by arterial IL-1ßand IL-6 concentrations. Conclusions. Dopexamine protects colonic, but not gastric mucosalepithelium in experimental endotoxin shock. This may be relatedto redistribution of blood flow within the splanchnic circulation. Br J Anaesth 2003; 91: 878–85