British Journal of Anaesthesia, 2003, Vol. 91, No. 6 878-885
© 2003 The Board of Management and Trustees of the British Journal of Anaesthesia
Laboratory Investigations |
Dopexamine reverses colonic but not gastric mucosal perfusion defects in lethal endotoxin shock
Department of Anesthesiology and Intensive Care, Kuopio University Hospital, Kuopio, Finland
*Corresponding author: Department of Critical Care Medicine, Room 1055, Scaife Hall, 3550 Terrace Street, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261, USA. E-mail: tenhjj@anes.upmc.edu
Background. Whilst dopexamine appears to increase overall splanchnic blood flow in postoperative and septic patients, the effects on gastric mucosal perfusion are controversial and based on concomitantly increasing mucosal to arterial PCO2 gradients (PdCO2). We hypothesized that dopexamine alters splanchnic blood flow distribution and metabolism during experimental endotoxin shock and modifies the inflammatory response induced by endotoxin.
Methods. In an experiment with anaesthetized normovolaemic, normoventilated pigs, 21 animals were randomized into: (i) subacute lethal endotoxin shock for 14 h (n=7 at baseline); (ii) endotoxin shock with dopexamine infusion (aiming to exceed baseline cardiac output, n=7); or (iii) controls (n=7). Regional blood flow and metabolism were monitored.
Results. Endotoxin produced a hypodynamic phase followed by a normo/hyperdynamic, hypotensive phase. Despite increasing systemic blood flow in response to dopexamine, proportional splanchnic 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 augmented the gastric PdCO2 gradient while colonic luminal lactate release and colonic PdCO2 gradient were reversed. Dopexamine did not modify the inflammatory response as evaluated by arterial IL-1ß and IL-6 concentrations.
Conclusions. Dopexamine protects colonic, but not gastric mucosal epithelium in experimental endotoxin shock. This may be related to redistribution of blood flow within the splanchnic circulation.
Br J Anaesth 2003; 91: 87885
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