Apparent heterogeneity of regional blood flow and metabolic changes within splanchnic tissues during experimental endotoxin shock.
We conducted a randomized, controlled experiment of prolonged lethal endotoxin shock in pigs aiming at 1) simultaneously measuring perfusion at different parts of the gut to study the potential heterogeneity of blood flow within the splanchnic region; 2) studying the association among regional blood flows, oxygen supply, and different metabolic markers of perfusion; and 3) analyzing the association between histological gut injury and markers of perfusion and metabolism. The primary response to endotoxin was a decrease in systemic and splanchnic blood flow followed by hyperdynamic systemic circulation. Redistribution of blood flows occurred within the splanchnic circulation: superior mesenteric artery blood flow was maintained, whereas celiac trunk blood flow was compromised. Mucosal to arterial PCO(2) gradients did not reflect changes in total splanchnic perfusion, but they were associated with regional blood flows during the hypodynamic phase of shock. During hyperdynamic systemic circulation, PCO(2) gradients increased heterogeneously in the gastrointestinal tract, whereas luminal lactate increased only in the colon. Histological analysis revealed mucosal epithelial injury only in the colon. We conclude that markers of perfusion and metabolism over one visceral region do not reflect perfusion and metabolism in other splanchnic vascular areas. Intestinal mucosal epithelial injury occurs in the colon during 12 h of endotoxin shock while the epithelial injury is still absent in the jejunum. Hyperdynamic and hypotensive shock induces gut luminal lactate release in the colon but not in the jejunum. The association or causality between the mucosal epithelial injury and luminal lactate release remains to be elucidated.


CONCLUSIONS
Surrogate regional markers of tissue perfusion over one region do not reflect the state of perfusion over another. Therefore, regional metabolic monitoring (microdialysis) in multiple locations is needed. Although tonometry does not differentiate between macro-level regional perfusion defect and tissue injury, intestinal luminal microdialysis detects mucosal lactate release, which may be associated with epithelial injury. The degree of correlation or causality between the two remains to be evaluated.
Tenhunen
Jyrki J
JJ
Departments of *Anesthesiology and Intensive Care, †Clinical Pathology, and ‡Surgery, Kuopio University Hospital, Kuopio, Finland.
Uusaro
Ari
A
Kärjä
Vesa
V
Oksala
Niku
N
Jakob
Stephan M
SM
Ruokonen
Esko
E
D000818:Animals; D001783:Blood Flow Velocity; D002245:Carbon Dioxide / Q000378:metabolism; D003106:Colon / Q000473:pathology; D004731:Endotoxins; D004926:Escherichia coli; D005260:Female; D005753:Gastric Mucosa / Q000378:metabolism; D006439:Hemodynamics; D007413:Intestinal Mucosa / Q000378:metabolism; D007583:Jejunum / Q000473:pathology; D019344:Lactic Acid / Q000097:blood; D010100:Oxygen / Q000097:blood; D012772:Shock, Septic / Q000378:metabolism / Q000503:physiopathology*; D013152:Splanchnic Circulation; D013552:Swine
D004731:Endotoxins; D002245:Carbon Dioxide; D019344:Lactic Acid; C044101:endotoxin, Escherichia coli; D010100:Oxygen