Dysregulation of the veno-arterial response in the superior mesenteric artery during endotoxic shock
Revelly, J.P.; Ayuse, T.; Brienza, N.; Robotham, J.L.
Critical Care Medicine 23(9): 1519-1527
1995
ISSN/ISBN: 0090-3493 PMID: 7664554 Document Number: 452938
Objective: To investigate whether the vascular dysfunction in endotoxic shock is associated with inhibition of the veno-arterial response of the superior mesenteric artery. Design: Prospective, concurrent trial. Setting. Animal laboratory. Subjects: Domestic pigs. Interventions: Two groups of pigs were anesthetized with ketamine and pentobarbital, mechanically ventilated, and hemodynamically monitored. One group (n = 8) was challenged with Escherichia coli endotoxin (30 mu-g/ kg iv), while the other group (n = 4) served as time controls. Portal vein pressure was transiently increased in a series of steps from baseline to 25 mm Hg by partially obstructing portal venous flow. Measurements and Main Results: The effects of increases in portal pressure on superior mesenteric artery resistance, superior mesenteric artery fractional flow, and cardiac output were assessed. Under pre-endotoxin conditions, raising portal pressure induced an increase in superior mesenteric artery resistance, a decrease in superior mesenteric artery fractional flow, and no significant change in cardiac output (i.e., a normally regulating veno-arterial response). After endotoxin administration, raising portal pressure induced a decrease in superior mesenteric artery resistance, no change in superior mesenteric artery fractional flow, and a decrease in cardiac output (i.e., a dysregulated veno-arterial response). Conclusions: Under baseline conditions, a normally regulating veno-arterial response in the mesenteric vascular bed should minimize intestinal blood pooling with acute portal hypertension. Under conditions of endotoxemic shock, the dysregulation of the veno-arterial response could substantially contribute to blood pooling and edema formation in the intestinal vascular bed during septic shock. This phenomenon may account for many of the macro- and microcirculatory manifestations of septic shock.