The mechanisms and prevention of intravascular fluid loss after occlusion of the supraceliac aorta in dogs

Abstract

Mechanisms of intravascular fluid depletion after temporary occlusion of the supraceliac aorta were investigated in a canine model. During ischemia and reperfusion, hemodynamic parameters, superior mesenteric artery flow, intestinal mucosal perfusion, and mucosal permeability were monitored. After 12 hours of reperfusion, the volumes of intravenous electrolyte fluid required to maintain hemodynamic stability and fluid lost into the gastrointestinal tract and peritoneal cavity were measured. The distribution of total body water was analyzed by use of radionuclide dilution techniques. Group A animals underwent laparotomy only, group B had the supraceliac aorta occluded for 45 minutes, group C had superoxide dismutase administered after 45 minutes of aortic occlusion, and group D animals were exposed to mild hypothermia during a similar ischemia and reperfusion period. No significant difference was found in mean superior mesenteric artery flow or mucosal perfusion during ischemia among groups B, C, and D. During reperfusion superior mesenteric artery flow returned to values similar to control in all groups. Aortic occlusion increased mucosal permeability most significantly in group B (p < 0.01). Mean intravenous fluid requirements (ml/mg) were the following: group A, 80 ± 5; group B, 201 ± 9 (p < 0.01); group C, 116 ± 7 (p < 0.05); group D, 245 ± 24 (p < 0.05). Mean gastrointestinal fluid loss was highest in the hypothermic group and smallest if superoxide dismutase was given. Mean intracellular fluid volume was increased in groups B and D compared with group A (p < 0.01). We conclude that aortic occlusion and reperfusion results in increased requirement for intravenous fluid as fluid shifts into the intracellular space and is lost into the gastrointestinal tract. These fluid shifts are increased by hypothermia but can be minimized by superoxide dismutase.