• J S Young, M Fernandez, and J W Meredith.
• Department of Surgery, University of Virginia Health Sciences Center, Charlottesville, 22906, USA.
• J. Surg. Res. 1997 Jul 15;71(1):87-92.

BackgroundGut and hepatic dysfunction, during and after hypovolemic shock, have been implicated as causative mechanisms in the development of multiple system organ failure in the trauma patient. Current techniques of assessment of perfusion only detect changes in systemic oxygen transport. We designed an animal model that can measure changes in oxygen transport in the liver and gut during hypovolemic shock and resuscitation.Materials And MethodsAnimals were hemorrhaged to a mean arterial pressure (MAP) of 60 mm Hg and maintained at 60 mm Hg for 60 min. Animals were then assigned to one of three groups. Group I served as nontreatment controls. Group II received shed blood and saline in sufficient volumes to restore MAP to baseline. Group III animals were resuscitated with shed blood, saline, and donor blood to restore systemic oxygen delivery to the preshock value.ResultsThe animals resuscitated to their baseline systemic oxygen delivery, Group III, had significantly higher systemic, hepatic, and splanchnic oxygen delivery than the remaining groups. In addition, Group III had higher oxygen consumption, portal flow, and hepatic artery flow than the blood pressure-directed group, Group II. The decrease in oxygen extraction ratio in the gut and liver was significantly greater in Group III than in Group II.ConclusionsThese data show that hepatic and gut vascular beds are better perfused when resuscitation from hemorrhage is guided by systemic oxygen transport measurements compared to resuscitation guided by blood pressure.

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