OBJECTIVES: To develop a reproducible model to measure transmural gut tissue PO2, to determine the gradient from serosa to mucosa during normovolemia and hypovolemia, and to determine the effect of resuscitation with heparan sulfate (danaparoid sodium) on this gradient. DESIGN: Fluorescent tissue oxygen sensors were placed onto serosal and mucosal surfaces of rat colon. Hemorrhagic shock was induced using a fixed pressure (mean arterial pressure, 40 mm Hg) model and resuscitated with either saline solution or heparan. RESULTS: Control animals had stable mean (+/- SD) serosal and mucosal tissue oxygen tensions (PO2) of 64 +/- 4 and 10 +/- 2 mm Hg, respectively. In shocked animals, baseline serosal PO2 decreased to 37 +/- 2 mm Hg at a mean (+/- SD) of 19 +/- 7 minutes after the initiation of hemorrhage. Mucosal values decreased to a minimum of 4 +/- 2 mm Hg at 45 +/- 15 minutes after the initiation of hemorrhage. Serosal PO2 returned to baseline during resuscitation in both control and heparan-resuscitated animals. Mucosal PO2 did not return to baseline in the shock/no heparan group. In the heparan-resuscitated animals, however, mucosal PO2 increased above baseline (13 +/- 3 mm Hg at 3 hours after completion of hemorrhage). CONCLUSIONS: A transmural gradient of PO2 exists across the colon with mucosal PO2 far lower than serosal PO2. Both serosal and mucosal PO2 decrease during hypovolemia. During hypovolemia, the PO2 of the entire gut wall is in a range in which phagocytic killing is impaired by hypoxia. Heparan improved mucosal PO2 and it may restore and/or protect gut function by oxygen-related mechanisms.
OBJECTIVES: To develop a reproducible model to measure transmural gut tissue PO2, to determine the gradient from serosa to mucosa during normovolemia and hypovolemia, and to determine the effect of resuscitation with heparan sulfate (danaparoid sodium) on this gradient. DESIGN: Fluorescent tissue oxygen sensors were placed onto serosal and mucosal surfaces of rat colon. Hemorrhagic shock was induced using a fixed pressure (mean arterial pressure, 40 mm Hg) model and resuscitated with either saline solution or heparan. RESULTS: Control animals had stable mean (+/- SD) serosal and mucosal tissue oxygen tensions (PO2) of 64 +/- 4 and 10 +/- 2 mm Hg, respectively. In shocked animals, baseline serosal PO2 decreased to 37 +/- 2 mm Hg at a mean (+/- SD) of 19 +/- 7 minutes after the initiation of hemorrhage. Mucosal values decreased to a minimum of 4 +/- 2 mm Hg at 45 +/- 15 minutes after the initiation of hemorrhage. Serosal PO2 returned to baseline during resuscitation in both control and heparan-resuscitated animals. Mucosal PO2 did not return to baseline in the shock/no heparan group. In the heparan-resuscitated animals, however, mucosal PO2 increased above baseline (13 +/- 3 mm Hg at 3 hours after completion of hemorrhage). CONCLUSIONS: A transmural gradient of PO2 exists across the colon with mucosal PO2 far lower than serosal PO2. Both serosal and mucosal PO2 decrease during hypovolemia. During hypovolemia, the PO2 of the entire gut wall is in a range in which phagocytic killing is impaired by hypoxia. Heparan improved mucosal PO2 and it may restore and/or protect gut function by oxygen-related mechanisms.