• K S Ephgrave, R L Kleiman-Wexler, K Broadhust, and B Booth.
• VA Medical Center, Iowa City, Iowa 52246.
• J. Surg. Res. 1994 May 1;56(5):424-33.

AbstractGastric mucosal injury after hemorrhagic shock may be a consequence of both ischemia and reperfusion, as toxic oxygen-derived compounds are generated when ischemic tissues are reperfused. The present study was designed to estimate the magnitude of the reperfusion component of gastric mucosal injury, in comparison with the known capacity of the gastric mucosal surface to rapidly restore or restitute its surface after removal of various insults. Twelve dogs were subjected to 2 hr of hemorrhagic shock, with intragastric acid infused to produce gastric mucosal injury. Half were sacrificed 15 min after return of shed blood, while half were fully resuscitated with additional crystalloids and sacrificed 2 hr later. Gross and microscopic injury to the gastric mucosal surface were not increased by resuscitation. Particularly in the antrum, the resuscitated animals had significantly less gastric mucosal injury than unresuscitated animals. The amount of gastric mucosal injury was strongly inversely related to the success of resuscitation after 2 hr, specifically correlating with left ventricular pressure, cardiac index, mean arterial pressure, and systemic pH. Our data suggest that gastric mucosal restitution rather than reperfusion injury may predominant within a few hours of hemorrhagic shock and show that the degree of shock-induced gastric mucosal injury is inversely related to hemodynamic performance after resuscitation.

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