BACKGROUND: It has been suggested that multiple sublethal insults are commonly associated with the development of multiple organ failure (MOF). The gut is considered to be pivotal in the pathogenesis of MOF. This study investigated the effects of repeated ischemia-reperfusion of the rat small intestine. METHODS: Groups of rats underwent 30 min of superior mesenteric artery occlusion or sham operation followed by 24 h of reperfusion. They then received an additional 30 min of superior mesenteric artery occlusion and 2 h of reperfusion or sham operation. Small intestine was examined for mucosal injury, neutrophil infiltration, goblet cell number, and generation of the eicosanoids, prostaglandin E2, and leukotriene B4. Activation of neutrophils was assessed in systemic venous blood. RESULTS: Animals subjected to two insults of ischemia-reperfusion demonstrated significantly less mucosal injury than animals undergoing one episode of ischemia and 2 h of reperfusion, despite increased neutrophil infiltration, leukotriene B4, and activated systemic neutrophils. Goblet cell number was elevated in animals 24 h after the first ischemia-reperfusion insult and remained enhanced after the second episode of ischemia-reperfusion. CONCLUSIONS: The initial episode of ischemia-reperfusion caused an adaptive response associated with cytoarchitectural preservation following the subsequent insult. Increased mucus production was associated with mucosal protection. Nevertheless, repeated ischemia-reperfusion potentiated the local inflammatory response and the systemic activation of neutrophils.
BACKGROUND: It has been suggested that multiple sublethal insults are commonly associated with the development of multiple organ failure (MOF). The gut is considered to be pivotal in the pathogenesis of MOF. This study investigated the effects of repeated ischemia-reperfusion of the rat small intestine. METHODS: Groups of rats underwent 30 min of superior mesenteric artery occlusion or sham operation followed by 24 h of reperfusion. They then received an additional 30 min of superior mesenteric artery occlusion and 2 h of reperfusion or sham operation. Small intestine was examined for mucosal injury, neutrophil infiltration, goblet cell number, and generation of the eicosanoids, prostaglandin E2, and leukotriene B4. Activation of neutrophils was assessed in systemic venous blood. RESULTS: Animals subjected to two insults of ischemia-reperfusion demonstrated significantly less mucosal injury than animals undergoing one episode of ischemia and 2 h of reperfusion, despite increased neutrophil infiltration, leukotriene B4, and activated systemic neutrophils. Goblet cell number was elevated in animals 24 h after the first ischemia-reperfusion insult and remained enhanced after the second episode of ischemia-reperfusion. CONCLUSIONS: The initial episode of ischemia-reperfusion caused an adaptive response associated with cytoarchitectural preservation following the subsequent insult. Increased mucus production was associated with mucosal protection. Nevertheless, repeated ischemia-reperfusion potentiated the local inflammatory response and the systemic activation of neutrophils.