Abstract
Acute mesenteric ischemia (AMI) is a life-threatening condition that can result in multiple organ injury and death. A timely diagnosis and treatment would have a significant impact on the morbidity and mortality in high-risk patient population. The purpose of this study was to investigate if intestinal fatty acid binding protein (I-FABP) and α-defensins can be used as biomarkers for early AMI and resultant lung injury. C57BL/6 mice were subjected to intestinal ischemia by occlusion of the superior mesenteric artery. A time course of intestinal ischemia from 0.5 to 3 h was performed and followed by reperfusion for 2 h. Additional mice were treated with N-acetyl-cysteine (NAC) at 300 mg/kg given intraperitoneally prior to reperfusion. AMI resulted in severe intestinal injury characterized by neutrophil infiltrate, myeloperoxidase (MPO) levels, cytokine/chemokine levels, and tissue histopathology. Pathologic signs of ischemia were evident at 1 h, and by 3 h of ischemia, the full thickness of the intestine mucosa had areas of coagulative necrosis. It was noted that the levels of α-defensins in intestinal tissue peaked at 1 h and I-FABP in plasma peaked at 3 h after AMI. Intestinal ischemia also resulted in lung injury in a time-dependent manner. Pretreatment with NAC decreased the levels of intestinal α-defensins and plasma I-FABP, as well as lung MPO and cytokines. In summary, the concentrations of intestinal α-defensins and plasma I-FABP predicted intestinal ischemia prior to pathological evidence of ischemia and I-FABP directly correlated with resultant lung injury. The antioxidant NAC reduced intestinal and lung injury induced by AMI, suggesting a role for oxidants in the mechanism for distant organ injury. I-FABP and α-defensins are promising biomarkers, and may guide the treatment with antioxidant in early intestinal and distal organ injury.
Highlights
Acute mesenteric ischemia (AMI) can occur through many mechanisms
D, MPO activity mirrored the number of neutrophils found infiltrating the intestinal tissue, where compared to sham treated mice, significant neutrophil infiltrate was found after 1, 2, and 3 h ischemia (n53 for all groups)
We have found that AMI results in both direct intestinal injury and acute lung injury
Summary
Acute mesenteric ischemia (AMI) can occur through many mechanisms. There are occlusive causes such as arterial embolus or thrombosis, or venous thrombosis as well as non-occlusive causes such as non-occlusive mesenteric infarction (NOMI) secondary to low flow states. The gastrointestinal tract forms an important defensive barrier. Its unique vascular supply and predisposition towards both ischemia and mucosal hypoxia put it at high risk for injury. As the result of an injury, the gastrointestinal tract becomes a major pathogenic source of bacteria and inflammatory mediators that subsequently lead to a septic response. The mortality rates in patients with AMI have not changed since the 1940’s, with rates ranging from 60–80% [1,2,3]. As such, finding novel biomarkers that can predict gastrointestinal injury prior to pathological changes is needed
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