Article révisé par les pairs
Résumé : Background: Long periods of ischemia can cause organ injury and dysfunction. The protein degradation occurring in the muscular layer and in the mucosa of the intestinal wall during ischemia may release amino acids into the intestinal lumen or into the circulation. The small intestine, like skeletal muscle, cannot synthesize or degrade tyrosine. Thus, the tyrosine concentration released from the gut mucosa reflects the balance between protein synthesis and degradation. We aimed to determine whether tyrosine can be used as a marker of intestinal injury during ischemia. Methods: In 19 anesthetized rabbits, an ultrasonic flow probe was placed around the superior mesenteric artery to estimate blood flow. A segment from the ileum was isolated using two multilumen catheters with inflated balloons to create a closed segment for perfusion. Animals were allocated into three groups: a sham group without intervention (group I); a group submitted to superior mesenteric artery ligation only (group II); and a group submitted to 1 h of SMA clamping followed by 1 h of reperfusion (group III). Concentrations of lactate and tyrosine (fluorometry) were determined in the serum and the gut luminal perfusate. Results: Gut luminal perfusate tyrosine concentrations increased significantly in group II (from 10 ± 8 to 93 ± 63 mm/mL at 2 h) and were significantly higher than in group I (26 ± 24 mm/mL) and group III (11 ± 13 mm/mL) (P < 0.05 for all). Conclusion: Tyrosine is released from cells into the lumen during severe intestinal ischemia. Regional measurements of tyrosine levels may be a useful indicator of severe intestinal villus compromise. © 2009 Elsevier Inc. All rights reserved.

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