Prostaglandin E-major urinary metabolites as a new biomarker for acute mesenteric ischemia

Abstract

Background Acute mesenteric ischemia (AMI) is an emergent vascular disease caused by cessation of the blood supply to the small intestine. Despite advances in the diagnosis, intervention, and surgical procedures, AMI remains a life-threatening condition. Prostaglandin E2 Major Urinary Metabolite (PGE-MUM), the urinary metabolite of Prostaglandin E2, is known to be stable in urine and has been suggested to be a valuable biomarker for intestinal mucosal inflammation, such as ulcerative colitis. We therefore investigated whether or not PGE-MUM levels reflect the degree of ischemia in an intestinal ischemia-reperfusion (IR) model. Methods Male rats were used to establish a superior mesenteric artery occlusion (SMAO) group, in which the superior mesenteric artery was clamped, and a sham group. The clamping times in the SMAO group were either 30 or 60 min, and reperfusion times were either 3 or 6 h, after which PGE-MUM values were measured. Results The histological injury score of the SMAO (30-min ischemia and 6-h reperfusion group: 1.8 ± 0.4 and 60-min ischemia and 6-h reperfusion group: 4.7 ± 0.5) and were significantly greater than that of the sham group (0.4 ± 0.7, p < 0.05). The PGE-MUM levels in the SMAO group (30-min ischemia and 6-h reperfusion group:483 ± 256 and 60-min ischemia and 6-h reperfusion group:889 ± 402 ng/mL) were significantly higher than in the sham group (30-min and 6-h observation group:51 ± 20, and 60-min and 6-h observation group:73 ± 32 ng/mL p < 0.05). Furthermore, the PGE-MUM value was corrected by the concentration of urinary creatinine (Cr). The PGE-MUM/urinary Cr levels in the SMAO group were also significantly higher than in the sham group (p < 0.05). Conclusions We found that intestinal IR increased urinary PGE-MUM levels depending on the ischemic time. This suggests the potential utility of PGE-MUM as a noninvasive marker of intestinal ischemia.