Superior mesenteric artery occlusion models shock-induced gut ischemia-reperfusion.

INTRODUCTION Superior mesenteric artery occlusion (SMAO) is a simple and reproducible model of shock-induced gut ischemia/reperfusion, but some argue that it is not clinically relevant. The purpose of the current study was to compare SMAO to a standard model of controlled hemorrhage (CH) and uncontrolled hemorrhage (UH). METHODS Rats had femoral lines and a jejunal mucosal laser Doppler placed followed by SMAO (60 min of ischemia, no resuscitation), controlled hemorrhage (40 mm Hg for 60 min, 2:1 resuscitation shed blood and lactated Ringers), or uncontrolled hemorrhage (liver injury, 3:1 resuscitation with lactated Ringers). Base deficit, lactate, and jejunal mucosal flow (as a percentage of baseline) were recorded during ischemia and for 120 min after reperfusion. Jejunal tissue was harvested for morphological evaluation. Comparison among groups was by analysis of variance (ANOVA), and significance was set at P < 0.05. RESULTS Mucosal blood flow was similar among groups at the onset of reperfusion (CH, 16.9 +/- 5.0% versus UH, 10.9 +/- 3.1% versus SMAO, 13.9 +/- 6.2%) and during the initial period of reperfusion. By 120 min, however, flow in CH (75.4 +/- 2.5%) was significantly higher that in either UH (36.4 +/- 13.1%) or SMAO (31.7 +/- 8.4%). Histological injury was less with CH, while base deficit was significantly higher in CH at the onset of reperfusion (-24 +/- 2 versus UH, -10 +/- 3 and SMAO, -6 +/- 3 mM/L) but comparable by the end (CH, -17 +/- 4 versus UH, -16 +/- 3 and SMAO, -17 +/- 2 mM/L). CONCLUSIONS SMAO is a clinically relevant model of shock-induced gut ischemia/reperfusion.