Establishment of a swine experimental model of non-occlusive mesenteric ischemia: Combining induced hemorrhagic shock and vasopressor administration.

Abstract

Non-occlusive mesenteric ischemia (NOMI) is associated with high mortality rates, but definitive treatments have not yet been established. Although experimental animal models are worthwhile, reproducible models that reflect the pathophysiology of NOMI have not been developed. We combined risk factors for NOMI, comprising hemorrhagic shock, systemic vasopressor infusion, and local vasopressor infusion from the superior mesenteric artery (SMA) in swine under maintained anesthesia. Experiment 1 involved full-intensity (40%) phlebotomy and systemic vasopressor (norepinephrine and epinephrine). Experiment 2 involved full-intensity (40%) phlebotomy, systemic norepinephrine, and local vasopressor infusion into the SMA. Experiment 3 involved moderate (27%) phlebotomy, systemic norepinephrine infusion, and local epinephrine infusion. We evaluated serum lactate levels, intestinal serosa color, computed tomography (CT) angiography, and pathological findings. After inducing hemorrhage, systemic vasopressor alone and in combination with local vasopressin or norepinephrine infusion did not induce ischemic color changes in the intestine. The combination of systemic norepinephrine and local epinephrine (0.5 μg/kg/min) after moderate (27% blood loss) hemorrhage induced gross color change, pathological destruction, and elevation of serum lactate. Patent flow in the SMA was confirmed on CT angiography. We established a swine NOMI model with systemic norepinephrine infusion and local epinephrine with moderate hemorrhagic shock.