Intestinal ischemia shock in normal and Dibenzyline-protected dogs

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Abstract
An experimental model was developed to facilitate study of the intestinal-hepatic complex in shock. Shock was produced by ischemic injury to the intestine by temporary (4-hr) ligation of the superior mesenteric artery (SMA shock). Protection against shock was induced by Dibenzyline injected into the portal vein. Blood samples before, during, and after arterial occlusion were taken from the femoral, portal, and hepatic veins for hemoglobin, hematocrit, plasma proteins, bacterial culture, endotoxin detoxifying component (EDC), and vasotropic assays (rat mesoappendix). Liver biopsies were taken for carbon distribution in the Kupffer cells. Blood pressure and tissue temperatures were monitored. The data indicate that these parameters of SMA shock are predictable and typical of other types of experimental shock and can be attenuated by Dibenzyline. Bacterial organisms and polysaccharides (EDC) were not present in irreversible shock. Vasotropic assays demonstrated vasodepressor (epinephrine inhibiting) materials, in the peripheral blood. Vasodepressor responses were abolished by the action of Dibenzyline on hepatic function, possibly by sustaining hepatic reticuloendothelial system activity.