Reticuloendothelial depression with superior mesenteric artery occlusion

Abstract

Normotensive, splenectomized dogs were subjected to intestinal ischemia by occlusion of the superior mesenteric artery (SMA) for periods of 15–90 min. Autoperfusion of the liver with arterial blood at normal flow rates was maintained in order to prevent hepatic ischemia during the period of SMA occlusion. The phagocytic activity of the hepatic reticuloendothelial system was assessed by measuring the clearance of carbon particles. Intestinal ischemia for 30 min led to a significant (P < 0.01) depression of carbon clearance. However, increasing the duration of ischemia to as long as 90 min did not produce a significantly greater depression of the clearance rate. Portal venous flow measurements, made just prior to the time of carbon injections, demonstrated that reduced phagocytic activity could not be attributed to reduced hepatic blood flow. Since ischemia of the hepatic RES was prevented during the period of SMA occlusion, it is probable that a humoral reticuloendothelial substance was produced by the ischemic intestine, as previously demonstrated in dogs subjected to hemorrhagic hypotension. In dogs treated with antibiotics to eliminate the gram-negative fecal flora, occlusion of the SMA for 1 hr caused depression of granulopectic activity. This suggests that gram-negative bacterial products are not required for the formation of the reticuloendothelial depressing substance.