Hemodynamic effects of cecal ligation sepsis in dogs.

Cecal ligation sepsis was studied in eight pentobarbital-anesthetized dogs with hemodynamic measurements at baseline, 2 days after cecal ligation, and following Ringer’s lactate resuscitation. Microsphere techniques were used to measure peripheral arteriovenous (A-V) shunting and distribution of cardiac output. Cecal ligation sepsis was manifested by pyrexia, leukocytosis, decreased blood pressure, and purulent peritonitis. Although cardiac index (CI) increased in two, decreased in four, and was unchanged in two dogs, femoral artery blood flow (FAQ) decreased in all animals (125 to 84 ml/mitt, P < 0.01). Hindlimb A-V 0, difference increased while 0, consumption and A-V shunting did not change. Distribution of cardiac output increased significantly to the kidneys (f63%, P < 0.01) and liver (Tl68%, P < O.Ol), but was unchanged to skin, pancreas, and skeletal muscle. Intrarenal distribution of blood flow did not change despite increased total renal blood flow during sepsis. Ringer’s lactate resuscitation (20 ml/kg) during sepsis increased CI, while FAQ and A-V Or differences returned to baseline values. Hindlimh A-V shunting remained low and unchanged. In contrast to the effects of local inflammation in canine septic hindlimbs, there does not appear to be a specific vasodilator released during cecal ligation sepsis which causes increased peripheral blood flow and elevated A-V shunting. Cecal ligation in dogs, however, does not mimic the disproportionately low peripheral resistance and reduced 0, extraction seen in hyperdynamic human sepsis. These results should, therefore, be interpreted with caution.