Effect of perfusion of liver on properdin titers in dogs subjected to hemorrhagic shock

Abstract

Previously it was demonstrated that plasma properdin levels decline in dogs as a result of hemorrhagic shock. The possibility that the liver may be a source of properdin and also a site for detoxification of the endotoxins formed during oligemia suggested that perfusion of the liver might prevent this fall in properdin titer. Seventeen dogs, in which the liver was autoperfused by way of the splenic vein, were bled to 35 mm Hg arterial pressure and maintained at this level until they took back 40% of their maximum bled volume, or were in oligemia for 4–5 hours. Liver perfusion failed to prevent the decline in properdin titer; in fact, there was a significantly greater ( P = 0.04) fall in the liver-perfused group than in the control animals. Furthermore, there were no significant differences in survival time or duration of oligemia.