Abstract
The sequence of hemorrhagic shock was studied in dogs with functional absence of the liver produced by ligation of vascular inflow circuits. Establishment of a portal to jugular shunt permitted continual measurement of intestinal blood flow. It was found that this vascular bed exhibited the characteristic hyperemic response previously observed in dogs with intact livers, studied under similar conditions. Other hemodynamic changes symptomatic of irreversibility were observed. It is concluded that the liver made anoxic during shock does not contribute to irreversibility, and that it is more likely that it exerts a protective role. An hypothesis is advocated that hypotension creates conditions in the intestinal bed which favor production or release of vasodepressor agents or material toxic to the cardiovascular system. In the absence, or impairment of the normal protective role of the liver, these gain access into the general circulation with deleterious consequences to circulatory homeostasis.