Behaviour of Lysosomes in Hæmorrhagic Shock

Abstract

IN a series of detailed publications^1–5, Fine et al. have maintained that the probable cause of death in traumatic shock is the irretrievable collapse of the circulation caused by a bacterial toxin which intensifies vasoconstrictor activity so as to injure the splanchnic viscera, with resulting decline in vascular reactivity to catechol amines and functional damage in key organs, especially the liver and intestine. In the absence of any obvious systemic or local infection, these workers have considered that the most likely source of the toxin is an endotoxin derived from the intestinal flora. The difference between that type of shock which responds to resuscitative measures, that is, ‘reversible shock’, and the irreversible form would appear to depend on the ability of the reticulo-endothelial system, particularly in the liver and spleen, to inactivate this toxin. This ability declines if the animal is in shock for 2 h or longer. There are indications that this detoxication process is concurrent with an esterase-like protein in spleen and liver that releases phosphate. Abolition of vasoconstrictor activity in the splanchnic area by cœliac blockade preserves this process as well as the vascular integrity of the portal and systemic circulation. Under these circumstances the animals are able to survive an otherwise lethal exposure to shock. It is noteworthy, however, that while functional differences in the spleens and livers of normal and shocked animals have been observed, no histological abnormalities have been detected.