Humoral deficiency and reticuloendothelial depression after traumatic shock

Circulating opsonin levels and reticuloendothelial (RE) phagocytic activity were investigated in anesthetized rats subjected to Noble-Collip drum (NCD) trauma. Reticuloendothelial function was assessed by colloid clearance kinetics and circulating opsonin levels by in vitro tissue slice bioassay. After sublethal shock, both hepatic RE phagocytosis and plasma opsonic activity were significantly (P less than 0.001) depressed in the 0.5- to 6-h posttrauma period. Pulmonary and bone marrow localization of the blood-borne test microparticles significantly (P less than 0.05) increased during hepatic RES depression. Hepatic RE cells from animals during the interval of posttraumatic in vivo phagocytic depression exhibited normal phagocytosis when incubated in normal pretrauma plasma and decreased phagocytic activity when incubated in posttrauma plasma. After sublethal shock, restoration or opsonin levels by 24 h after shock resulted in hepatic RE recovery. Plasma opsonin levels declined in direct relationship to the degree of trauma. Progressive hepatic RE failure was correlated with the progressive decline in circulating plasma opsonic activity. The findings indicate that opsonic depletion may be involved in the etiology of hepatic reticuloendothelial depression after traumatic shock.

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