Tissue Damage by Immune Reactions

The phenomenon has dassically been produced in the rabbit by bacterial endotoxins (2) and results from the widespread occlusion of glomerular capillaries by dense fibrin deposits (3-5). Two basic conditions (3) appear essential for the development of the lesion: (a) the slow activation of intravascular coagulation with the formation of fibrin aggregates in the circulating blood, and (b) the inhibition of the protective mechanism concerned with the intravascular removal of fibrin. In the rabbit it has recently been shown that the phagocytic dearance mechanism of the reticuloendothelial system is largely responsible for the elimination of circulating fibrin aggregates, and that unless reticuloendothelial blockade occur concurrently with intravascular coagulation, fibrin is not generally deposited in sufficient quantity to produce occlusive vascular lesions (3, 6). In view of these findings it has been suggested (3) that bacterial endotoxins produce the generalized Shwartzman reaction by virtue of their capacity not only to initiate intravascular coagulation (7) but also to cause profound depression of reticuloendothelial function (8).