STUDIES ON THE GENERALIZED SHWARTZMAN REACTION* IV . PREVENTION OF THE Loc~a~ AND GENERALIZED SIIWARTZMAN REACTIONS WITH HEPARIN

I t has been shown that thrombosis of small blood vessels is a constant pathological feature of both the generalized and local Shwartzman phenomena (1-3). Studying the dermal Shwartzman reaction, Stetson found that leukocyteplatelet thrombi occur in the small blood vessels of prepared skin shortly after the provoking intravenous injection of toxin (3). He attributed this to the development of adhesiveness of the white blood cells and platelets, and associated it with the occurrence of leukopenia following the intravenous injection of meningococcal toxin. On the basis of his observation that occlusion of small blood vessels regularly occurred prior to the development of hemorrhagic necrosis of the skin, Stetson suggested that thrombosis of capillaries and venules plays an essential role in the pathogenesis of the local Shwartzman reaction. The initial histological event in the development of bilateral cortical necrosis of the kidneys, in the generalized Shwartzman reaction, is occlusion of the glomerular capillaries by acellular, eosinophilic material having tinctorial properties characteristic of "fibrinoid" (4, 5). Although usually homogenous, this material occasionally possesses a fibrillary structure resembling that of fibrin. Neither platelets nor leukocytes are identifiable as a basic constituent of this material (6). In studies of the pathology of the developing renal lesion (7), it was observed that fibrinoid plugs appeared in the glomerular capillaries between 2 and 4 hours after the second, or provoking intravenous injection of toxin, their formation thus antedating by several hours the appearance of hemorrhagic necrosis of the renal cortex. This sequence of events suggested that bilateral cortical