The Prevention of the Generalized Shwartzman Reaction With Sodium Warfarin

Studies are reported on the effect of immunologically induced thrombocytopenia upon the local and generalized Shwartzman phenomena. Intravenous injection of antiplatelet serum to rabbits produced profound but transient thrombocytopenia unaccompanied by significant changes in circulating leucocytes. Platelet antiserum alone given to rabbits prepared with thorotrast produced renal lesions characteristic of the Shwartzman reaction. Thrombocytopenia induced by platelet antiserum did not inhibit the cutaneous hemorrhagic lesion of the local Shwartzman phenomenon produced by sequential injections of endotoxin intracutaneously and intravenously. The implications of these observations in the pathogenesis of the local cutaneous and generalized Shwartzman reaction are discussed.

Section: Discussionmentioning

confidence: 99%

Section: (From the Department Of Medicine The Johns Hopkins Universimentioning

confidence: 99%

Platelets and the Shwartzman Phenomenon

Levin

Cluff

1965

“…Deposition of this material can be blocked by the administration of heparin (5) or coumarin compounds (6) in doses rendering the blood incoagniable. Administration of streptokinase, in doses that have been demonstrated to produce in ~qvo fibrinolysis, also prevents the accumulation of these intravascular deposits (7).…”

mentioning

confidence: 99%

Reticuloendothelial Clearance of Circulating Fibrin in the Pathogenesis of the Generalized Shwartzman Reaction

Lee

1962

188

“…Furthermore, both agents were known to prevent not only the local but also the generalized Shwartzman reac-PATHOGENESIS OP INFLAMMATION. III tion; a lesion in which leucocytic sticking figures prominently (3,4). This as well as other evidence has been regarded as support for the contention that polymerization of fibrinogen to fibrinoid is essential for development of the Shwartzman lesion (5).…”

mentioning

confidence: 59%

Studies on the Pathogenesis of Acute Inflammation

Allison

Lancaster

1961

The mechanism responsible for the sticking of white blood cells to blood vessel walls in early inflammation continues to pose a challenging problem since this reaction represents the key to an overall understanding of the exudatire events set off by injury.In studies reported earlier, interference with the clotting of blood in vivo failed to prevent the vigorous sticking of leucocytes to vascular endothelium within rabbit ear chambers damaged by heat. As a specific example, maximal activation of the endogenous fibrinolytic system of rabbits by streptokinase (SK) administration did not diminish adherence of circulating white blood cells to endothelium. Since lysis of fibrin in vitro was brisk, failure to modify the sticking reaction could be explained only by assuming that destruction of fibrin on the surfaces of both white cells and endothelium failed to keep pace with newly formed material. In a more direct approach to the problem, the behavior of white cells in damaged chambers was followed after removal of all chemically detectable fibrinogen from the systemic circulation. Even under these conditions, when fibrinogen levels were too low to measure, brisk leucocytic sticking still developed after ear chambers had been damaged by heat (1). From these data it was concluded that the sticking reaction was not causally related to formation of fibrin.Such consistent failure to halt white cell sticking led to an investigation of specific pharmacological substances known to block the clotting of blood in vivo. From preliminary observations previously reported, it was anticipated that one such agent, heparin, would materially impede the reaction (2). Although many anticoagulants were available, heparin and warfarin sodium were selected because of extensive use by others; both were of low toxicity in the ranges used; and because each could be administered parenterally to insure adequate blood levels. Furthermore, both agents were known to prevent not only the local but also the generalized Shwartzman reac-*