Studies were made in 5 monkeys, 7 rabbits, and 33 cats of the effect of gram-negative endotoxin on aortic, pulmonary artery (PAP), and portal venous (PVP) pressures; and on changes in weight of a short segment of intestine. Studies of blood pooling were also made in 12 cats. The responses in these species were compared with those previously observed in the dog. Although variable degrees of hypotension developed at one time or another in all animals following injection of endotoxin, the early precipitous hypotension that characteristically occurs in the dog was observed only in the cat. However, in this species the dramatic fall in pressure could be ascribed to pulmonary vascular constriction and acute right ventricular hypertension and failure, and not to splanchnic pooling. PAP also became elevated in the monkey and the rabbit, but usually was of lesser magnitude and did not appear to explain the development of the relatively late hypotension that occurred in these species. The absence of significant increases in gut weight and the minor increments in PVP in all animals indicate that in none of these species is hepatic vein constriction and splanchnic pooling a significant mechanism in producing early shock as it is in the dog. Pathologic gross and microscopic studies in the monkey and gross examinations in the other species supported this conclusion.
The earliest histologic lesion in the generalized Shwartzman reaction, which is produced in rabbits by two appropriately spaced intravenous injections of endotoxin derived from Gram-negative microorganisms, is the deposition of a homogenous, eosinophilic material with the staining properties of fibrinoid within the lumen of the glomerular capillaries of the kidneys. Occlusion of the glomerular circulation is followed by the development of bilateral renal cortical necrosis, the characteristic gross lesion which identifies the reaction (1-3). The fibrinoid material becomes visible as a layer along the inner surface of the capillary walls, or as masses which fill the lumen of the vessels, within the first 6 or 8 hours after the second injection of endotoxin. Similar material appears within the walls of the coronary arteries, in the substance of the mitral and aortic valves, and in the sinusoids of the liver and spleen (2, 3).A central problem in the pathogenesis of the generalized Shwartzman reaction is the origin and nature of the fibrinoid material. Histologic studies, reported elsewhere (2, 3), indicate that it is derived from the circulating blood. The demonstration that its appearance can be prevented by treatment of the animals with heparin at the time of the second injection of endotoxin (4) sug-
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