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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Pathogenesis of experimental adrenal hemorrhagic necrosis ("apoplexy"): ultrastructural, biochemical, neuropharmacologic, and blood coagulation studies with acrylonitrile in the rat.

The pathogenesis of experimental adrenal hemorrhagic necrosis produced by acrylonitrile in the rat was investigated by various morphologic, biochemical, and pharmacologic methods. One dose of this chemical injected intravenously caused 100 per cent incidence of adrenal hemorrhage and necrosis in 90 to 120 minutes. Electron microscopy, histochemistry, and light microscopy combined with colloidal carbon labeling suggested an early damage (30 minutes after administration of acrylonitrile) to the vascular endothelium in the adrenal cortex, prominent at 60 minutes, when lesion to the parenchymal cells was not visible. The use of extracellular diffusion tracer horseradish peroxidase further indicated that parenchymal cell injury was a late event. Damage to the vascular endothelium in the adrenal cortex was associated with retrograde embolization of medullary cells and cell fragments into the cortical capillaries. The ultrastructurally demonstrated platelet aggregation and fibrin precipitation at the sites of discontinuous vascular endothelium were accompanied by a decrease in circulating platelets and fibrinogen as well as prolongation of prothrombin, partial thromboplastin, and thrombin time. The concentration of dopamine, unlike that of noradrenaline, in the adrenals but not in the brain of rats injected with acrylonitrile showed a time-dependent elevation. Pretreatment with phenoxybenzamine (alpha-adrenergic antagonist) or labetalol (alpha- and beta-adrenergic blocker) or metyrapone (11-beta-hydroxylase inhibitor) and the depletion of catecholamines by reserpine or prior medullectomy prevented the chemically induced adrenal necrosis. These results indicate that the presence of a functional adrenal cortex is necessary for the development of cortical damage which is associated with early vascular lesion caused and/or modulated by vasoactive amines from the medulla and/or (metabolites of) acrylonitrile.[1]


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