Abstract
A recent hypothesis concerning host susceptibility to shock postulates that the basic etiology of shock phenomena centers on vascular smooth muscle injuries (Palmerio and Fine, 1969). Palmerio and Fine (1969) presented evidence that resistance to shock is dependent upon the antibacterial and detoxification potential of the RES. A shock model in which the critical nature of the RES has been implicated is endotoxin-induced shock (Beeson, 1947 a, b). Beeson in 1947 first demonstrated the importance of RES function in host defense against endotoxin-induced pathology (Beeson, 1947 a, b). Rabbits, previously tolerant to the febrile effects of endotoxin and subsequently treated with a large dose of colloidal materials which were known to temporarily depress RES activity, responded to the pyrogenic effects of endotoxin (Beeson, 1947a). In addition, an RES “blockading” dose of colloidal material resensitized tolerant rabbits to the Shwartzman reaction and enhanced lethality when endotoxin was subsequently administered (Beeson, 1947b). Passive plasma transfer studies indicated that RES blockade retarded the clearance of circulating endotoxin (Beeson, 1947a). Beeson speculated that diminution in phagocytosis of endotoxin enabled the endotoxin to injure various tissues as reflected by fever (Beeson, 1947a).
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Di Luzio, N.R., Crafton, C.G. (1970). A Consideration of the Role of the Reticuloendothelial System (RES) in Endotoxin Shock. In: Bertelli, A., Back, N. (eds) Shock: Biochemical, Pharmacological, and Clinical Aspects. Advances in Experimental Medicine and Biology, vol 9. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-3201-5_3
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DOI: https://doi.org/10.1007/978-1-4684-3201-5_3
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