Titlebook: Shock, Sepsis, and Organ Failure; Second Wiggers Berna Günther Schlag,Heinz Redl,Daniel L. Traber Conference proceedings 1991 Springer-Verl

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Modulation of Hepatic Function in Endotoxemia by Intercellular Communicationa pivotal role in the homeostasis of blood glucose. Glycogen synthesis and breakdown, and gluconeogenesis are under strict hormonal regulation. Besides the well known stimulators of glycogenolysis, i.e. glucagon, epinephrine, vasopressin (VP) (Kraus-Friedman 1984; Exton 1985), other factors e.g. the

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Cytokine-Dependent Interleukin-8 Expression and its Role in Cell Communicationsuccessful leukodiapedesis to occur, granulocytes must first physically adhere to endothelial cells that line post-capillary venules and then undergo directed migration in response to established chemotactic gradients. The transendothelial trafficking of these inflammatory cells occurs in the presen

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Trauma and Sepsis Induced Activation of Granulocytes, Monocytes/Macrophages and Endothelial Cells inarly) and bacterial products (late) induced generalized inflammation. Organ failure is the final result of the action of inflammatory mediators, which cause a permeability increase as well as cellular edema.

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Mechanisms of Vascular Impairment During Endotoxaemia with Special Reference to the Role of the L-arular resistance, often with a normal or elevated cardiac output (Siegel et al. 1971; Groeneveld et al. 1986; Thijs and Groeneveld 1988). This loss of vascular tone can be persistent (‘unrelenting hypotension’: Thijs et al. 1987) and is one of the major causes of death in these patients (Parker et al

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Experimental Evidence of Bacterial Translocation in Traumaerformed in the 1960’s (10,11) documented that bacteria and endotoxin originating in the gut may gain access to the systemic circulation in a wide variety of patients, this concept was largely ignored until the middle to late 1970’s.