Shock, Sepsis, and Organ Failure

Gut as a Source of Organ Failure.- Hypoxic Damage of the Gut in Shock.- Experimental Evidence of Bacterial Translocation in Trauma.- Bacterial Translocation in a Baboon Model of Hypovolemic-Traumatic Shock.- Bacterial Translocation Across a Histologically Intact Intestinal Mucosa.- Clinical Evidence of Bacterial Translocation from the Gut.- Role of Bacterial Translocation and Selective Gut Decontamination in the Development of Multiple Organ Failure.- Metabolic Aspects of the Liver in Sepsis.- The Liver as Modulator of the Host-Defense Response: Host-Defense Failure Disease as a Manifestation of Hepatic Decompensation.- Concepts of Liver Protein Metabolism in Sepsis.- Increased Glucose Uptake and Superoxide Anion Production After Priming of Activation of Hepatic Phagocytes: A Potential Source of Liver Damage.- Modulation of Hepatic Function in Endotoxemia by Intercellular Communication.- Endothelium as a Target in Sepsis.- Cytokine-Dependent Interleukin-8 Expression and its Role in Cell Communication.- Trauma and Sepsis Induced Activation of Granulocytes, Monocytes/Macrophages and Endothelial Cells in Primates.- Molecular Mechanisms of Neutrophil-Mediated Pulmonary Microvascular Injury: Role of Adhesion Proteins.- Pathogenetic Linkages Between Gram Negative Septic Shock and the Cellular Initiation and Regulation of Coagulation.- Sepsis, Disseminated Intravascular Coagulation and Multiorgan Failure: Catastrophic Events in Severe Burns.- Mechanisms of Vascular Impairment During Endotoxaemia with Special Reference to the Role of the L-arginine Pathway.- Permeability Changes During Experimental Endotoxemia and Sepsis.