Metabolism during shock and sepsis.
The shock-induced changes in the cells of both peripheral tissues and vital organs apparently occur mainly in the energy pathways. The normal flow of these pathways is inhibited by the lack of oxygen; and both this anoxia and the consequent energy deficit inhibit the function of membranes. As a result, the active transport of gluconeogenic substrates, such as glucose, amino acid, and fatty acid, is blocked; this allows potassium efflux and sodium influx. Gluconeogenesis is inhibited either by a direct effect of endotoxin on the gluconeogenic enzymes or by the lack of ATP. Prolonged anoxia interferes with the oxidation of pyruvate and increases the intracellular and extracellular levels of lactate. The intracellular acidosis or the direct effect of endotoxin on the membranes finally causes the permeability or lysis of cellular and lysosomal membranes. Lysosomal hydrolases have been implicated in the cellular pathology of shock, the production of MDF, and the adverse effects on endothelial cells of the vascular system. Further ATP deficiency may alter protein biosynthesis.
D050260:Carbohydrate Metabolism; D002462:Cell Membrane / Q000378:metabolism; D004734:Energy Metabolism; D006801:Humans; D050356:Lipid Metabolism; D008247:Lysosomes / Q000201:enzymology; D011506:Proteins / Q000378:metabolism; D018805:Sepsis / Q000378:metabolism*; D012769:Shock / Q000378:metabolism*
D011506:Proteins