| pubmed-article:2254978 | pubmed:abstractText | Following resuscitation from shock, the clinical phase of persistent hypermetabolism is entered from which a substantial number of patients transcend into progressive organ failure and expire. The available epidemiologic, physiologic, and metabolic data are consistent with the position that a persistent degree of microcirculatory hypoxia, although it may be present in amounts that are below the sensitivity of current detection systems, becomes an increasingly less important etiologic factor as the organ failure disease progresses. Rather, aerobic metabolism appears to be the dominant mechanism of meeting the increased work loads and energy demands. There is an increasing body of evidence that cytokine release systemically, and increased cell-cell interaction through cytokines and prostanoids locally, may alter not only parenchymal function in the proximity of these mononuclear cells, but organ function at distant sites. If this latter hypothesis continues to be substantiated, it implies that the underlying cell and organ dysfunction may indeed be reversible if appropriate counter-regulatory mechanisms could be developed and the appropriate timing of their application understood. | lld:pubmed |
