title: Hypoxic signal transduction in critical illness.
abstract: Derangements in tissue perfusion occur during critical illness, and the resulting deficit in oxygen delivery may play an important role in the pathogenesis of hemorrhagic and septic shock. Cells and organisms have developed a variety of adaptive strategies to maintain adequate energy production to maintain normal cellular function under hypoxic conditions. Recent studies from our laboratory suggest that certain proinflammatory cytokines, which are likely to be elaborated during or after shock, can interfere with the ability of cells to adapt to hypoxia, and thereby contribute to the development of organ system dysfunction.
authors.affiliation: Department of Surgery, University of Pittsburgh Medical School, PA, USA.
authors.forename: D J
authors.initials: DJ
authors.lastname: Bertges
authors.forename: M P
authors.initials: MP
authors.lastname: Fink
authors.forename: R L
authors.initials: RL
authors.lastname: Delude
mesh_terms: D016638:Critical Illness; D016207:Cytokines / Q000009:adverse effects*; D005786:Gene Expression Regulation; D006801:Humans; D000860:Hypoxia / Q000150:complications / Q000235:genetics / Q000378:metabolism / Q000503:physiopathology*; D009102:Multiple Organ Failure / Q000209:etiology; D010101:Oxygen Consumption; D012771:Shock, Hemorrhagic / Q000378:metabolism / Q000503:physiopathology*; D015398:Signal Transduction / Q000502:physiology*
chemical_list: D016207:Cytokines