Effect of endotoxin on oleic acid lung injury does not depend on priming.

Recent studies have demonstrated significant synergistic physiological and biochemical effects between low-dose endotoxin (Etx) administration and oleic acid (OA)-induced canine lung injury. To evaluate whether this interaction depends on Etx priming of some key cell population, we compared the effects of giving low-dose Etx both after as well as before inducing lung injury with OA. In addition to hemodynamic and blood-gas measurements, positron emission tomographic imaging was used to measure edema accumulation and intrapulmonary blood flow distribution. Biochemical measurements of the stable metabolites of prostacyclin and thromboxane were obtained as well as measurements of isoprostanes and reactive sulfhydryls as evidence for possible concomitant oxidant production. We found that the physiological and biochemical effects of low-dose Etx developed 30-45 min after its administration, regardless of whether Etx was administered before or after OA. No increase in either isoprostane or reactive sulfhydryl production after Etx and/or OA was detected. These data suggest that the synergistic effect of low-dose Etx and OA-induced lung injury is not due to a priming effect of Etx.

[1]  R. Bellomo,et al.  The effect of intensive plasma water exchange by hemofiltration on hemodynamics and soluble mediators in canine endotoxemia. , 2000, American journal of respiratory and critical care medicine.

[2]  D. Schuster,et al.  Role of cyclooxygenase-2 in oleic acid-induced acute lung injury. , 1999, American journal of respiratory and critical care medicine.

[3]  D. Schuster,et al.  Response to inhaled nitric oxide in acute lung injury depends on distribution of pulmonary blood flow prior to its administration. , 1999, American journal of respiratory and critical care medicine.

[4]  J. Mitchell,et al.  Synergy between cyclo‐oxygenase‐2 induction and arachidonic acid supply in vivo: consequences for nonsteroidal antiinflammatory drug efficacy , 1999, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[5]  A P Wheeler,et al.  Treating patients with severe sepsis. , 1999, The New England journal of medicine.

[6]  J. Morrow,et al.  Mass spectrometric quantification of F2-isoprostanes in biological fluids and tissues as measure of oxidant stress. , 1999, Methods in enzymology.

[7]  A. Matsukawa,et al.  Crucial role of group IIA phospholipase A(2) in oleic acid-induced acute lung injury in rabbits. , 1999, American journal of respiratory and critical care medicine.

[8]  D. Schuster.  The evaluation of lung function with PET. , 1998, Seminars in nuclear medicine.

[9]  Caroline Gilbert,et al.  Expression and activity of prostaglandin endoperoxide synthase‐2 in agonist‐activated human neutrophils , 1998, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[10]  D. Schuster,et al.  Synergistic hemodynamic effects of low-dose endotoxin and acute lung injury. , 1998, American journal of respiratory and critical care medicine.

[11]  W. Seeger,et al.  Endotoxin priming of thromboxane-related vasoconstrictor responses in perfused rabbit lungs. , 1997, Journal of applied physiology.

[12]  W. Seeger,et al.  Synergism of alveolar endotoxin "priming" and intravascular exotoxin challenge in lung injury. , 1996, American Journal of Respiratory and Critical Care Medicine.

[13]  A. Baue.  MOF/MODS, SIRS: AN UPDATE , 1996, Shock.

[14]  J. Maclouf,et al.  Cyclooxygenases-1 and −2 of Endothelial Cells Utilize Exogenous or Endogenous Arachidonic Acid for Transcellular Production of Thromboxane (*) , 1996, The Journal of Biological Chemistry.

[15]  C. Thiemermann,et al.  Cytokine‐mediated induction of cyclo‐oxygenase‐2 by activation of tyrosine kinase in bovine endothelial cells stimulated by bacterial lipopolysaccharide , 1995, British journal of pharmacology.

[16]  D. Schuster,et al.  What is acute lung injury? What is ARDS? , 1995, Chest.

[17]  R. Allen,et al.  Prior exposure to endotoxin exacerbates lipopolysaccharide-induced hypoxemia and alveolitis in anesthetized swine. , 1994, Shock.

[18]  D. Schuster.  ARDS: clinical lessons from the oleic acid model of acute lung injury. , 1994, American journal of respiratory and critical care medicine.

[19]  D. Schuster,et al.  Thromboxane receptor stimulation/inhibition and perfusion redistribution after acute lung injury. , 1993, Journal of applied physiology.

[20]  C. McCall,et al.  Lipopolysaccharide-induced expression of prostaglandin H synthase-2 in alveolar macrophages is inhibited by dexamethasone but not by aspirin. , 1993, Biochemical and biophysical research communications.

[21]  D. Schuster,et al.  Eicosanoid balance and perfusion redistribution of oleic acid-induced acute lung injury. , 1992, Journal of applied physiology.

[22]  A. Hamvas,et al.  Inflammation and oxygen free radical formation during pulmonary ischemia-reperfusion injury. , 1992, Journal of applied physiology.

[23]  D. Herndon,et al.  Time course of hypoxic pulmonary vasoconstriction after endotoxin infusion in unanesthetized sheep. , 1991, Journal of applied physiology.

[24]  D. Schuster,et al.  Perfusion redistribution after alveolar flooding: vasoconstriction vs. vascular compression. , 1991, Journal of applied physiology.

[25]  N. Suttorp,et al.  Endotoxin alters arachidonate metabolism in pulmonary endothelial cells. , 1987, The American journal of physiology.

[26]  R. Snyderman,et al.  The NADPH oxidase of human polymorphonuclear leukocytes. Evidence for regulation by multiple signals. , 1984, The Journal of biological chemistry.

[27]  E. K. Weir,et al.  Endotoxin and prevention of hypoxic pulmonary vasoconstriction. , 1976, The Journal of laboratory and clinical medicine.