Changes in extravascular lung water and fatty acids in a hyperdynamic canine model of sepsis.
Several mediators, including fatty acids, have been postulated to induce the increase in permeability of the pulmonary endothelium and subsequent accumulation of extravascular lung water (EVLW) which are generally considered to be among the first events in the development of adult respiratory distress syndrome. In a canine model of hyperdynamic sepsis (hemodynamically similar to human sepsis) changes in EVLW and in concentrations of different fatty acids in the aortic and pulmonary arterial blood were measured. Two days after induction of sepsis, EVLW increased from 6.6 +/- 0.6 to 9.2 +/- 1.0 ml/kg, and the pulmonary arterial concentration of oleic acid increased from 52 +/- 4 to 73 +/- 5 mg/dl. Three days after induction of sepsis, EVLW increased further to 14.4 +/- 3.8 ml/kg and the mean concentration of oleic acid increased to 74 +/- 7 mg/dl. Twenty-four hours later, both EVLW and the mean pulmonary arterial concentration of oleic acid were not different from basal. We postulate that oleic acid, a known inducer of experimental ARDS, is one of the mediators of endothelial damage of the lung during sepsis.
D000818:Animals; D004285:Dogs; D004927:Escherichia coli Infections / Q000378:metabolism; D005110:Extracellular Space / Q000378:metabolism*; D005227:Fatty Acids / Q000378:metabolism*; D008168:Lung / Q000378:metabolism*; D011651:Pulmonary Artery / Q000378:metabolism; D011654:Pulmonary Edema / Q000378:metabolism; D012128:Respiratory Distress Syndrome / Q000378:metabolism*; D018805:Sepsis / Q000378:metabolism
D005227:Fatty Acids