The effect of furosemide infusion on serum epidermal growth factor concentration after acute lung injury

Acute lung injury and its more severe form, acute respiratory distress syndrome, are clinical syndromes of progressive hypoxemia and ventilation-perfusion mismatch with decreasing pulmonary compliance in the absence of congestive heart failure. Epidermal growth factor is involved in the pathogenesis of airway inflammation as well as a proinflammatory effect in other tissues. Furosemide has been shown to improve pulmonary gas exchange and intrapulmonary shunt by a nondiuretic mechanism in animal models of acute respiratory distress syndrome. The current study was undertaken to clarify whether furosemide attenuates the inflammatory response by changing the epidermal growth factor level in patients with acute lung injury. A prospective, randomized clinical trial involving 30 patients with acute lung injury was designed and conducted over 7 days. The measured outcomes included hemodynamics, acute physiology and chronic health evaluation (APACHE II) scores, and oxygenation. The serum specimens were analyzed with enzyme-linked immunoassay (ELISA) for epidermal growth factor at baseline, then 3 and 7 days after acute lung injury. The ratio of partial pressure of arterial oxygen (PaO2) to fraction of inspired oxygen (FIO2) improved in the furosemide-treated group within 24 hours (from 180 to 264; P = .01). The mean arterial pressure and heart rate was greater in this group than in the control group (that received no furosemide) on day 7 (P = .027). The mean arterial pressure increased and the heart rate decreased over time in the treatment group, but not significantly. Serum epidermal growth factor levels also were not significantly different between the furosemide treatment group and the control group (P > .05). Continuous furosemide infusion improves oxygenation and hemodynamics in patients with acute lung injury, but not through a change in the serum epidermal growth factor level. Further study is needed to determine the exact mechanism of furosemide action in patients with acute lung injury and acute respiratory distress syndrome.