The effect of lung edema on pulmonary vasoactivity of furosemide

Previous data suggest that furosemide improves gas exchange in pulmonary edema by preferential perfusion of nonedematous lung units. To test whether this is a direct effect of furosemide on the pulmonary vasculature as opposed to a secondary phenomenon resulting from the known peripheral effects of this drug, the effect of furosemide on the pressure-flow characteristics of the pulmonary vasculature was studied in six isolated perfused canine lungs with different degrees of gravimetrically determined edema. Furosemide shifted the pressure-flow curve by decreasing the mean intercept or average closing pressure of the pulmonary vascular bed from 13.8 +/- 5.3 to 9.5 +/- 5.4 cm H2O and the zero-flow critical closing pressure from 9.3 +/- 4.3 to 4.7 +/- 3.5 cm H2O (P less than 0.05). The slopes of these curves did not change between control and furosemide treatment. The decrease in intercept and the decrease in zero-flow critical closing pressures were closely correlated with the increase in edema (r = 0.895 for average closing pressure and r = -0.928 for critical closing pressure) (P less than 0.05). Furosemide doubled the pulmonary blood flow in the isolated lobe for the same driving pressure and the greater the amount of lobar edema the less pronounced was this furosemide-associated increase in blood flow. This direct effect of furosemide on the pulmonary vasculature could explain the improved gas exchange seen before a decrease in pulmonary edema, since this pulmonary vasoactivity would result in preferential perfusion of nonflooded alveolar units.