To test the hypothesis that pulmonary vasoactivity of
furosemide redistributes blood away from edematous lung, thus improving gas exchange, we studied two groups of 10 dogs each with unilobar
oleic acid edema, treating one group with 1 mg/kg
furosemide 2 h after the
oleic acid. Pulmonary perfusion distribution was determined with radio
microspheres. Shunts of the injured lobe, measured from O2 contents of lower lobar pulmonary venous blood, increased significantly (P less than 0.05) at 2 h after injury in both groups. Within 0.5 h after
furosemide the lobar shunt decreased in the treated animals from 40.1 +/- 20.6 to 28.6 +/- 20.1% and increased from 21.4 +/- 14.0 to 53.8 +/- 26.9% in the control group (P less than 0.05). Mean fractional lobar perfusion to the injured lobe increased from 18.2 +/- 4.8 to 21.6 +/- 6.4% (P less than 0.05) in the
furosemide group but decreased from 20.1 +/- 3.5 to 16.1 +/- 4.4% (P less than 0.05) in the controls.
Wet lung-to-
body weight ratios of the edematous lobes did not differ between the two groups. Our data suggest the possibility that, before decreasing
edema,
furosemide improved shunt through pulmonary vascular effects by preferential perfusion of nonflooded alveolar units.