Am. J. Respir. Crit. Care Med.,
Volume 156, Number 2, August 1997, 478-483
Dilatory Effect of Furosemide on Rat Tracheal
Arterioles and Venules
MICHEL R.
CORBOZ,
STEPHEN T.
BALLARD,
SARAH K.
INGLIS,
and
AUBREY E.
TAYLOR
Department of Physiology, College of Medicine, University of South Alabama, Mobile, Alabama
Furosemide pretreatment greatly reduces the severity of an asthmatic response to several types of
bronchoconstrictor challenge. Indirect evidence suggests that furosemide exerts its protective effects
by dilating the airway vasculature during thermal stress. To test the hypothesis that furosemide dilates airway microvessels, the tracheas of anesthetized rats were surgically exposed and continuously
suffused with Krebs Ringer bicarbonate warmed to 37° C. Tracheal adventitial arterioles (13.0 to 41.0 µm initial diameter, n = 47) and venules (50.0 to 99.0 µm initial diameter, n = 46) were visualized
with a videomicroscope, and vessel diameters were measured using videocalipers. When vessels were
preconstricted with 10
4 M phenylephrine, a selective 
1-adrenergic agonist, and then treated with
104 M furosemide, significant (p < 0.05) dilation was observed in both arterioles (from 64.6 to
79.5% of their initial diameter) and venules (from 52.1 to 65.4% of their initial diameter). When vessels were preconstricted with 104 phenylephrine, after pretreatment with the cyclooxygenase inhibitor indomethacin (5.0 mg/kg), 104 M furosemide significantly dilated arterioles (from 77.5 to 93.0% of their initial diameter) and venules (from 58.5 to 80.1% of their initial diameter). In vessels preconstricted with 103 M L-NAME, an inhibitor of nitric oxide synthesis, addition of 104 M furosemide to
the suffusion still caused significant dilation in arterioles, from 77.4 to 88.8% of their initial diameter,
and in venules from 79.5 to 86.7% of their initial diameter. These data confirm that furosemide,
when applied topically, dilates tracheal arterioles and venules by cyclooxygenase- and nitric oxide-
independent mechanisms.
