Allicin, an extract from garlic, has been shown to be a systemic and pulmon
ary arterial vasodilator that acts by an unknown mechanism. In the present
experiments, pulmonary vascular responses to allicin (10-100 mu g), allyl m
ercaptan (0.3-1 mg), and diallyl disulfide (0.3-1 mg) were studied in the i
solated lung of the rat under constant-flow conditions. When baseline tone
in the pulmonary vascular bed of the rat was raised to a high-steady level
with the thromboxane A(2) mimic U-46619, dose-related decreases in pulmonar
y arterial pressure were observed. In terms of the mechanism of action of a
llicin vasodilator activity in the rat, responses to allicin were not signi
ficantly different after administration of the nitric oxide synthase inhibi
tor N-omega-nitro-L-arginine methyl ester, the K-ATP(+), channel antagonist
U-37883A, or the cyclooxygenase inhibitor sodium meclofenamate, or when lu
ng ventilation was interrupted. These data show that allicin has significan
t vasodilator activity in the pulmonary vascular bed of the rat, whereas al
lyl mercaptan and diallyl disulfide produced no significant changes in pulm
onary arterial perfusion pressure. The present data suggest that pulmonary
vasodilator :responses to allicin are independent of the synthesis of nitri
c oxide, ATP-sensitive K+ channels, activation of cyclooxygenase enzyme, or
changes in bronchomotor tone in the pulmonary vascular bed of the rat.