Isolated third-order pulmonary arteries and veins from sheep were exam
ined for the effects of septicemia on norepinephrine-induced contracti
ons, nitric oxide INO)-mediated dilation, and basal cyclic GMP levels.
The groups studied were as follows: control sheep (n = 7); sheep give
n live Pseudomonas aeruginosa (Ps, n = 6) for 48 h; and sheep given N-
G-mono-methyl-L-arginine during the last 24 h of Ps infusion (Ps-L-NMM
A, n = 4). The norepinephrine-induced contractions were significantly
greater (p < .05) in arteries from septic (Ps and Ps-L-NMMA) sheep. Ba
sal cyclic GMP levels were similar in all of the arteries. The norepin
ephrine-induced contractions were significantly depressed (p < .05) in
veins from septic (Ps and Ps-L-NMMA) sheep. Basal cyclic GMP levels i
n veins from Ps sheep were markedly elevated (p < .01). N-omega-nitro-
L-arginine methyl ester (L-NAME) ex vivo decreased cyclic GMP in both
arteries and veins. Removal of endothelium enhanced contractions and d
ecreased cyclic GMP in arteries and veins only from control sheep. The
results show that septicemia differently affects the pulmonary artery
and vein. The enhanced vasoconstriction of the artery is due to decre
ased endothelium-dependent NO release; the attenuated vasoconstriction
of the vein is associated with NO-mediated increased cyclic GMP level
s.