2005b. Nω-nitroL-arginine methyl ester (L-NAME) amplifies the pulmonary hypertensive response to microparticle injections in broilers

ABSTRACT The pulmonary hypertensive response to bacterial lipopolysaccharide (LPS, endotoxin) varies widely among individual broilers, leading to the sugges-tion that innate variability may exist in the proportions or profiles of chemical mediators released during the en-suing inflammatory cascade. LPS induces the expression of nitric oxide synthase (iNOS), which produces the vaso-dilator nitric oxide (NO) to modulate the responses to concurrently produced vasoconstrictors. In experiment 1, broilers were given the NOS inhibitor Nω-nitro-L-arginine methyl ester (L-NAME), followed by a supra-maximal dose of LPS while the pulmonary arterial pressure was recorded. In experiment 2 the cardiac output also was recorded before and following the i.v. injection of L-NAME. In both experiments, injection with L-NAME modestly increased the pulmonary arterial pressurewhen compared with control values, confirming previous re-ports that tonic/basal NO synthesis is required to pro-mote flow-dependent pulmonary vasodilation in chick-ens. This response to L-NAME occurred in spite of a ten-dency for cardiac output and stroke volume to decline and, therefore, can be attributed to pulmonary vasocon