SUPPLEMENTAL L-ARGININE ATTENUATES PULMONARY-HYPERTENSION SYNDROME (ASCITES) IN BROILERS

The incidence of pulmonary hypertension syndrome (PHS; ascites) was ev aluated in two experiments using broiler breeder male by-product chick s exposed after 3 wk of age to cool environmental temperatures (10 to 15 C). In Experiment 1, 3- to 6-wk-old birds were fed a grower diet to which 0 (Control), .25, .5, or 1% supplemental L-arginine HCl had bee n added. During Weeks 7 to 8, all groups in Experiment 1 were fed a fi nisher diet containing no supplemental arginine. In Experiment 2, the Control group received no supplemental arginine, a second group was fe d a grower diet supplemented with 1% L-arginine HCl (Weeks 3 to 6), an d a third group was fed grower and finisher diets supplemented with 1% L-arginine HCl (Weeks 3 to 8). Cumulative PHS mortality was significa ntly reduced by 1% L-arginine HCl on Days 34 to 46 in Experiment 1. Wh en data from all birds fed grower or finisher diets supplemented with 1% L-arginine HCl were pooled in Experiment 2, cumulative PHS mortalit y was marginally lower (P = .065) than for the Control group. Suppleme ntal L-arginine HCl had no effect on final body weights, weight gain, or feed conversion in either experiment. Neither body weight on Day 1 or 21 nor net weight gain from Days 1 to 21 determined susceptibility to PHS during the subsequent grower and finisher intervals in either e xperiment. On Day 55 of Experiment 2, large healthy birds fed diets su pplemented with 1% L-arginine HCl had significantly lower right:total ventricle weight ratios than Control birds, indicating that L-arginine HCl supplementation reduced right ventricular hypertrophy, presumably by reducing pulmonary arterial pressure. These results are consistent with the hypothesis that supplemental L-arginine, above levels requir ed for maximal growth, is required as a substrate for the production o f nitric oxide, a powerful endogenous pulmonary vasodilator.