Concurrent supplementation of arginine, vitamin E, and vitamin C improve cardiopulmonary performance in broilers chickens
2009
Ruiz-Feria, C.A.
Two experiments were conducted to evaluate the effects of arginine, vitamin E (VE), and vitamin C (VC) on cardiopulmonary performance and ascites parameters of broilers reared under a cold environmental temperature. One-day-old male broilers were fed a basal corn-soybean meal diet (control, 1.2% arginine and 40 IU of VE), or the basal diet supplemented with 1% arginine and either 200 IU vitamin E (AE), 500 mg of vitamin C (AC), or a combination of VE and VC at the same amounts (AEC) per kilogram of feed. Pulmonary arterial pressure (PAP) and mean arterial pressure were recorded in clinically healthy, anesthetized birds (28 to 42 d old) before and after an epinephrine (Epi) challenge (0.5 mg/kg of BW, i.v.), an aminoguanidine hemisulfate challenge (100 mg/kg of BW, i.v.), and an N-nitro-L-arginine methyl ester challenge (50 mg/kg of BW, i.v.) at 20-min intervals. Data were analyzed by repeated measures ANOVA, and the Student Newman-Keuls test was used to separate means within groups. The PAP increased 30 s after the Epi challenge in all birds, but the peak PAP was lower in the AEC group than in all the other groups, whereas birds in the AE and AC groups had lower PAP peaks than did the control group. After 120 s of challenge, the PAP was lower in AEC birds compared with the other birds. The PAP returned to pre-Epi amounts within 300 s in all groups. The PAP was increased (P < 0.05) within 60 s after the aminoguanidine hemisulfate and N-nitro-L-arginine methyl ester challenges in all groups, but no differences were found among groups. The mean arterial pressure responses did not differ among groups. Plasma NO was greater in the AEC group than in all the other groups before and after the Epi challenge. These results showed that Epi elicited lower amplitude PAP and less prolonged increases in PAP in birds from the AEC group, and this may have been related to the increased vasodilation attributable to NO production. The AEC may have had complementary effects against oxidative stress, protecting the endothelium and preserving NO function.
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