Two experiments were conducted to evaluate the effects of arginine, vitamin E, and their combination on cardiopulmonary performance and nitric oxide synthase (NOS) activity in broilers undergoing cold-induced ascites (pulmonary hypertension) after an acute challenge with epinephrine. One day-old male broilers ( n = 25/treatment) were supplemented with arginine (0.3% water supplementation), vitamin E (400 IU/L or kg, water or feed supplementation; experiment 1 and 2 respectively) or both compounds, above NRC (1994) recommendations. From day 28 to 42, a catheterization was performed (n = 8/treatment) to evaluate pulmonary and mean arterial pressures, and heart rate. After recording baseline values, two injections of epinephrine (1 or 0.5 mg/kg body weight, experiment 1 and 2, respectively) were administered in a 20 min interval. The NOS activity was estimated through the conversion of 14C-arginine to 14C-citrulline in isolated pulmonary arteries ( n = 8/treatment). Overall, the time taken for pulmonary arterial pressure to return to values no different from initial baseline levels was longer for the birds consuming high levels of vitamin E (alone or in combination with arginine) compared to birds supplemented only with arginine. Although NOS activity was highly variable, birds fed with high arginine levels tended to have the lowest NOS activity. These results showed that vitamin E supplementation at the levels used in these experiments has detrimental effects on cardiopulmonary performance, and does not improve NOS activity in isolated pulmonary arteries.

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Two identical experiments were conducted to evaluate the combined effects of arginine (AR), vitamin E (VE) and vitamin C (VC) on cardiopulmonary performance and ascites parameters of broilers reared under cold environmental temperature. One d old male broilers were fed a basal corn-soybean meal diet (CTL, 1.2 % AR and 40 IU VE), the basal diet supplemented with 1% AR and either 200 IU VE (AE group), or 500 mg of VC (AC group), or a combination of VE and VC (AEC group) at the same level per kg of feed. Pulmonary arterial pressure (PAP) and mean arterial pressure (MAP) were recorded in clinically healthy anesthetized birds (28-42 d old) before and after an epinephrine challenge (EPI, 0.5 mg/kg BW i.v.), Amino-guanidine Hemisulphate (AG, 100 mg/kg BW i.v.) and N-Nitro L-Arginine Methyl Ester (L-NAME 50 mg/kg BW, i.v.) at 20 min intervals. The PAP increased 30 s after EPI in all birds, but the peak PAP was lower in the AEC group than in all the other birds. After 120 s of challenge the PAP was lower in AEC birds compared to the other birds. The PAP returned to pre-EPI levels within 300 s in all groups. The PAP was increased ( P< 0.05) within 60 s after the AG and L-NAME challenge in all groups, but no differences were found among groups. Plasma nitric oxide (NO) was higher in the AEC birds than in all the other groups before and after challenge. Our results showed that birds fed AEC maintained a lower PAP than the CTL birds after EPI elicited an increase in cardiac output and this can be explained by a higher production of NO. A combination of AR, VE, and VC may have complementary effects against oxidative stress, protecting the endothelium and preserving NO function.

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