- Effects of arginine and antioxidant vitamins on pulmonary artery reactivity to phenylephrine in the broiler chicken.
Effects of arginine and antioxidant vitamins on pulmonary artery reactivity to phenylephrine in the broiler chicken.
The effects of supplemental l-arginine (Arg), vitamin E (VE), and vitamin C (VC) on vascular reactivity to phenylephrine (PE) were examined in clinically healthy hypoxemic male broiler chickens. One-day-old chicks were housed in wire cages and randomly allocated to 1 of 3 dietary treatments: control (CTL; n = 80; 3,200 kcal of ME/kg, 23% CP, 1.55% Arg and 40 IU of VE/kg of feed), high-Arg (HA; n = 40; CTL + 0.8% Arg), or high-Arg and high antioxidant-vitamin diet (AEC; n = 40; HA + 200 IU of VE/kg of feed and 500 mg of VC/kg of feed). At d 14, 40 CTL birds and all the HA and AEC birds had a primary pulmonary bronchus surgically occluded (PBO). Forty CTL broilers underwent surgery without occluding the bronchus (SHAM). Pulmonary artery (PA) rings were mounted for isometric tension recordings 14 to 21 d postsurgery. The HA-PBO and AEC-PBO PA were immersed in Krebs-Henseleit buffer plus a vehicle (VehCtl) or Krebs-Henseleit buffer plus supplemental Arg, or Arg, VE, and VC (A-E-C). Maximal contractile response to PE of the CTL-SHAM PA (16 ± 14 mg/mg of dry tissue) was one-tenth compared with that of the CTL-PBO PA (159 ± 13 mg/mg), whereas the PA contractility in the supplemented groups was one-ninth compared with those of the CTL-PBO (17.9 ± 13.0 mg/mg, 17.90 ± 13.0 mg/mg for the HA-PBO+Arg and AEC-PBO+A-E-C treatments, respectively). Supplementing the bath with Arg did not change the maximal response to PE compared with the vehicle control (16.7 ± 12.2 mg/mg for HA-PBO-VehCtl). However, supplementing the bath with A-E-C produced a one-fourth reactivity compared with that of the vehicle control (80.7 ± 13.0 mg/mg for AEC-PBO-VehCtl). The PBO increased PA reactivity to PE, but supplemental Arg plus VE and VC significantly reduced it. Differential reactivity responses to PE may have been the result of protective effects of Arg, VE, and VC, implicating oxidative stress in endothelial dysfunction as well as in the upregulation of smooth muscle contractility.