TITLE:
Body Weight and Steroidal Implants Impact Animal Growth Performance, Sera Metabolites, and Pulmonary Arterial Pressure in Feedlot Cattle
AUTHORS:
Tyler A. Vogel, Joseph M. Neary, Zachary K. Smith, Bradley J. Johnson
KEYWORDS:
Cattle, Estradiol, Pulmonary Pressure, Trenbolone
JOURNAL NAME:
Open Journal of Animal Sciences,
Vol.10 No.3,
June
19,
2020
ABSTRACT: The study objective was to evaluate steer growth performance, sera metabolite responses, carcass characteristics, and pulmonary arterial pressure as affected by body weight at time of implantation and steroidal implant administration. Crossbred steers (n = 20) were used in a 2 × 2 factorial arrangement of treatments in a completely randomized design experiment, Factors included: body weight: light (L), or heavy (H) and implant: Non-implanted (NoIMP), or Implanted (IMP) with steer serving as the experimental unit for all analyses. Initial weights for L and H steers were 398 ± 27.6 and 547 ± 25.2 kg, respectively. Implanted steers received a terminal implant (200 mg trenbolone acetate and 20 mg estradiol-17β; Revalor-200; Merck Animal Health, Madison, NJ) on d 0. Cattle within treatments were group housed in common pens (n = 5 steers/pen). Bodyweight, blood samples, and pulmonary arterial pressure were collected on d 0, 14, 35, 70 and 104. Cattle were fed a common diet once daily to provide ad libitum access to feed. The finishing diet contained (DM basis) 13.3% CP, 2.13 Mcal/kg NEm, and 1.45 Mcal/kg NEg. Growth performance (body weight and ADG) and carcass traits were analyzed using the MIXED procedure of SAS 9.4 (SAS Inst. Inc., Cary, NC). Sera metabolites were analyzed as repeated measures over time, with day as the repeated measure. For all analyses, α level 0.05) in ADG were observed in NoIMP vs. IMP cattle beyond d 70 (1.21 vs. 1.01 ± 0.16 kg; P = 0.38). Sera urea-N concentrations were decreased (P 0.49). The study reaffirms the effects of implanting on animal growth performance and carcass characteristics in cattle. In addition, elevated BW leads to increased pulmonary arterial pressures which may increase the risk of right-sided heart failure.