0354 Angus cattle at high elevation: Comparison of models to estimate breeding values of yearling pulmonary arterial pressure

2016 ◽  
Vol 94 (suppl_5) ◽  
pp. 170-171
Author(s):  
X. Zeng ◽  
T. N. Holt ◽  
S. E. Speidel ◽  
R. M. Enns ◽  
M. G. Thomas
2020 ◽  
Vol 98 (5) ◽  
Author(s):  
Scott E Speidel ◽  
Milton G Thomas ◽  
Timothy N Holt ◽  
R Mark Enns

Abstract Pulmonary arterial pressure (PAP) is a diagnostic measure used to determine an individual’s susceptibility to developing high-altitude disease. The importance of PAP measures collected at elevations lower than the intended breeding elevation of the bulls (i.e., ≥1,520 m) is unknown. Therefore, the objective of this study was to determine the genetic relationship between PAP measures collected in a range of elevations using reaction norm models. A total of 9,177 PAP and elevation observations on purebred Angus cattle, which averaged 43.49 ± 11.32 mmHg and 1,878.6 ± 296.8 m, respectively, were used in the evaluation. The average age of the individuals in the evaluation was 434.04 ± 115.9 d. A random regression model containing the effects of sex, a linear covariate of age, a quadratic fixed covariate of elevation, and random effects consisting of a contemporary group and a linear regression of PAP on elevation was used for the evaluation of PAP. Two forms of PAP were evaluated with this model. First, to address the non-normality of the data, PAP was raised to the power of −2.6 (ptPAP) based on the results of a Box–Cox analysis. Second, raw PAP (rPAP) phenotypes were evaluated to compare the results to those obtained from the transformed data. For ptPAP, heritability ranged from 0.25 to 0.37 corresponding to elevations of 1,900 and 1,215 m, respectively. For rPAP, heritability ranged from 0.22 to 0.41 corresponding to elevations of 1,700 and 2,495 m, respectively. Generally, lower elevations corresponded to decreased heritabilities while higher elevations corresponded to increased heritability estimates. For ptPAP, genetic correlations ranged from 0.18 (elevation: 1,215 and 2,495 m) to 1.00. For rPAP, genetic correlations ranged from 0.08 (elevation: 1,215 and 2,495 m) to 1.00. In general, the closer the elevations in which PAP was measured, the greater the genetic relationship. The greater the difference in elevation between PAP measures resulted in lower genetic correlations. The rank correlation between expected progeny differences (EPD) for 1,215 and 2,495 m was 0.65 and 0.49 for the ptPAP and rPAP, respectively. These results suggested that PAP measures collected in lower elevations may be used as an indicator of high-altitude adaptability. In the estimation of EPD to rank sires for their suitability for use in high-elevation production systems, it is important to account for the relationships among varied altitudes.


2020 ◽  
Vol 98 (Supplement_4) ◽  
pp. 197-197
Author(s):  
Emma A Briggs ◽  
Scott Speidel ◽  
Mark Enns ◽  
Milt Thomas ◽  
Tim Holt

Abstract The objective of the study was to evaluate if a genetic relationship exists between pulmonary arterial pressure (PAP) measured at high elevation with traits associated with moderate elevation feedlot and carcass traits. For this analysis, PAP, feed intake, and carcass data were taken from 6,898, 558, and 1,627 animals, respectively. At an elevation of 2,115 m, PAP measurements were collected, then a selective group of steers was relocated to a moderate elevation feedlot (1,500 m) where feed intake data were collected. Genetic relationships were evaluated with 5-trait animal models using REML statistical analysis. For all traits in the analysis, fixed effects and contemporary groups were assigned as well as a direct genetic random effect. For weaning weight, a maternal permanent environmental effect was applied in the analysis. For PAP, the heritability estimate was 0.29 ± 0.03. Genetic correlations between PAP with feedlot traits was positive, with estimates of 0.34 ± 0.20 (average dry matter intake) and 0.05 ± 17 (average daily gain). The strongest genetic correlation between PAP and carcass performance traits were those of rib eye area (-0.30 ± 0.12) and calculated yield grade (0.29 ± 0.13). Genetic correlations between PAP and marbling score, back fat, or hot carcass weight were 0.00 ± 0.13, -0.07 ± 0.13, and 0.14 ± 0.10, respectively. These results suggest a favorable genetic relationship exists between PAP with feedlot and carcass traits.


2018 ◽  
Vol 96 (9) ◽  
pp. 3599-3605 ◽  
Author(s):  
Rachel C Pauling ◽  
Scott E Speidel ◽  
Milton G Thomas ◽  
Timothy N Holt ◽  
Richard M Enns

2019 ◽  
Vol 3 (Supplement_1) ◽  
pp. 1669-1672
Author(s):  
Kaysie J Jennings ◽  
Greta M Krafsur ◽  
R Dale Brown ◽  
Timothy N Holt ◽  
Stephen J Coleman ◽  
...  

2001 ◽  
Vol 90 (1) ◽  
pp. 261-268 ◽  
Author(s):  
Leonardo C. Clavijo ◽  
Mary B. Carter ◽  
Paul J. Matheson ◽  
Mark A. Wilson ◽  
William B. Wead ◽  
...  

In vivo pulmonary arterial catheterization was used to determine the mechanism by which platelet-activating factor (PAF) produces pulmonary edema in rats. PAF induces pulmonary edema by increasing pulmonary microvascular permeability (PMP) without changing the pulmonary pressure gradient. Rats were cannulated for measurement of pulmonary arterial pressure (Ppa) and mean arterial pressure. PMP was determined by using either in vivo fluorescent videomicroscopy or the ex vivo Evans blue dye technique. WEB 2086 was administered intravenously (IV) to antagonize specific PAF effects. Three experiments were performed: 1) IV PAF, 2) topical PAF, and 3) Escherichia coli bacteremia. IV PAF induced systemic hypotension with a decrease in Ppa. PMP increased after IV PAF in a dose-related manner. Topical PAF increased PMP but decreased Ppa only at high doses. Both PMP (88 ± 5%) and Ppa (50 ± 3%) increased during E. coli bacteremia. PAF-receptor blockade prevents changes in Ppa and PMP after both topical PAF and E. coli bacteremia. PAF, which has been shown to mediate pulmonary edema in prior studies, appears to act in the lung by primarily increasing microvascular permeability. The presence of PAF might be prerequisite for pulmonary vascular constriction during gram-negative bacteremia.


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