0169 Pulmonary arterial pressure in yearling Angus cattle managed at high altitude: Study of a non-synonymous SNP in the oxygen-dependent degradation domain of the endothelial PAS domain-containing protein 1 gene

2016 ◽  
Vol 94 (suppl_5) ◽  
pp. 82-82
Author(s):  
N. F. Crawford ◽  
X. Zeng ◽  
S. J. Coleman ◽  
T. N. Holt ◽  
S. E. Speidel ◽  
...  
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.


2019 ◽  
Vol 53 (6) ◽  
pp. 1802040 ◽  
Author(s):  
Rodrigo Soria ◽  
Matthias Egger ◽  
Urs Scherrer ◽  
Nicole Bender ◽  
Stefano F. Rimoldi

Up to 10% of the more than 140 million high-altitude dwellers worldwide suffer from chronic mountain sickness (CMS). Patients suffering from this debilitating problem often display increased pulmonary arterial pressure (PAP), which may contribute to exercise intolerance and right heart failure. However, there is little information on the usual PAP in these patients.We systematically reviewed and meta-analysed all data published in English or Spanish until June 2018 on echocardiographic estimations of PAP at rest and during mild exercise in CMS patients.Nine studies comprising 287 participants fulfilled the inclusion criteria. At rest, the point estimate from meta-analysis of the mean systolic PAP was 27.9 mmHg (95% CI 26.3–29.6 mmHg). These values are 11% (+2.7 mmHg) higher than those previously meta-analysed in apparently healthy high-altitude dwellers. During mild exercise (50 W) the difference in mean systolic PAP between patients and high-altitude dwellers was markedly more accentuated (48.3 versus 36.3 mmHg) than at rest.These findings indicate that in patients with CMS PAP is moderately increased at rest, but markedly increased during mild exercise, which will be common with activities of daily living.


PLoS ONE ◽  
2021 ◽  
Vol 16 (2) ◽  
pp. e0247107
Author(s):  
Chunyan He ◽  
Hedong Xiang ◽  
Chuan Liu ◽  
Shiyong Yu ◽  
Jie Yang ◽  
...  

Background High altitude exposure induces overload of right-sided heart and may further predispose to supraventricular arrhythmia. It has been reported that atrial mechanical dyssynchrony is associated with atrial arrhythmia. Whether high altitude exposure causes higher right atrial (RA) dyssynchrony is still unknown. The aim of study was to investigate the effect of high altitude exposure on right atrial mechanical synchrony. Methods In this study, 98 healthy young men underwent clinical examination and echocardiography at sea level (400 m) and high altitude (4100 m) after an ascent within 7 days. RA dyssynchrony was defined as inhomogeneous timing to peak strain and strain rate using 2D speckle-tracking echocardiography. Results Following high altitude exposure, standard deviation of the time to peak strain (SD-TPS) [36.2 (24.5, 48.6) ms vs. 21.7 (12.9, 32.1) ms, p<0.001] and SD-TPS as percentage of R–R’ interval (4.6 ± 2.1% vs. 2.5 ± 1.8%, p<0.001) significantly increased. Additionally, subjects with higher SD-TPS (%) at high altitude presented decreased right ventricular global longitudinal strain and RA active emptying fraction, but increased RA minimal volume index, which were not observed in lower group. Multivariable analysis showed that mean pulmonary arterial pressure and tricuspid E/A were independently associated with SD-TPS (%) at high altitude. Conclusion Our data for the first time demonstrated that high altitude exposure causes RA dyssynchrony in healthy young men, which may be secondary to increased pulmonary arterial pressure. In addition, subjects with higher RA dyssynchrony presented worse RA contractile function and right ventricular performance.


2016 ◽  
Vol 190 ◽  
pp. 76-80 ◽  
Author(s):  
Derek W. Bailey ◽  
Milton G. Thomas ◽  
Tim N. Holt ◽  
Mitch B. Stephenson ◽  
R. Mark Enns ◽  
...  

1993 ◽  
Vol 74 (1) ◽  
pp. 312-318 ◽  
Author(s):  
B. M. Groves ◽  
T. Droma ◽  
J. R. Sutton ◽  
R. G. McCullough ◽  
R. E. McCullough ◽  
...  

Elevated pulmonary arterial pressure in high-altitude residents may be a maladaptive response to chronic hypoxia. If so, well-adapted populations would be expected to have pulmonary arterial pressures that are similar to sea-level values. Five normal male 22-yr-old lifelong residents of > or = 3,600 m who were of Tibetan descent were studied in Lhasa (3,658 m) at rest and during near-maximal upright ergometer exercise. We found that resting mean pulmonary arterial pressure [15 +/- 1 (SE) mmHg] and pulmonary vascular resistance (1.8 +/- 0.2 Wood units) were within sea-level norms and were little changed while subjects breathed a hypoxic gas mixture [arterial O2 pressure (PaO2) = 36 +/- 2 Torr]. Near-maximal exercise [87 +/- 13% maximal O2 uptake (VO2max)] increased cardiac output more than threefold to values of 18.3 +/- 1.2 l/min but did not elevate pulmonary vascular resistance. Breathing 100% O2 during near-maximal exercise did not reduce pulmonary arterial pressure or vascular resistance. We concluded that this small sample of healthy Tibetans with lifelong residence > or = 3,658 m had resting pulmonary arterial pressures that were normal by sea-level standards and exhibited minimal hypoxic pulmonary vasoconstriction, both at rest and during exercise. These findings are consistent with remarkable cardiac performance and high-altitude adaptation.


Sign in / Sign up

Export Citation Format

Share Document