The genetic factor influencing pulmonary hypertension in cattle at high altitude

Weir, Ε. Kenneth; Tucker, Adam; Reeves, John Τ.; Will, D. H.; Grover, R. F.

doi:10.1093/cvr/8.6.745

Cited by 86 publications

(47 citation statements)

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“…The studies that support the hypothesis that pulmonary adaptative responses to high altitude are determined by environmental and/or developmental factors 665 EXERCISE PERFORMANCE OF TIBETAN AND HAN ADOLESCENTS (2,4,6,10,11,19,22) seem to argue against the presumptions that are in accord with the genetic hypothesis implication (3,9,16,26,33,35). It could be proposed, however, that the mechanisms responsible for the process of pulmonary adaptation to highaltitude environment may include both considerations.…”

Section: Exercise Performance Of Tibetan and Han Adolescentsmentioning

confidence: 98%

Exercise performance of Tibetan and Han adolescents at altitudes of 3,417 and 4,300 m

Chen

Wang

et al. 1997

Journal of Applied Physiology

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Yoshimura. Exercise performance of Tibetan and Han adolescents at altitudes of 3,417 and 4,300 m. J. Appl. Physiol. 83(2): 661-667, 1997.-The difference was studied between O 2 transport in lifelong Tibetan adolescents and in newcomer Han adolescents acclimatized to high altitude. We measured minute ventilation, maximal O 2 uptake, maximal cardiac output, and arterial O 2 saturation during maximal exercise, using the incremental exercise technique, at altitudes of 3,417 and 4,300 m. The groups were well matched for age, height, and nutritional status. The Tibetans had been living at the altitudes for a longer period than the Hans (14.5 6 0.2 vs. 7.8 6 0.8 yr at 3,417 m, P , 0.01; and 14.7 6 0.3 vs. 5.3 6 0.7 yr at 4,300 m, P , 0.01, respectively). At rest, Tibetans had significantly greater vital capacity and maximal voluntary ventilation than the Hans at both altitudes. At maximal exercise, Tibetans compared with Hans had higher maximal O 2 uptake (42.2 6 1.7 vs. 36.7 6 1.2 ml · min 21 ·kg 21 at 3,417 m, P , 0.01; and 36.8 6 1.9 vs. 30.0 6 1.4 ml · min 21 ·kg 21 at 4,300 m, P , 0.01, respectively) and greater maximal cardiac output (12.8 6 0.3 vs. 11.4 6 0.2 l/min at 3,417 m, P , 0.01; 11.5 6 0.5 vs. 10.0 6 0.5 l/min at 4,300 m, P , 0.05, respectively). Although the differences in arterial O 2 saturation between Tibetans and Hans were not significant at rest and during mild exercise, the differences became greater with increases in exercise workload at both altitudes. We concluded that exposure to high altitude from birth to adolescence resulted in an efficient O 2 transport and a greater aerobic exercise performance that may reflect a successful adaptation to life at high altitude. cardiac output; maximal oxygen consumption; ventilation; developmental adaptation; genetic adaptation MAXIMAL O 2 UPTAKE (V O 2 max ), an integrated index of the overall functional capacity of the O 2 transport system, invariably decreases with altitude during both acute and chronic exposure to high altitude in lowland adults (31,34). This is due to the reduction of ambient O 2 pressure at high altitude. Although comparative studies of V O 2 max between high altitude natives and lowland residents at high-altitude have been done, the conclusions are controversial (10-13, 30). High-altitude adult natives in either Andean or Himalayan populations have higher exercise performance and maintain better arterial O 2 saturation (Sa O 2 ) during exercise compared with newcomers (17,20,30,38). These characteristics, which are associated with more efficient pulmonary gas exchange (38) and better adaptation to high-altitude stress, are acquired through many generations of lifelong high-altitude exposure. The Tibetans are believed to have lived at high altitude longer than other highaltitude residents. The effects of high-altitude hypoxia on the physiological responses of Tibetan and Han adolescents to exercise have never been reported. Whether the pulmonary adaptations in humans are determined purely by environment or relate to genetic character...

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Section: Exercise Performance Of Tibetan and Han Adolescentsmentioning

confidence: 98%

Exercise performance of Tibetan and Han adolescents at altitudes of 3,417 and 4,300 m

Chen

Wang

et al. 1997

Journal of Applied Physiology

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“…In later studies, extensive vascular remodeling was reported, characterized by collagen deposition, adventitial and medial thickening, and arteriolar muscularization (527,594,596). As with humans, there is variability in the development of hypoxic PH in cattle, which may have a genetic basis (575,681,698). Recently, SNP analysis of four candidate genes in cattle with severe hypoxic PH failed to uncover obvious SNPs associated with high-altitude susceptibility, although SNPs in additional candidate genes were identified and will require further investigation (456).…”

Section: Hypoxiamentioning

confidence: 99%

Lung Circulation

Suresh

Shimoda

2016

Comprehensive Physiology

111

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The circulation of the lung is unique both in volume and function. For example, it is the only organ with two circulations: the pulmonary circulation, the main function of which is gas exchange, and the bronchial circulation, a systemic vascular supply that provides oxygenated blood to the walls of the conducting airways, pulmonary arteries and veins. The pulmonary circulation accommodates the entire cardiac output, maintaining high blood flow at low intravascular arterial pressure. As compared with the systemic circulation, pulmonary arteries have thinner walls with much less vascular smooth muscle and a relative lack of basal tone. Factors controlling pulmonary blood flow include vascular structure, gravity, mechanical effects of breathing, and the influence of neural and humoral factors. Pulmonary vascular tone is also altered by hypoxia, which causes pulmonary vasoconstriction. If the hypoxic stimulus persists for a prolonged period, contraction is accompanied by remodeling of the vasculature, resulting in pulmonary hypertension. In addition, genetic and environmental factors can also confer susceptibility to development of pulmonary hypertension. Under normal conditions, the endothelium forms a tight barrier, actively regulating interstitial fluid homeostasis. Infection and inflammation compromise normal barrier homeostasis, resulting in increased permeability and edema formation. This article focuses on reviewing the basics of the lung circulation (pulmonary and bronchial), normal development and transition at birth and vasoregulation. Mechanisms contributing to pathological conditions in the pulmonary circulation, in particular when barrier function is disrupted and during development of pulmonary hypertension, will also be discussed.

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“…It was noted some years ago that imported Hereford cows reared at altitude in the high plains of the Colorado Rocky Mountains in the United States were susceptible to high altitude pulmonary hypertension 8 . This manifested as 'brisket disease' where the region at the front of the cow's chest (the brisket) becomes oedematous.…”

Section: Evidence For Genetic Susceptibility To Hypoxia-induced Pulmomentioning

confidence: 99%

“…This manifested as 'brisket disease' where the region at the front of the cow's chest (the brisket) becomes oedematous. This trait affected only a minority of the cows and was found to be inherited 8 . It was subsequently possible to breed the trait out of the herds by only breeding from resistant animals.…”

Section: Evidence For Genetic Susceptibility To Hypoxia-induced Pulmomentioning

confidence: 99%

Genetic and molecular mechanisms of pulmonary hypertension

Morrell

Wilkins

2001

Clinical Medicine

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-Pulmonary arterial hypertension frequently occurs secondary to common cardiopulmonary diseases, and more rarely as a primary condition. Observations in animals and man have suggested genetic influences underlying the susceptibility to pulmonary hypertension. A gene underlying many cases of familial and apparently sporadic cases of primary pulmonary hypertension has now been identified, and a genetic approach to hypoxia-induced pulmonary hypertension promises to reveal new insights into the unique nature of the pulmonary circulation. The exploration of potential candidate genes influencing susceptibility and the identification of new genes promise new therapeutic approaches to the treatment of pulmonary hypertension. The unique nature of the pulmonary circulationThe main role of the pulmonary circulation is to deliver deoxygenated blood to the alveolar capillaries where gas exchange occurs. To achieve this vital role the pulmonary circulation has developed as a high flow, low resistance vascular bed to protect the thin blood-gas barrier from high intravascular pressures that would otherwise promote alveolar oedema formation. Consequently the mean pulmonary arterial pressure (~13mmHg) is approximately one fifth of the systemic arterial pressure, and because of the great capacity of the pulmonary circulation to recruit normally closed vessels, rarely rises above 30mmHg even at very high levels of cardiac output 1 . In contrast to the systemic circulation, the normal pulmonary circulation exhibits minimal resting tone, and appears to be almost maximally dilated under resting conditions. The maximum resistance in the pulmonary circulation lies in the precapillary arterioles, the site of some of the earliest pathological changes during the development of pulmonary hypertension. One of the intriguing features of the pulmonary circulation is vasoconstriction to hypoxia 2 , whereas the systemic circulation responds by vasodilatation. This mechanism, when localised to a particular lung segment or lobe, serves to preserve arterial oxygenation by reducing blood flow to underventilated lung regions, for example in pneumonia or acute asthma 3 . However, the importance of this role should not be overestimated, since it is only about 50% efficient at preserving arterial oxygenation in man and the intensity of hypoxic pulmonary vasoconstriction varies greatly between species. Indeed, it could be argued that the mechanism is a vestigial response representing the equivalent of the amphibian reflex that diverts blood flow from the lungs to the skin, which serves as an alternative organ of gas exchange during hibernation 4 ! Hypoxia-induced pulmonary hypertensionWhen alveolar hypoxia involves most of the lung and is prolonged, any usefulness of acute hypoxic pulmonary vasoconstriction is offset by a rise in pulmonary arterial pressure. This is accompanied by structural changes in small peripheral pulmonary arteries, consisting of increased wall thickness of muscular arteries and the appearance of new muscle in normally non...

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The genetic factor influencing pulmonary hypertension in cattle at high altitude

Cited by 86 publications

References 0 publications

Exercise performance of Tibetan and Han adolescents at altitudes of 3,417 and 4,300 m

Exercise performance of Tibetan and Han adolescents at altitudes of 3,417 and 4,300 m

Lung Circulation

Genetic and molecular mechanisms of pulmonary hypertension

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