Inherited susceptibility of cattle to high-altitude pulmonary hypertension

Will, D. H.; Hicks, J. L.; Card, Cynthia; Alexander, A. F.

doi:10.1152/jappl.1975.38.3.491

Cited by 51 publications

(29 citation statements)

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“…It was previously documented that some subjects are more susceptible (high responders) to the development of pulmonary hypertension in hypoxic conditions than others (nonresponders) [22,23]. However, in the present study no significant correlations were found between diurnal vascular response to hypoxia and hypercapnia, daytime Ppa and the slope of Ppa changes during the night.…”

Section: Discussioncontrasting

confidence: 84%

Time course of pulmonary artery pressure during sleep in sleep apnoea syndrome: role of recurrent apnoeas

Sforza

Laks²,

Grunstein³

et al. 1998

Eur Respir J

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The increase in pulmonary arterial pressure (Ppa) during acute hypoxia is mainly related to alveolar hypoxaemia inducing vasoconstriction of precapillary pulmonary arterioles [1,2] whereas during chronic hypoxia, mechanical and hormonal factors make the vessels adapt to hypoxia and modify their response to chemical stimulus [3]. Furthermore, the temporal profile of the hypoxaemic stimulus may have a substantial effect on the pulmonary vascular response [4] as suggested by experimental studies allowing that repeated exposure to intermittent hypoxaemia [5] enhances the pulmonary hypoxic pressor response.Previous studies [6] in obstructive sleep apnoea (OSAS) patients have shown that repeated desaturations from obstructive apnoeas induce a transient increase in Ppa that, together with daytime hypoxaemia, is considered to be the key factor responsible for daytime pulmonary hypertension [7,8]. Recent evidence in animals [9][10][11] has demonstrated that repetitive hypoxic stimuli, simulating the chemical changes produced by apnoeas lead to systemic hypertension either during the exposure or during the recovery period. A more direct approach to the pulmonary vascular effects of repetitive hypoxaemia has been used by IWASE et al. [12]. Using a canine model they have demonstrated a progressive increase in systemic and pulmonary arterial pressure during repetitive hypoxaemic exposure. On the basis of these latter findings a trend in the pulmonary arterial pressure response to repetitive hypoxaemia similar to the one produced experimentally may occur in patients with OSAS.The two aims of the present study were: 1) to ascertain whether recurrent apnoea-related oxygen desaturations are associated with a progressive rise in Ppa during the night in OSAS patients; 2) if there was a rise in the expected direction, to determine whether diurnal and nocturnal variables would predict the degree of progressive nocturnal increase in Ppa. Patients and methods PatientsThirty five consecutive patients referred to the sleep laboratory for habitual snoring and possible sleep apnoea We have, therefore, examined the nocturnal trend of Ppa in seven obstructive sleep apnoea syndrome (OSAS) patients and in five snorers. Mean Ppa was measured before, at the start, at the end and after the selected apnoeas. The analysis was performed for each 1 h period for at least 7 h throughout the night on at least 10 randomly selected apnoeas per hour. In snorers, 100 randomly chosen values were measured during every hour of the night. In the morning after the nocturnal study, the Ppa responses to acute hypoxia and hypercapnia were measured.No Ppa changes throughout the 7 h were found during sleep in snorers (Ppa slope:-0.002±0.10 mmHg·h -1 ). In OSAS patients a small but significant increase in Ppa throughout the night was noted, affecting the values before (Ppa slope: 0.7±0.16 mm Hg·h -1 ), at the start of apnoea (Ppa slope: 0.53±0.1 mmHg·h -1 ) as well as at the end (Ppa slope: 0.44±0.08 mmHg·h -1 ) and in the postapnoeic period (Ppa slope: 0.55±0.1 mmHg...

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Section: Discussioncontrasting

confidence: 84%

Time course of pulmonary artery pressure during sleep in sleep apnoea syndrome: role of recurrent apnoeas

Sforza

Laks²,

Grunstein³

et al. 1998

Eur Respir J

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“…Sakai et al (26) studied the differences in pulmonary hemodynamic characteristics between pikas (genus Ochotona), as high-altitude-adapted animals, and Wistar rats. They clearly demonstrated that significantly lower values of Ppa, PVR, and the ratio of right to left ventricular weight were observed in pikas than in rats at various altitudes of 4,460, 3,300, 2,300, and 610 m. Will et al (35) and Weir et al (33) demonstrated that offspring of cattle that were found to be either susceptible or resistant to the development of ''brisket disease'' retained their respective susceptible or resistant trait for at least two generations. These reports suggest that the differences in pulmonary vascular responses to high altitude between highland natives and lowlanders could be attributable to genetic adaptation.…”

Section: Exercise Performance Of Tibetan and Han Adolescentsmentioning

confidence: 96%

“…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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“…Los valores de PAPm obtenidos en la altura (Cuadro 1) estuvieron elevados y similares a los obtenidos por Tucker et al (1975) y Will et al (1975) en condiciones similares. Para Ames (2001), estos valores de PAPm están dentro del rango aceptable para introducir ganado bovino en la altura (PAPm < 41 mm Hg) pudiendo considerarse como un buen indicador.…”

Section: Discussionunclassified

Efecto Del Ketoprofeno Sobre La Presión Arterial Pulmonar en Terneros Jersey Sometidos a Hipoxia De La Altura.

et al. 2012

Rev. investig. vet. Perú

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Inherited susceptibility of cattle to high-altitude pulmonary hypertension

Cited by 51 publications

References 0 publications

Time course of pulmonary artery pressure during sleep in sleep apnoea syndrome: role of recurrent apnoeas

Time course of pulmonary artery pressure during sleep in sleep apnoea syndrome: role of recurrent apnoeas

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

Efecto Del Ketoprofeno Sobre La Presión Arterial Pulmonar en Terneros Jersey Sometidos a Hipoxia De La Altura.

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