Protective effect of female sex hormones against pulmonary hypertension in Bolivian high altitude natives
Fecha
2003-02-19Autor
Sartori, Claudio
Allemann, Yves
Salinas Salmón, Carlos E
Turini, Pierre
Rodríguez, Armando
Hutter, Damián
Thalmann, Sébastien
Vargas, Enrique
Villena, Mercedes
Scherrer, Urs
Metadatos
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There is abundant evidence that female sex hormones have protective effects in the systemic circulation in both animals and humans,
but little is known regarding their role in the regulation of the pulmonary circulation. Observations in rats suggest that estrogens may
have protective effects against hypoxia-induced pulmonary hypertension. We hypothesized that female sex may confer resistance
against pulmonary hypertension in high altitude natives. To test our
hypothesis, we performed echocardiographic measurements of the
transtricuspid pressure gradient as an index of systolic pulmonaryartery pressure in young healthy Bolivians of Aymara ancestry. We
studied 82 females and 99 males between 0 and 35 years of age, who
were born and living at high altitude (4000 m). To provide additional
information, we also measured arterial oxygen saturation and hemoglobin. The main new findings were two-fold. We found a strong
direct relationship between age and systolic pulmonary artery pressure in male (r = 0.48, P< 0.001), but not in female (r = 0.16, P > 0.1)
high altitude natives. Moreover, starting at the age of 12 years hemoglobin levels were significantly higher in males than in females,
and there was a direct relationship between hemoglobin and pulmonary artery pressure in male (r = 0.51, P < 0.001), but not female
(r = 0.14, P > 0.1) subjects. The gender-related differences in pulmonary-artery pressure were not related to differences in arterial oxygen saturation which were comparable in the two groups. These findings provide the first evidence for an age-related increase in
pulmonary-artery pressure in young healthy male, but not female
high-altitude natives. We speculate that female sex may protect
against hypoxia-induced pulmonary hypertension in humans, either
via decreased hemoglobin concentration and blood viscosity or by
favorable effects of female sex hormones on pulmonary endothelial
responsiveness to hypoxia.