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1.
Cells ; 11(19)2022 09 20.
Artículo en Inglés | MEDLINE | ID: mdl-36230894

RESUMEN

The role of microparticles (MPs) and cold in high altitude pulmonary hypertension (HAPH) remains unexplored. We investigated the impact of long-term cold exposure on the pulmonary circulation in lowlanders and high-altitude natives and the role of MPs. Pulmonary hemodynamics were evaluated using Doppler echocardiography at the end of the colder and warmer seasons. We further examined the miRNA content of MPs isolated from the study participants and studied their effects on human pulmonary artery smooth muscle (hPASMCs) and endothelial cells (hPAECs). Long-term exposure to cold environment was associated with an enhanced pulmonary artery pressure in highlanders. Plasma levels of CD62E-positive and CD68-positive MPs increased in response to cold in lowlanders and HAPH highlanders. The miRNA-210 expression contained in MPs differentially changed in response to cold in lowlanders and highlanders. MPs isolated from lowlanders and highlanders increased proliferation and reduced apoptosis of hPASMCs. Further, MPs isolated from warm-exposed HAPH highlanders and cold-exposed highlanders exerted the most pronounced effects on VEGF expression in hPAECs. We demonstrated that prolonged exposure to cold is associated with elevated pulmonary artery pressures, which are most pronounced in high-altitude residents. Further, the numbers of circulating MPs are differentially increased in lowlanders and HAPH highlanders during the colder season.


Asunto(s)
Hipertensión Pulmonar , MicroARNs , Altitud , Mal de Altura , Células Endoteliales , Humanos , Estaciones del Año , Factor A de Crecimiento Endotelial Vascular
2.
Wilderness Environ Med ; 28(3): 234-238, 2017 Sep.
Artículo en Inglés | MEDLINE | ID: mdl-28673745

RESUMEN

High altitude pulmonary edema (HAPE) is a potentially life-threatening form of noncardiogenic pulmonary edema that may develop in otherwise healthy individuals upon ascent to high altitude. A constitutional susceptibility has been noted in some individuals, whereas others appear not to be susceptible at all. In our report, we present a case of HAPE triggered by concurrent respiratory tract infection and strenuous exercise in a mining worker with an abnormal rise in pulmonary artery pressure in response to acute hypoxia, without a prior history of HAPE during almost a year of commuting between high altitude and lowland areas.


Asunto(s)
Mal de Altura/diagnóstico , Ejercicio Físico , Hipertensión Pulmonar/diagnóstico , Hipoxia/complicaciones , Infecciones del Sistema Respiratorio/complicaciones , Adulto , Humanos , Kirguistán , Masculino
3.
High Alt Med Biol ; 4(4): 455-63, 2003.
Artículo en Inglés | MEDLINE | ID: mdl-14672548

RESUMEN

Chronic alveolar hypoxia due to disease or low atmospheric pressure at high altitude results in the development of hypoxic pulmonary hypertension. The effects of intermittent hypoxia on pulmonary hemodynamics in healthy men have not been studied. We aimed to investigate, prospectively, pulmonary hemodynamics in workers commuting between an elevation of 3700 and 4200 m (4-week working shift) and lowland, below 500 m (4 weeks of holiday). Pulmonary hemodynamics has been investigated by Doppler echocardiography in 26 healthy Caucasian males, mean age 42 +/- 9 yr. First at lowland (760 m) and next during the fourth week of work at high altitude. Investigations were repeated in 21 subjects 1 year later at the end of the high-altitude exposure. The third series of investigations was performed 2 yr after the initial ones in 10 subjects who earlier had shown the strongest hypoxic vasoconstriction. At lowland, subjects presented with normal pulmonary hemodynamics. At high altitude, mean pulmonary artery pressure (PAPm) rose from 14.7 +/- 2.7 mmHg to 25.8 +/- 8.3 mmHg. One year later the PAPm remained unchanged in hypoxic conditions (25.0 +/- 7.3 mmHg). At the end of a 2-year follow-up of 10 "hyperreactors," PAPm measured at the end of the hypoxic exposure was the same as at the initial investigation, averaging 28 +/- 4.0, 28 +/- 3.5, and 29 +/- 2.5 mmHg at the beginning and at 1 and after 2 yr of intermittent exposure to high altitude. We concluded that intermittent exposure to 4000 m lasting 3 yr does not lead to development of permanent pulmonary hypertension.


Asunto(s)
Aclimatación , Mal de Altura , Altitud , Hipertensión Pulmonar/fisiopatología , Exposición Profesional/efectos adversos , Circulación Pulmonar , Adulto , Mal de Altura/diagnóstico por imagen , Mal de Altura/fisiopatología , Asia , Ecocardiografía Doppler , Monitoreo del Ambiente/métodos , Estudios de Seguimiento , Hemodinámica , Humanos , Hipertensión Pulmonar/diagnóstico por imagen , Hipertensión Pulmonar/etiología , Kirguistán , Masculino , Persona de Mediana Edad , Minería , Estudios Prospectivos , Pruebas de Función Respiratoria , Factores de Riesgo , Factores de Tiempo
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