Browsing by Autor "Antezana, AM"

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    Adrenergic system in high altitude residents
    (Facultad de Medicina, Enfermería, Nutrición y Tecnología Médica, 1992) Antezana, AM
    Abstract. Heart rate (HR) response to isoproterenol (ISO) infusion (IP) is decreased in normal sea level (SL) natives exposed to high altitude (HA). Since norepinephrine plasma concentration is higher in HA hypoxia, a downregulation of beta-adrenoceptors (PAR) was evoked. We explored this phenomenon at 3600 m in a HA normal population (HAN) and in polycythemic subjects (HAP). Results are compared to SL natives in normoxia (SLN), and during chronic hypoxia at 4800 m (SLH) (J Appl Physiol 65: 1957 - 1961, 1988). ISO dose required to raise HR by 25 min-1(l 25) is not different in HAN or HAP group when compared to SLN. Density of ẞAR on lymphocytes was 39% and 25% lower in HAN and HAP than in SLN group, respectively. Chronotropic response to IP is similar in SL and HA subjects under their usual environmental conditions, while SL natives show a blunted response under hypoxia, probably due to a decrease in ẞAR density. No adrenergic desensitization was found in highlanders. Lower ẞAR density in HA groups could be an adaptive mechanism to chronic hypoxia. Polycythemia does not affect this responsiveness.
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    Pulmonary hypertension in high-altitude chronic hypoxia : response to nifedipine
    (Facultad de Medicina, Enfermería, Nutrición y Tecnología Médica, 1998) Antezana, AM
    ABSTRACT. Permanent residents at high altitude may develop excessive polycythaemia (H-Hb) and pulmonary hypertension, which often leads to cardiac failure. Inhibitors of calcium channels have been shown to reverse pulmonary hypertension in respiratory diseases and in primary pulmonary hypertension, but their efficiency has not been evaluated in high-altitude-induced pulmonary hypertension. Systolic pulmonary arterial pressure (Ppa) was studied by Doppler echocardiography, at rest and after sublingual nifedipine, in 31 asymptomatic residents at 3,600 m. Individuals were separated into two groups according to resting Ppa: a group with low Ppa (ð4.7 kPa, n=17) and a group with high Ppa (>4.7 kPa, n=14). Individuals were also split into two groups according to haemoglobin (Hb) concentration: a normocy-thaemic (L-Hb) group ([Hb] ð180 g·L-1, n=17) and a H-Hb group ([Hb] >180 g·L-1, n=14). No significant difference in Ppa was observed between the L-Hb and H-Hb groups. There was no correlation between [Hb] and Ppa. Nifedipine induced a decrease of >20% in Ppa in two-thirds of the subjects. This response was correlated with higher levels of basal Ppa (p<0.001) and was inversely correlated with age in the L-Hb group (p<0.05). Pulmonary vasoreactivity to nifedipine was independent of the degree of H-Hb. Pulmonary hypertension secondary to chronic altitude hypoxia may be reversible, despite a possible remodelling of the pulmonary arterioles.