The vasoconstrictive effect of hypoxia upon pulmonary artery vessels is well known in most mammalian species, including humans. A pure form of hypoxic pulmonary artery hypertension can be seen in high-altitude residents. A loss of adaptation to chronic hypoxia, known as chronic mountain sickness (CMS), is observed in 5-10% of people sojourning above 3,000 m and is characterized by excessive polycythaemia (H-Hb), pulmonary hypertension and nonspecific neurological symptoms [1]. Ongoing pulmonary vasoconstriction leads to increased vascular resistance and pulmonary artery pressure (Ppa), which are probable maladaptive responses to high altitude since they result in minimal improvement in ventilation-perfusion matching and increased workload for the right ventricle.In addition to vasoconstriction, chronic alveolar hypoxia is associated with structural changes in the media of terminal portions of pulmonary arterioles [2], such as smooth muscle cell proliferation, thickening of the media, proliferation and turgescence of endothelial cells. Recently, this vascular remodelling has been found in only a few residents at high altitude [3], but it is admitted that sustained hypoxia is able to increase muscularization of the small pulmonary vessels and to increase even further the pulmonary vascular resistance.A reduction in Ppa, under hypoxic conditions, has been obtained by the calcium channel-blocker nifedipine in healthy humans exposed to acute normobaric hypoxia [4] or in subjects suffering from high-altitude pulmonary oedema in hypobaric hypoxia [5]. In other aetiologies of pulmonary hypertension, such as primary pulmonary hypertension [6] or secondary to obstructive pulmonary disease [7,8], nifedipine and felodipine were efficient in decreasing Ppa. Calcium antagonists have also been shown to be efficient in experimental hypoxic pulmonary vasoconstriction [9,10].Reversal of hypoxic pulmonary hypertension with calcium channel-blockers has not been evaluated in a population chronically exposed to high altitude. Venesection has been used to treat CMS, but no modification of pulmonary haemodynamics has been reported.The objectives of this study were to assess pulmonary hypertension in native residents at high-altitude by echocardiography, to analyse the relationship between Ppa and H-Hb, and to study the effect of acute administration of nifedipine on pulmonary pressure. In the presence of reversible vascular changes in altitude-induced pulmonary hypertension, a nifedipine-induced vasodilatation could be anticipated. Materials and methods SubjectsThirty males and one females, native residents of La Paz (3,500-4,100 m), Bolivia, were included in this nonrandomized study. Asymptomatic subjects were recruited 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). Ind...
The electrocardiographic (ECG) changes in Bolivian patients with mucocutaneous leishmaniasis, treated with meglumine antimoniate and allopurinol, were evaluated. Electric changes due to the antimonial compound appeared in 45% of the patients, and consisted of repolarization alteration, principally affecting the T wave and the S-T segment. The changes disappeared within 2 months following the end of the antimonial treatment. In patients with associated Chagas disease and leishmaniasis, antimonial therapy did not aggravate the ECG changes characteristic of Chagasic cardiopathy.
Acute and chronic exposure to high-altitude (HA) hypoxia inhibits the renin-angiotensin-aldosterone system and may modify the release of atrial natriuretic peptide (ANP) in sea-level (SL) natives. In HA natives, the release of these hormones could be influenced by changes in blood volume or pulmonary arterial pressure. Twenty-four men residing in La Paz, Bolivia, at 3,600 m were separated into two groups: one normocythemic (HAN; with hematocrit < 57%; n = 13) and the other polycythemic (HAP; with hematocrit > 57%; n = 11). A control group of 9 SL residents was studied in normoxia (SLN) as well as after 4 days spent at 4,350 m (SLH). The groups were tested for plasma active renin (PAR), plasma aldosterone concentration, ANP, and potassium and norepineprine concentrations at rest and after a maximal exercise. Pulmonary arterial systolic pressure was assessed by a Doppler technique. It was observed that PAR and plasma aldosterone concentration at rest and after exercise were lower in the SLH than in the SLN group. PAR and norepineprine concentration were higher among highlanders than in the SLN group. Renin response to exercise was normal among the HAN group and slightly decreased among the HAP group, and an exercise-induced increase in aldosterone was attenuated in both HA groups. Aldosterone response to renin was maintained among the SLH group but was attenuated in the HA groups, possibly owing to a protective mechanism against salt and water retention. Resting and exercise ANP was lower in the HA groups than in the SLN group.(ABSTRACT TRUNCATED AT 250 WORDS)
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 (beta AR) 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 (I 25) is not different in HAN or HAP group when compared to SLN. Density of beta AR 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 beta AR density. No adrenergic desensitization was found in highlanders. Lower beta AR density in HA groups could be an adaptive mechanism to chronic hypoxia. Polycythemia does not affect this responsiveness.
Pulmonary vascular pressures and blood flow were measured with and without unilateral pulmonary arterial occlusion (UPAO) at rest and during exercise in 10 normal highlanders at La Paz, Bolivia (altitude, 3,750 m). In 6 other highlanders at rest and during exercise, pulmonary pressures, flow, and blood volume were measured during air breathing (PIO2 congruent to 100 Torr) and 29-30% oxygen (PIO2 congruent to 150 Torr). During air breathing, pulmonary vascular resistance was elevated at rest and did not change with exercise. Pulmonary arterial pressure rose less at rest with UPAO than during exercise without UPAO, and pulmonary vascular resistance was less in the former. Raising PaO2 to normal sea-level values had no effects on the pulmonary circulation at rest but prevented to a large extent the rise in pulmonary arterial pressure during exercise. Hence pulmonary vascular resistance during exercise was lower with oxygen than without. Thus, hypoxic vasoconstriction contributed to the pulmonary hypertension during exercise in normal highlanders. Circumstantial evidence suggests that this is related to the profound mixed venous hypoxemia caused by exercise in a hypoxic environment.
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