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Pulmonary artery pressure increases at high altitude. It has been speculated that augmented respiratory synthesis of the vasodilator nitric oxide (NO) protects high-altitude natives from pulmonary hypertension, but direct evidence for this speculation is lacking. We, therefore, measured systolic pulmonary artery pressure (right ventricular to right atrial pressure gradient, Doppler-echocardiography), exhaled NO (NIOX MINO®) and oxygen saturation in 34 healthy adult Bolivian high altitude natives and in 35 healthy age- and sex-matched, well acclimatized European low altitude natives living at high-altitude (3′600 m). Mean±SD systolic pulmonary artery pressure (29.3±5.9 mm Hg, range 16 to 40, vs. 29.6±4.9 mm Hg, range 22 to 42), exhaled NO (19.2±7.2 ppb, range 8 to 41, vs. 22.5±9.5 ppb, range 9 to 52) and arterial oxygen saturation (92.4±3.2, range 80 to 97, vs. 92.5±2.4, range 87 to 97) were similar in Bolivians and Europeans. There was no relationship between pulmonary artery pressure and respiratory NO neither in Bolivians (r=0.14, p=0.44), nor in Europeans (r=0.19, p=0.29). These findings provide the first evidence that at high altitude, pulmonary artery pressure in European low altitude natives is not elevated, but similar to the one measured in Bolivian high altitude natives. These findings challenge the concept that Bolivian high altitude natives are protected from hypoxic pulmonary hypertension. [ABSTRACT FROM AUTHOR]

Excessive erythrocytosis is a hallmark of Chronic Mountain Sickness (CMS). By scavenging nitric oxide (NO), erythrocytosis may impair NO bioavailability, and, in turn, increase pulmonary artery tone. Little is known, however, about pulmonary vasoregulation at rest and during exercise in CMS. We measured systolic pulmonary artery pressure (echocardiography) at rest and during exercise (bicycle ergometer) in 20 male subjects with CMS (primary erythrocytosis, Hb level >20g/dl) and 40 healthy controls in La Paz (3600 m). All subjects were Bolivian high-altitude natives. Hemoglobin levels, as expected, were markedly higher in CMS than in control subjects (22.1±2.0 vs. 16.7±0.8, mean±SD, p<0.001), and were associated with an increased resting systolic pulmonary artery pressure (35.5±8.7 vs. 29.5±4.9 mm Hg, p<0.002). Most importantly, the exercise-induced increase in pulmonary artery pressure was roughly twice as large in patients with CMS than in control subjects: at 50 Watts systolic-pulmonary artery pressure increased to 59.3±14.5 mm Hg in the patients, but to only 43.3±8.3 mm Hg in the control subjects (P<0.001). These data provide the first evidence for a strikingly exaggerated pulmonary artery pressure response to mild exercise in CMS. This exaggerated pulmonary vasoconstrictor response, which is possibly related to impaired NO biodisponibility, may contribute to impaired exercise tolerance in CMS. [ABSTRACT FROM AUTHOR]

Offspring of mothers suffering from preeclampsia and subjects with a history of reentry high-altitude pulmonary edema (re-entry HAPE) display sustained hypoxic pulmonary hypertension when living at high altitude and a predisposition to pulmonary edema. The underlying mechanisms are unknown. We hypothesized that the predisposition to pulmonary edema could be caused by capillary stress failure related to exaggerated pulmonary hypertension. We, therefore, estimated the pulmonary artery pressure response (Doppler echocardiography) to mild exercise in 18 re-entry HAPE-prone subjects, 12 offspring of preeclampsia and 29 controls, all born and living in La Paz, Bolivia (3600 m). As expected, mean±SD systolic pulmonary artery pressure at rest was higher in re-entry HAPE prone subjects and offspring of preeclampsia than in controls (42±7 and 37±8 vs. 30±7 mm Hg, P<0.001). Most importantly, the exercise-induced increase in pulmonary artery pressure was 50 percent larger in the two groups of subjects at risk than in controls (21±8 and 21±10 vs. 14±7 mm Hg, P=0.02). These data provide the first evidence for a markedly exaggerated pulmonary vasoconstrictor response to exercise in high altitude dwellers known to have an augmented susceptibility to develop pulmonary edema. We speculate that this exaggerated response may predispose them to pulmonary edema by causing capillary stress failure. [ABSTRACT FROM AUTHOR]