Inhaled Nitric Oxide for High-Altitude Pulmonary Edema

Scherrer, Urs; Vollenweider, L; Delabays, Alain; Savcic, Milos; Eichenberger, Urs; Kleger, Gian‐Reto; Fikrle, A; Ballmer, Peter E.; Nicod, Pascal; Bärtsch, Peter

doi:10.1056/nejm199603073341003

Cited by 292 publications

(200 citation statements)

References 24 publications

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“…The initial impetus for the study was the inverse relation between pulmonary NO and pulmonary arterial pressure found in animal and human experiments (6,7,9,14,15,22,23,27,28). That relation was not found in this study, despite adequate statistical power.…”

Section: Discussionmentioning

confidence: 60%

“…1) Exhaled NO does not increase after experimental elevation of cardiac output (12). 2) Exhaled NO is decreased on acute exposure to high altitude, despite elevation of cardiac output (11,23,30). 3) Experimental inhibition of NO synthesis causes a decrease in cardiac index at sea level (6,27).…”

Section: Discussionmentioning

confidence: 99%

“…An animal study using NO synthase gene transfer to the airway demonstrates elegantly that increasing NO decreases hypoxic pulmonary vasoconstriction (7). Studies of humans are consistent and have demonstrated that 1) NO is critical in regulating basal pulmonary vascular tone (10,27), 2) inhibiting NO synthesis exacerbates hypoxic pulmonary vasoconstriction, and 3) inhaling gas mixtures with high concentrations of NO diminishes hypoxic pulmonary vasoconstriction at sea level (6,15) and lowers pulmonary artery systolic pressure at high altitude (23). Moreover, sea-level natives exposed to acute hypoxia (and who have relatively high levels of exhaled NO) have less hypoxic pulmonary vasoconstriction, as measured by pulmonary artery systolic pressure (8,11).…”

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confidence: 96%

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Nitric oxide and cardiopulmonary hemodynamics in Tibetan highlanders

Hoit

Dalton

Erzurum³

et al. 2005

Journal of Applied Physiology

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When O 2 availability is reduced unavoidably, as it is at high altitude, a potential mechanism to improve O 2 delivery to tissues is an increase in blood flow. Nitric oxide (NO) regulates blood vessel diameter and can influence blood flow. This field study of intrapopulation variation at high altitude tested the hypothesis that the level of exhaled NO (a summary measure of pulmonary synthesis, consumption, and transfer from cells in the airway) is directly proportional to pulmonary, and thus systemic, blood flow. Twenty Tibetan male and 37 female healthy, nonsmoking, native residents at 4,200 m (13,900 ft), with an average O 2 saturation of hemoglobin of 85%, participated in the study. The geometric mean partial pressure of NO exhaled at a flow of 17 ml/s was 23.4 nmHg, significantly lower than that of a sea-level reference group. However, the rate of NO transfer out of the airway wall was seven times higher than at sea level, which implied the potential for vasodilation of the pulmonary blood vessels. Mean pulmonary blood flow (measured by cardiac index) was 2.7 Ϯ 0.1 (SE) l/min, and mean pulmonary artery systolic pressure was 31.4 Ϯ 0.9 (SE) mmHg. Higher exhaled NO was associated with higher pulmonary blood flow; yet there was no associated increase in pulmonary artery systolic pressure. The results suggest that NO in the lung may play a key beneficial role in allowing Tibetans at 4,200 m to compensate for ambient hypoxia with higher pulmonary blood flow and O 2 delivery without the consequences of higher pulmonary arterial pressure. high altitude; oxygen delivery; oxygen availability; hypoxia WHEN OXYGEN AVAILABILITY is reduced, as it is at high altitude, an increased blood flow could potentially improve O 2 delivery to tissues. However, the pulmonary vasoconstriction response to hypoxia decreases blood flow in the lung, the first point of contact with the circulation. This response probably evolved at sea level to maintain gas exchange by redistribution of blood flow from temporarily small, poorly oxygenated to betteroxygenated areas of the lung (17, 32). At high altitude, the entire lung is always hypoxic, and the resulting general vasoconstriction does not redistribute blood flow; instead, it increases pulmonary arterial pressure, sometimes causing pathological remodeling of the heart and lungs (30). However, many people live at high altitude without pulmonary hypertension or cardiac hypertrophy, which suggests that another factor may intervene to maintain blood flow when the blood carries less O 2 and the usual vasoconstriction response increases pulmonary resistance. That factor may be nitric oxide (NO), a vasodilator found in high concentrations in the lungs of high-altitude natives, particularly among Tibetans (5).A wealth of studies support a key role for NO in determining basal pulmonary vascular tone at sea level and in effecting the hypoxic vasoconstriction response. An animal study using NO synthase gene transfer to the airway demonstrates elegantly that increasing NO decreases hypoxic pulmonary v...

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Section: Discussionmentioning

confidence: 60%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 96%

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Nitric oxide and cardiopulmonary hemodynamics in Tibetan highlanders

Hoit

Dalton

Erzurum³

et al. 2005

Journal of Applied Physiology

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“…Persons who are prone to the condition have higher PAP at rest and in response to hypoxia, altitude and exercise than those who are resistant to it. Inhalation of nitric oxide is reported to be beneficial in subjects prone to HAPO by reducing PAP [17]. Oelz [IS] and Bartsch [191 have demonstrated protective and therapeutic effects of lowering PAP with nifedipine without impairing performance in climbers prone to HAPO.…”

Section: Discussionmentioning

confidence: 99%

High Altitude Pulmonary Oedema – An Experience in Eastern Himalaya

Virmani

1997

Medical Journal Armed Forces India

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Lt Col SK VIRMANI ABSTRACi Three hundred and five cases of high altitude pulmonary oedema (HAPO) hospitalised in eastern Himalayan region have been analyzed. Incidence of HAPO was 5.S per cent. Eighty per cent cases occurred during latter half of the year. Fifty six per cent of cases belonged to the third decade of life. HAPO cases occurred most commonly between the height of 2740 m to 5960 m, Eighty three per cent cases developed symptoms within 72 hours of induction to high altitude and 65.9 per cent suffered from the illness despite complete acclimatization. Breathlessness, headache and cough were the commonest symptoms. Tachycardia and tachypnoea was present in all cases. Twenty five per cent cases showed various EeG abnormalities. Mortality rate was 0.98 per cent.

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“…24 Color Doppler echocardiography was used to locate the tricuspid-regurgitation jet. The maximal velocity was then determined by careful application of the continuous-wave sampler on the regurgitation jet.…”

Section: Echocardiographymentioning

confidence: 99%

Salmeterol for the Prevention of High-Altitude Pulmonary Edema

2002

N Engl J Med

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Inhaled Nitric Oxide for High-Altitude Pulmonary Edema

Cited by 292 publications

References 24 publications

Nitric oxide and cardiopulmonary hemodynamics in Tibetan highlanders

Nitric oxide and cardiopulmonary hemodynamics in Tibetan highlanders

High Altitude Pulmonary Oedema – An Experience in Eastern Himalaya

Salmeterol for the Prevention of High-Altitude Pulmonary Edema

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