Acute Hypoxic Pulmonary Vascular Response Does Not Accompany Plasma Endothelin-1 Elevation in Subjects Susceptible to High Altitude Pulmonary Edema.

Droma, Yunden; Ge, Ri-Li; Tanaka, Masao; Koizumi, Tomonobu; Hanaoka, Masayuki; Miyahara, Takashige; Yamaguchi, Shinjiro; Okada, Kazuyoshi; Yoshikawa, Sumiko; Matsuzawa, Y.; Kubo, Keishi; Kobayashi, Toshio; Sekiguchi, Morie

doi:10.2169/internalmedicine.35.257

Cited by 5 publications

(1 citation statement)

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“…49] and decreased NO synthesis [21] have been sug gested to account for higher Ppa in HAPE-susceptible subjects. While a brisk HPVR in HAPE-susceptible sub jects is not accompanied by increased endothelin-1 in plasma [50] and thus does not support the former con cept, production of NO by the pulmonary vasculature in HAPE-susceptible subjects has not been examined.…”

Section: Laboratory Evaluationmentioning

confidence: 94%

High Altitude Pulmonary Edema

Bärtsch

1997

Respiration

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Altitude, speed and mode of ascent and, above all, individual susceptibility are the most important determinants for the occurrence of high-altitude pulmonary edema (HAPE). This illness usually occurs only 2-5 days after acute exposure to altitudes above 2,500-3,000 m. Chest radiographs and CT scans show a patchy predominantly peripheral distribution of edema. Wedge pressure is normal at rest, and there is an excessive rise in pulmonary artery pressure (Ppa) which precedes edema formation. Bronchoalveolar lavage in patients with advanced HAPE shows evidence of inflammatory response with increased capillary permeability. There are, however, no prospective data indicating whether the inflammatory response is a primary cause of HAPE or a consequence of edema formation. Excessive rise in Ppa appears to be a crucial pathophysiologic factor for HAPE. Recent observations of high Ppa in HAPE-susceptible sujects who did not develop pulmonary edema after rapid ascent to high altitude suggest either that Ppa does not necessarily reflect capillary pressure in these individuals or else that additional factors, such as an inflammatory response and/or a decreased fluid clearance from the lung, are necessary for the development of pulmonary edema. The treatment of choice is immediate descent. When this is impossible and supplemental oxygen is not available, treatment with nifedipine is recommended until descent is possible.

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Section: Laboratory Evaluationmentioning

confidence: 94%

High Altitude Pulmonary Edema

Bärtsch

1997

Respiration

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High‐Altitude Pulmonary Edema

Swenson

Bärtsch²

2012

Comprehensive Physiology

138

123

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High-altitude pulmonary edema (HAPE), a not uncommon form of acute altitude illness, can occur within days of ascent above 2500 to 3000 m. Although life-threatening, it is avoidable by slow ascent to permit acclimatization or with drug prophylaxis. The critical pathophysiology is an excessive rise in pulmonary vascular resistance or hypoxic pulmonary vasoconstriction (HPV) leading to increased microvascular pressures. The resultant hydrostatic stress causes dynamic changes in the permeability of the alveolar capillary barrier and mechanical injurious damage leading to leakage of large proteins and erythrocytes into the alveolar space in the absence of inflammation. Bronchoalveolar lavage and hemodynamic pressure measurements in humans confirm that elevated capillary pressure induces a high-permeability noninflammatory lung edema. Reduced nitric oxide availability and increased endothelin in hypoxia are the major determinants of excessive HPV in HAPE-susceptible individuals. Other hypoxia-dependent differences in ventilatory control, sympathetic nervous system activation, endothelial function, and alveolar epithelial active fluid reabsorption likely contribute additionally to HAPE susceptibility. Recent studies strongly suggest nonuniform regional hypoxic arteriolar vasoconstriction as an explanation for how HPV occurring predominantly at the arteriolar level causes leakage. In areas of high blood flow due to lesser HPV, edema develops due to pressures that exceed the dynamic and structural capacity of the alveolar capillary barrier to maintain normal fluid balance. This article will review the pathophysiology of the vasculature, alveolar epithelium, innervation, immune response, and genetics of the lung at high altitude, as well as therapeutic and prophylactic strategies to reduce the morbidity and mortality of HAPE.

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