scholarly journals Doppler assessment of hypoxic pulmonary vasoconstriction and susceptibility to high altitude pulmonary oedema.

Thorax ◽  
1995 ◽  
Vol 50 (1) ◽  
pp. 22-27 ◽  
Author(s):  
J L Vachiery ◽  
T McDonagh ◽  
J J Moraine ◽  
J Berre ◽  
R Naeije ◽  
...  
Keyword(s):  
High Altitude ◽  
Pulmonary Oedema ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Pulmonary Vasoconstriction

scholarly journals Acute high-altitude sickness

2017 ◽  
Vol 26 (143) ◽  
pp. 160096 ◽  
Author(s):  
Andrew M. Luks ◽  
Erik R. Swenson ◽  
Peter Bärtsch
Keyword(s):  
High Altitude ◽  
Pulmonary Oedema ◽  
Cerebral Oedema ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Acute Mountain Sickness ◽  
Resonance Imaging ◽  
Altitude Sickness ◽  
Pulmonary Vasoconstriction ◽  
Prevention And Treatment ◽  
Mountain Sickness

At any point 1–5 days following ascent to altitudes ≥2500 m, individuals are at risk of developing one of three forms of acute altitude illness: acute mountain sickness, a syndrome of nonspecific symptoms including headache, lassitude, dizziness and nausea; high-altitude cerebral oedema, a potentially fatal illness characterised by ataxia, decreased consciousness and characteristic changes on magnetic resonance imaging; and high-altitude pulmonary oedema, a noncardiogenic form of pulmonary oedema resulting from excessive hypoxic pulmonary vasoconstriction which can be fatal if not recognised and treated promptly. This review provides detailed information about each of these important clinical entities. After reviewing the clinical features, epidemiology and current understanding of the pathophysiology of each disorder, we describe the current pharmacological and nonpharmacological approaches to the prevention and treatment of these diseases.

Ischemic Preconditioning Improves Oxygen Saturation and Attenuates Hypoxic Pulmonary Vasoconstriction at High Altitude

2014 ◽  
Vol 15 (2) ◽  
pp. 155-161 ◽  
Author(s):  
Gary P. Foster ◽  
Paresh C. Giri ◽  
Douglas M. Rogers ◽  
Sophia R. Larson ◽  
James D. Anholm
Keyword(s):  
Oxygen Saturation ◽  
High Altitude ◽  
Ischemic Preconditioning ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Pulmonary Vasoconstriction

Physiological aspects of high-altitude pulmonary edema

2005 ◽  
Vol 98 (3) ◽  
pp. 1101-1110 ◽  
Author(s):  
Peter Bärtsch ◽  
Heimo Mairbäurl ◽  
Marco Maggiorini ◽  
Erik R. Swenson
Keyword(s):  
Pulmonary Edema ◽  
High Altitude ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Right Heart Catheterization ◽  
Lung Edema ◽  
Heart Catheterization ◽  
Edema Formation ◽  
Pulmonary Vasoconstriction ◽  
Large Molecular Weight ◽  
High Altitude Pulmonary Edema

High-altitude pulmonary edema (HAPE) develops in rapidly ascending nonacclimatized healthy individuals at altitudes above 3,000 m. An excessive rise in pulmonary artery pressure (PAP) preceding edema formation is the crucial pathophysiological factor because drugs that lower PAP prevent HAPE. Measurements of nitric oxide (NO) in exhaled air, of nitrites and nitrates in bronchoalveolar lavage (BAL) fluid, and forearm NO-dependent endothelial function all point to a reduced NO availability in hypoxia as a major cause of the excessive hypoxic PAP rise in HAPE-susceptible individuals. Studies using right heart catheterization or BAL in incipient HAPE have demonstrated that edema is caused by an increased microvascular hydrostatic pressure in the presence of normal left atrial pressure, resulting in leakage of large-molecular-weight proteins and erythrocytes across the alveolarcapillary barrier in the absence of any evidence of inflammation. These studies confirm in humans that high capillary pressure induces a high-permeability-type lung edema in the absence of inflammation, a concept first introduced under the term “stress failure.” Recent studies using microspheres in swine and magnetic resonance imaging in humans strongly support the concept and primacy of nonuniform hypoxic arteriolar vasoconstriction to explain how hypoxic pulmonary vasoconstriction occurring predominantly at the arteriolar level can cause leakage. This compelling but as yet unproven mechanism predicts that edema occurs in areas of high blood flow due to lesser vasoconstriction. The combination of high flow at higher pressure results in pressures, which exceed the structural and dynamic capacity of the alveolar capillary barrier to maintain normal alveolar fluid balance.

High-altitude pulmonary oedema

ESC CardioMed ◽  
2018 ◽  
pp. 1078-1080
Author(s):  
Samuel Verges ◽  
Patrick Levy
Keyword(s):  
High Altitude ◽  
Pulmonary Oedema ◽  
Acute Mountain Sickness ◽  
Arterial Oxygenation ◽  
Lower Altitude ◽  
Vasodilator Drugs ◽  
Oxygen Administration ◽  
Pulmonary Vasoconstriction ◽  
High Altitude Disease ◽  
Alveolar Capillary

At high altitude, the reduction in arterial oxygenation frequently leads to symptoms of acute mountain sickness. While these symptoms generally resolve spontaneously, high-altitude pulmonary oedema can develop and represents a potentially lethal form of high-altitude disease. High-altitude pulmonary oedema is a non-cardiogenic oedema due to exaggerated pulmonary vasoconstriction and altered alveolar–capillary permeability. In addition to descending to lower altitude, it requires specific emergency cares such as oxygen administration, a hyperbaric bag, and vasodilator drugs.

Insights by Peruvian scientists into the pathogenesis of human chronic hypoxic pulmonary hypertension

2005 ◽  
Vol 98 (1) ◽  
pp. 384-389 ◽  
Author(s):  
John T. Reeves ◽  
Robert F. Grover
Keyword(s):  
Pulmonary Hypertension ◽  
High Altitude ◽  
Structural Changes ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Elevated Pressure ◽  
Severe Pulmonary Hypertension ◽  
The Andes ◽  
Pulmonary Vasoconstriction ◽  
Oxygen Inhalation ◽  
High Altitude Natives

Pulmonary hypertension had long been suspected in high-altitude natives of the Andes. However, it remained for a team of Peruvian scientists led by Dante Penaloza to provide not only the first clear evidence that humans living at high altitude did indeed have chronic, and occasionally severe, pulmonary hypertension, but more importantly, that this was a consequence of structural changes in the pulmonary vascular bed. Novel histological findings by one of the team, Javier Arias-Stella, indicated that hypoxia-induced thickening of the pulmonary arteriolar walls was the primary cause of the elevated pressure. Because the hypertension was not promptly reversed by vasodilators (oxygen inhalation or acetylcholine infusion), they found it differed from acute hypoxic pulmonary vasoconstriction. The team's other novel findings included a delay in the normal fall in pulmonary vascular resistance after birth and, in adults, a lack of vasodilation with muscular exercise. Furthermore, the altitude-related pulmonary hypertension resolved over time at sea level.

Exaggerated Hypoxic Pulmonary Vasoconstriction Without Susceptibility to High Altitude Pulmonary Edema

2015 ◽  
Vol 16 (1) ◽  
pp. 11-17 ◽  
Author(s):  
Christoph Dehnert ◽  
Derliz Mereles ◽  
Sebastian Greiner ◽  
Dagmar Albers ◽  
Fabian Scheurlen ◽  
...  
Keyword(s):  
Pulmonary Edema ◽  
High Altitude ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Pulmonary Vasoconstriction ◽  
High Altitude Pulmonary Edema

Garlic prevents hypoxic pulmonary hypertension in rats

1998 ◽  
Vol 275 (2) ◽  
pp. L283-L287 ◽  
Author(s):  
Michael B. Fallon ◽  
Gary A. Abrams ◽  
Tarek T. Abdel-Razek ◽  
Jun Dai ◽  
Shi-Juan Chen ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
High Altitude ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Control Group ◽  
Nitric Oxide Synthase Inhibitor ◽  
Hypoxic Pulmonary Hypertension ◽  
Pulmonary Vasoconstriction ◽  
Pulmonary Arterial ◽  
Synthase Inhibitor

Hypoxic pulmonary vasoconstriction underlies the development of high-altitude pulmonary edema. Anecdotal observations suggest a beneficial effect of garlic in preventing high-altitude symptoms. To determine whether garlic influences pulmonary vasoconstriction, we assessed the effect of garlic on pulmonary pressures in rats subjected to alveolar hypoxia and on vasoconstriction in isolated pulmonary arterial rings. Garlic gavage (100 mg/kg body wt) for 5 days resulted in complete inhibition of acute hypoxic pulmonary vasoconstriction compared with the control group. No difference in mean arterial pressure or heart rate response to hypoxia was seen between the groups. Garlic solution resulted in a significant dose-dependent vasorelaxation in both endothelium-intact and mechanically endothelium-disrupted pulmonary arterial rings. The administration of N G-nitro-l-arginine methyl ester (a nitric oxide synthase inhibitor) inhibited the vasodilatory effect of garlic by 80%. These studies document that garlic blocks hypoxic pulmonary hypertension in vivo and demonstrate a combination of endothelium-dependent and -independent mechanisms for the effect in pulmonary arterial rings.

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