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.

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.

Hypoxic Pulmonary Vasoconstriction and Chronic Lung Disease

2013 ◽  
Vol 12 (3) ◽  
pp. 135-144 ◽  
Author(s):  
Erik R. Swenson
Keyword(s):  
Pulmonary Hypertension ◽  
Lung Disease ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
World Health ◽  
Disease States ◽  
Pulmonary Vasoconstriction ◽  
Local Ventilation ◽  
Pulmonary Vascular Endothelium ◽  
Health And Disease ◽  
Health Organization

Hypoxic vasoconstriction in the lung is a unique and fundamental characteristic of the pulmonary circulation. It functions in health and disease states to better preserve ventilation-perfusion matching by diverting blood flow to better ventilated regions when local ventilation is compromised. As more areas of lung become hypoxic either with high altitude or global lung disease, then hypoxic pulmonary vasoconstriction (HPV) becomes less effective in ventilation-perfusion matching and can lead to pulmonary hypertension. HPV is intrinsic to the vascular smooth muscle and its mechanisms remain poorly understood. In addition, the pulmonary vascular endothelium, red cells, lung innervation, and numerous circulating vasoactive agents also affect the strength of HPV. This review will discuss the pathophysiology of HPV and address its role in pulmonary hypertension associated with World Health Organization Group 3 diseases. When sustained beyond many hours, HPV may initiate pulmonary vascular remodeling and lead to more fixed and less oxygen-responsive pulmonary hypertension if the hypoxic stimulus is maintained.

scholarly journals Pulmonary Hypertension in Acute and Chronic High Altitude Maladaptation Disorders

2021 ◽  
Vol 18 (4) ◽  
pp. 1692
Author(s):  
Akylbek Sydykov ◽  
Argen Mamazhakypov ◽  
Abdirashit Maripov ◽  
Djuro Kosanovic ◽  
Norbert Weissmann ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
High Altitude ◽  
Clinical Experience ◽  
Current Knowledge ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Treatment Options ◽  
Right Heart Failure ◽  
Channel Blockers ◽  
The Right ◽  
Extensive Clinical Experience

Alveolar hypoxia is the most prominent feature of high altitude environment with well-known consequences for the cardio-pulmonary system, including development of pulmonary hypertension. Pulmonary hypertension due to an exaggerated hypoxic pulmonary vasoconstriction contributes to high altitude pulmonary edema (HAPE), a life-threatening disorder, occurring at high altitudes in non-acclimatized healthy individuals. Despite a strong physiologic rationale for using vasodilators for prevention and treatment of HAPE, no systematic studies of their efficacy have been conducted to date. Calcium-channel blockers are currently recommended for drug prophylaxis in high-risk individuals with a clear history of recurrent HAPE based on the extensive clinical experience with nifedipine in HAPE prevention in susceptible individuals. Chronic exposure to hypoxia induces pulmonary vascular remodeling and development of pulmonary hypertension, which places an increased pressure load on the right ventricle leading to right heart failure. Further, pulmonary hypertension along with excessive erythrocytosis may complicate chronic mountain sickness, another high altitude maladaptation disorder. Importantly, other causes than hypoxia may potentially underlie and/or contribute to pulmonary hypertension at high altitude, such as chronic heart and lung diseases, thrombotic or embolic diseases. Extensive clinical experience with drugs in patients with pulmonary arterial hypertension suggests their potential for treatment of high altitude pulmonary hypertension. Small studies have demonstrated their efficacy in reducing pulmonary artery pressure in high altitude residents. However, no drugs have been approved to date for the therapy of chronic high altitude pulmonary hypertension. This work provides a literature review on the role of pulmonary hypertension in the pathogenesis of acute and chronic high altitude maladaptation disorders and summarizes current knowledge regarding potential treatment options.

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.

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

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
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