The therapy of pulmonary hypertension has evolved rapidly in the last 10 years from the use of non-selective vasodilators to drugs that specifically target pulmonary vasodilation, endothelial function, and vascular remodeling. Sildenafil is a phosphodiesterase type 5 inhibitor that has an expanding role in the treatment of pulmonary hypertension. Case series and small studies, as well as the fi...

Hypoxia-induced and high altitude pulmonary hypertension are a major problem in the mountain areas of the world. The asymmetric methylarginines (ADMA) inhibit nitric oxide (NO) synthesis by competing with L-arginine, and high levels of plasma ADMA predict adverse outcomes in pulmonary hypertension. However, little is known about the regulation of the ADMA-NO pathway in animals adapted to high a...

The word ‘hypertension’ usually evokes thoughts of slowly rising systemic arterial blood pressure and increased risk for diseases like stroke, heart attack and congestive heart failure. However, hypertension in the pulmonary vasculature is an equally problematic disease (Rich et al. 1987, Rubin, 1997). Clinicians and medical students most often think about ‘primary pulmonary hypertension’, a de...

Altitude travel results in acute variations of barometric pressure, which induce different degrees of hypoxia, changing the gas contents in body tissues and cavities. Non ventilated air containing cavities may induce barotraumas of the lung (pneumothorax), sinuses and middle ear, with pain, vertigo and hearing loss. Commercial air planes keep their cabin pressure at an equivalent altitude of ab...

• The regulation of the pulmonary circulation is inextricably linked to the role of the lungs in gas exchange. Accordingly, it is not surprising that hypoxia and acidosis predominate as stimuli for vasomotor activity or that their main effects are exerted locally on the pulmonary vascular tree. Although pulmonary vasomotor nerves do exist, they operate more to adjust the distensibility of capac...

High-altitude illness is the collective term for acute mountain sickness (AMS), high-altitude cerebral oedema (HACE), and high-altitude pulmonary oedema (HAPE). The pathophysiology of these syndromes is not completely understood, although studies have substantially contributed to the current understanding of several areas. These areas include the role and potential mechanisms of brain swelling ...

Increased pulmonary arterial pressure (PAP) is a hallmark of high-altitude exposure and, if exaggerated, may be associated with morbidity and mortality. High altitude also alters nocturnal breathing and altered nocturnal respiration has recently been reported to be associated with altered pulmonary and systemic vascular function in Andean high-altitude dwellers [1], suggesting the possibility o...

BACKGROUND The degree of pulmonary hypertension in healthy subjects exposed to acute hypobaric hypoxia at high altitude was found to be related to increased plasma endothelin (ET)-1. The aim of the present study was to investigate the effects of ET-1 antagonism on pulmonary hypertension, renal water, and sodium balance under acute and prolonged exposure to high-altitude-associated hypoxia. ME...

When Paul Wood first described primary pulmonary hypertensionl 2 he believed it to have a vasoconstrictive origin and showed that the pulmonary vascular resistance could be selectively lowered in some but not all of these patients by infusion of acetyl choline into the pulmonary artery3 in contrast to patients with the Eisenmenger syndrome, who were invariably unresponsive.34 The pathogenesis h...

High-altitude pulmonary edema (HAPE), a potentially life-threatening complication of acute mountain sickness, is postulated to be a noncardiogenic permeability edema caused by acute pulmonary arteriolar vasoconstriction and resultant pulmonary hypertension in response to the hypoxia of rapid ascent to high altitudes. HAPE typically occurs unexpectedly in young, otherwise healthy mountaineers. A...