Been there done that1/14/2024 ![]() ![]() We recently observed very similar vascular intimal changes in the lungs of non-smoking normal subjects without COPD and without pulmonary hypertension. Whether this prominent feature of pulmonary vascular remodelling in COPD has any relationship to the development of pulmonary hypertension remains to be proven, however. The predominant type of pulmonary vascular remodelling in COPD is enlargement of the intimal layer in muscular arteries, which is very much unlike the type of remodelling seen in healthy highlanders and patients with chronic mountain sickness. observed endothelial dysfunction and vascular remodelling in lungs of normoxaemic patients with mild COPD and even in smokers with normal pulmonary function. The relationship between arterial oxygen tension and pulmonary artery pressure is very weak and long-term oxygen therapy does not fully reverse pulmonary hypertension or vascular remodelling in severe COPD. More recently, the role of hypoxia in the development of pulmonary hypertension in COPD was questioned. Accordingly, for many years HPV was the usual suspect when trying to explain the development of pulmonary hypertension in COPD. pneumonia and pulmonary oedema), HPV was long held responsible for the pathological alterations in lung vessels occurring in chronic lung diseases, particularly chronic obstructive pulmonary disease (COPD). While recognising the benefit of HPV to maintain arterial oxygen tension in many pathological conditions associated with impaired alveolar ventilation ( e.g. Mitochondria and NADPH oxidase (Nox) are considered as the major sources of ROS production in the pulmonary vasculature. It is generally accepted that the endothelial cell plays a central role in hypoxic sensing, and that hypoxic sensing involves changing levels of reactive oxygen species (ROS) – although the direction of this change (up or down) continues to be debated. Ever since von Euler and Liljestrand described their observations on pulmonary arterial blood pressure in the hypoxic cat, scientists have been dedicated to better understand the pulmonary vascular response to hypoxia. The unique property of small pulmonary arteries to constrict in response to a reduced alveolar oxygen tension allows us to cover not only the complexities of ventilation perfusion matching, but also to dive into the more exciting “physiological classics”, such as the fetal circulation and high altitude adaptation. To many of us involved in teaching pulmonary physiology and gas exchange to medical students, hypoxic pulmonary vasoconstriction (HPV) is a favourite topic. Hypoxic pulmonary vasoconstriction, mediated by p22phox, is a double-edged sword in COPD
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