The Cellular Effects Of Hypoxia In The Pulmonary Circulation


Scottish Pulmonary Vascular Unit, Glasgow, United Kingdom

Abstract: Hypoxia causes pulmonary hypertension in nearly all species studied. The pulmonary hypertension is accompanied and augmented by pulmonary vascular remodelling. Vascular remodelling is characterised largely by fibroblast, smooth muscle cell (SMC) and endothelial cell proliferation, which results in lumen obliteration. Chronic hypoxia elicits expression of several mitogens, growth factors and cytokines by pulmonary vascular cells and the suppression of anti-proliferative factors. Although hypoxic pulmonary vascular remodelling is associated with medial hypertrophy, in vitro hypoxia does not lead directly to an increase in smooth muscle cell proliferation. It is possible that hypoxia is sensed by fibroblasts, endothelial cells, or both, and intercellular signalling by growth factors, cytokines and other mitogens to adjacent pulmonary artery SMC is the underlying mechanism for the medial hypertrophy of pulmonary vascular remodelling.

Keywords: proliferation, remodelling, smooth muscle cells, endothelial cells, fibroblast and hypoxia


Since 1946 it has been known that hypoxia causes constriction of the pulmonary circulation. This was first shown in the intact vascular bed of the cat but subsequently also shown in isolated vessels (small resistance vessels) and isolated smooth muscle cells. The purpose of hypoxic pulmonary vasoconstriction is thought to be twofold. Firstly, in utero, it keeps the pulmonary circulation closed during gestation and allows it to open up quickly following birth. Secondly, it preserves ventilation-perfusion matching when there is obstruction of the airways. This benign physiological response becomes malign when the lung is faced with global hypoxia such as in the context of lung disease or for residents at high altitude. In this case all areas of the lung

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