Paul McLoughlin

TL;DR: It is shown that chronic hypoxia caused PH and remodeling of the blood vessel walls in rats but that this remodeling did not lead to structural narrowing of the vascular lumen, and sustained vasoconstriction had no role in ventilation-perfusion matching and optimization of gas exchange.

TL;DR: This review considers the evidence that protective lung ventilatory strategies improve survival and the current paradigms regarding the mechanisms underlying these effects and addresses the current evidence regarding the buffering of hypercapnic acidosis in ARDS.

TL;DR: It is found that chronic hypoxia resulted in increased total pulmonary vessel length, volume, endothelial surface area and number of endothelial cells in vivo, the first reported demonstration of Hypoxia‐induced angiogenesis in the mature pulmonary circulation, a structural adaptation that may have important beneficial consequences for gas exchange.

TL;DR: The notion that lung injury associated with atelectasis involves trauma to the distal airways is supported, with topographic and biochemical evidence that suchdistal airway injury is not localized solely to atelectatic areas, but is instead generalized in both atElectatic and nonatelectatic lung regions.

TL;DR: It is concluded that hypercapnic acidosis attenuates acute endotoxin-induced lung injury, and is efficacious both prophylactically and therapeutically.