{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,9]],"date-time":"2026-09-09T01:59:54Z","timestamp":1788919194186,"version":"build-2803163510"},"reference-count":91,"publisher":"Annual Reviews","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Annu. Rev. Physiol."],"published-print":{"date-parts":[[1999,3]]},"abstract":"<jats:p>\u25aa Abstract\u2002 The pulmonary blood-gas barrier needs to satisfy two conflicting requirements. It must be extremely thin for efficient gas exchange, but also immensely strong to withstand the extremely high stresses in the capillary wall when capillary pressure rises during exercise. The strength of the blood-gas barrier on the thin side is attributable to the type IV collagen in the basement membranes. However, when the wall stresses rise to very high levels, ultrastructural changes in the barrier occur, a condition known as stress failure. Physiological conditions that alter the properties of the barrier include intense exercise in elite human athletes. Some animals, such as Thoroughbred racehorses, consistently break their alveolar capillaries during galloping, causing hemorrhage. Pathophysiological conditions causing stress failure include neurogenic pulmonary edema, high-altitude pulmonary edema, left heart failure, and overinflation of the lung. Remodeling of the capillary wall occurs in response to increased wall stress, a good example being the thickening of the capillary basement membrane in diseases such as mitral stenosis. The blood-gas barrier is able to maintain its extreme thinness with sufficient strength only through continual regulation of its wall structure. Recent experimental work suggests that rapid changes in gene expression for extracellular matrix proteins and growth factors occur in response to increases in capillary wall stress. 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