blodluftbarriären

Blodluftbarriären, or the blood–air barrier, is the thin interface between the air in the alveoli and the blood in the pulmonary capillaries. It consists of the alveolar epithelium (primarily type I pneumocytes), the capillary endothelium, and their fused basement membranes, with a small interstitial space and a layer of alveolar surfactant. The barrier is ultra-thin and optimized for gas exchange, while also contributing to fluid regulation and host defense.

The barrier is typically about 0.2 to 0.6 micrometers thick and covers a large surface area—roughly 70 square meters in an adult. This extreme thinness, together with a large surface, enables rapid diffusion of gases between the air and the blood. The alveolar epithelium includes both type I and type II cells; type II cells produce surfactant, which reduces surface tension and helps maintain barrier stability.

Gas exchange occurs by diffusion driven by partial pressure differences of oxygen and carbon dioxide, described by diffusion principles such as Fick’s law. The barrier’s integrity supports efficient oxygen uptake and carbon dioxide removal, while its structure also influences fluid balance and immune defenses within the alveolar space.

Clinical relevance is seen when the barrier thickens or becomes damaged, impairing diffusion and causing hypoxemia. Conditions such as acute respiratory distress syndrome (ARDS), pulmonary edema, interstitial lung disease, and pneumonia can disrupt alveolar–capillary coupling. Diffusing capacity for carbon monoxide (DLCO) is commonly used to assess barrier function.

Surfactant from type II pneumocytes and alveolar macrophages contribute to barrier stability and immune surveillance. The blood–air barrier develops during lung maturation and can adapt in response to physiological or pathological changes.