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The response of segmental filtration coefficients (K[sub f]) to high peak inflation pressure (PIP) injury was determined in isolated perfused rat lungs. Total (E[sub f,t]), arterial (K[sub f,a]), and venous (K[sub f,v]) filtration coefficients were measured under baseline conditions and after ventilation with 40-45 cmH[sub 2]O PIP. K[sub f,a] and K[sub f,v] were measured under zone I conditions by increasing airway pressure to 25-27 cmH[sub 2]O. The microvascular segment K[sub f] (K[sub f,mv]) was then calculated by: K[sub f,mv] = K[sub f,t] - K[sub f,a] - K[sub f,v]. The baseline K[sub f,t] was 0.090 ± 0.022 ml·min[sup -1]·cmH[sub 2]O[sup -1]·100 g[sup -1] and segmentally distributed 18% arterial, 41% venous, and 41% microvascular. After high PIP injury, K[sub f,t] increased by 680%, whereas K[sub f,a], K[sub f,v], and K[sub f,mv] increased by 398, 589, and 975%, respectively. Pretreatment with 50 µM gadolinium chloride prevented the high PIP-induced increase in K[sub f] in all vascular segments. These data imply a lower hydraulic conductance for microvascular endothelium due to its large surface area and a gadolinium-sensitive high-PIP injury, produced in both alveolar and extra-alveolar vessel segments. [ABSTRACT FROM AUTHOR]