Abstract

We studied in isolated lungs the effects of oleic acid (OA) injury on the segmental distribution of vascular resistance. Vascular occlusion pressures were measured in control and OA-injured preparation over 90 min. Capillary filtration coefficient K F, C increased from 0.61(±0.10) to 0.91(±0.14) g·min −1·mmHg −1·(100 g) −1 in OA-injured lungs whereas it remained constant in control lungs. Total pulmonary vascular resistance changed little in both control and OA-injured lungs. OA injur resulted in a 15% increase of the double occlusion capillary pressure. In addition, the contribution of the microvasculature to the total vascular resistance rose from 8% to 22%. The increase in microvascular resistance was significant 15 min after OA on the arteriolar side and became significant 30 min later on the venular side. Oleic acid injury does not change the total pulmonary vascular resistance but alters the distribution of segmental resistances in the isolated rabbit lung, thereby contributing to the accumulation of lung water in this model of low pressure permeability edema.

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