Plasma fibronectin therapy and lung protein clearance with XXXX after surgery.

@entity1 @entity295 @entity796 @entity742 @entity2259
Plasma fibronectin modulates macrophage phagocytic function and can also incorporate into the insoluble tissue pool of fibronectin where it influences endothelial cell adhesion and tissue integrity. We studied the effect of postoperative @entity2259 on lung protein clearance in relation to plasma fibronectin levels using the unanesthetized @entity742 lung lymph fistula model and the effect of infusion of purified @entity1 plasma fibronectin on lung protein clearance. @entity742 received live @entity796 (5 X 10(8) iv) at a time of normal plasma fibronectin (590 +/- 37 micrograms/ml) or 5 days later at a time corresponding to elevation of plasma fibronectin (921 +/- 114 micrograms/ml). After the first bacterial challenge, there was a 22% decrease (P less than 0.05) in plasma fibronectin. Lung lymph flow (QL) initially increased 308% (P less than 0.05) by 2 h (0 h = 4.7 +/- 1.1 ml/h; 2 h = 14.4 +/- 3.5 ml/h), and the total protein lymph-to-plasma concentration ratio (L/P) declined. This was followed by a sustained second phase response over 3-12 h which was characterized by a 202-393% elevation in QL (P less than 0.05), an increase in the L/P ratio, and a 240-480% (P less than 0.05) increase in lung transvascular protein clearance (TVPC = QL X L/P). @entity742 with elevated fibronectin levels also manifested the early (2 h) elevation in QL (P less than 0.05) coupled with a decline in L/P ratio after the second bacterial challenge, but the second-phase increase in TVPC was markedly attenuated. Intravenous infusion of 500 mg of @entity1 plasma fibronectin into normal @entity742 to elevate the fibronectin level comparable to that in the hyperfibronectinemic @entity742 also attenuated (P less than 0.05) the second-phase (3-12 h) increase in lung protein clearance with @entity295 . Thus elevation of plasma fibronectin during postoperative Gram-negative @entity2259 may protect the lung vascular barrier. This response may be mediated by either fibronectin's opsonic support of phagocytic function or its influence on lung endothelial cell adhesion.
