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Department of Molecular and Cellular Physiology, Louisiana State University Medical Center, Shreveport, Louisiana 71130-3932
Fluid filtration rate (Jv/S) from rat mesenteric capillaries was measured using a modified Landis technique before and after superfusion with 100 µM NG-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase inhibitor. Three groups were studied: 1) control rats, 2) rats injected with antineutrophil serum (ANS), and 3) rats injected with a monoclonal antibody (CL26) against the leukocyte adhesion molecule CD18. The relative increase in Jv/S (L-NAME/baseline) in control rats averaged 1.66 ± 0.32 (n = 11), which was significantly higher (P < 0.05) than in ANS (0.51 ± 0.12; n = 5)- and CL26 (0.45 ± 0.16; n = 6)-injected rats exposed to L-NAME. The L-NAME-induced changes in Jv/S in each group were due to altered permeability rather than altered pressure gradients, as determined by measurements of arteriolar hydrostatic pressure (using a servo-null apparatus) and estimates of intravascular oncotic pressure (using plasma protein concentration). These findings indicate that nitric oxide synthase inhibition increases the permeability of mesenteric capillaries to water, a response that is dependent on neutrophil adhesion.
microvascular permeability; acute inflammation; endothelial barrier dysfunction
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