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J Appl Physiol 83: 1941-1946, 1997;
8750-7587/97 $5.00
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Vol. 83, Issue 6, 1941-1946, December 1997

Nitric oxide and endothelial permeability

Frank Hinder1, Michael Booke1, Lillian D. Traber2, and Daniel L. Traber2

1 Klinik und Poliklinik für Anästhesiologie und operative Intensivmedizin, der Westfälischen Wilhelms-Universität, Münster, Germany; and 2 Department of Anesthesiology, The University of Texas Medical Branch, Galveston, Texas 77555-1091

Received 20 August 1996; accepted in final form 25 July 1997.

Hinder, Frank, Michael Booke, Lillian D. Traber, and Daniel L. Traber. Nitric oxide and endothelial permeability. J. Appl. Physiol. 83(6): 1941-1946, 1997.---Nitric oxide synthase inhibition reverses systemic vasodilation during sepsis but may increase endothelial permeability. To assess adverse effects on the pulmonary vasculature, 12 sheep were chronically instrumented with lung lymph fistulas and hydraulic pulmonary venous occluders. Escherichia coli endotoxin (lipopolysaccharide; 10 ng · kg-1 · min-1) was continuously infused for 32 h. After 24 h, six animals received 25 mg/kg of Nomega -nitro-L-arginine methyl ester (L-NAME), and six received saline. All sheep developed a hyperdynamic circulatory response and elevated lymph flows by 24 h of lipopolysaccharide infusion. L-NAME reversed systemic vasodilation, increased pre- and postcapillary pulmonary vascular resistance index, pulmonary arterial pressure, and, transiently, effective pulmonary capillary pressure. Lung lymph flows were not different between groups at 24 h or thereafter. Calculated as changes from baseline, however, lung lymph flow was higher in the L-NAME group than in the control animals, with a trend toward lower lymph-to-plasma protein concentration ratio at 25 h. Permeability analysis at 32 h by the venous occlusion technique showed normal reflection coefficients and elevated filtration coefficients without differences between groups. Reversal by L-NAME of the systemic vasodilation during endotoxemia was associated with high pulmonary vascular resistance without evidence of impaired pulmonary endothelial barrier function.

nitric oxide synthase inhibition; lung; hyperdynamic sepsis; lung edema; vasodilation; pulmonary endothelial permeability

0161-7567/97 $5.00 Copyright © 1997 the American Physiological Society




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