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Nitric oxide and endothelial permeability

F Hinder1, M Booke, L D Traber

  • 1Klinik und Poliklinik für Anästhesiologie und operative Intensivmedizin, der Westfälischen Wilhelms-Universität, Münster, Germany.

Journal of Applied Physiology (Bethesda, Md. : 1985)
|February 14, 1998
PubMed
Summary
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Nitric oxide synthase inhibition reversed sepsis-induced vasodilation but increased pulmonary vascular resistance. This study found no evidence of impaired pulmonary endothelial barrier function with L-NAME treatment during endotoxemia.

Area of Science:

  • Physiology
  • Pharmacology
  • Critical Care Medicine

Background:

  • Sepsis causes systemic vasodilation, which nitric oxide synthase (NOS) inhibition can reverse.
  • However, NOS inhibition might negatively impact endothelial permeability, particularly in the pulmonary vasculature.

Purpose of the Study:

  • To investigate the effects of Nomega-nitro-L-arginine methyl ester (L-NAME), a NOS inhibitor, on pulmonary vascular resistance and endothelial permeability during endotoxemia in sheep.
  • To determine if reversing systemic vasodilation with L-NAME during sepsis adversely affects the pulmonary circulation.

Main Methods:

  • Twelve sheep were instrumented and infused with Escherichia coli endotoxin (lipopolysaccharide) for 32 hours.
  • After 24 hours, six sheep received L-NAME, while six received saline (control).

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  • Pulmonary hemodynamics, lung lymph flow, and endothelial permeability were assessed using various techniques, including venous occlusion plethysmography.

    • Main Results:

    • L-NAME reversed systemic vasodilation and increased pulmonary vascular resistance, pulmonary arterial pressure, and transiently, pulmonary capillary pressure.
    • Lung lymph flow did not differ between groups, but L-NAME administration showed a trend toward lower lymph-to-plasma protein concentration.
    • Endothelial permeability analysis revealed normal reflection coefficients and elevated filtration coefficients, with no significant differences between the L-NAME and control groups.

    Conclusions:

    • Reversal of systemic vasodilation by L-NAME during endotoxemia is associated with increased pulmonary vascular resistance.
    • Despite increased pulmonary vascular resistance, L-NAME treatment did not impair pulmonary endothelial barrier function in this ovine model of sepsis.