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Nitric oxide donor prevents hepatic and systemic perfusion decrease induced by endotoxin in anesthetized rabbits

C M Pastor1, M R Losser, D Payen

  • 1Department of Anesthesiology and Intensive Care, C.H.U. Lariboisière, Paris, France.

Hepatology (Baltimore, Md.)
|November 1, 1995
PubMed
Summary
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Nitric oxide (NO) donors like linsidomine may benefit liver blood flow during early endotoxemia. This study found linsidomine maintained systemic and hepatic perfusion, preventing lactic acidosis in rabbits.

Area of Science:

  • Physiology
  • Pharmacology
  • Sepsis Research

Background:

  • The role of nitric oxide (NO) in sepsis remains controversial, with conflicting results from human and animal studies regarding NO inhibitors.
  • Severe hypotension during sepsis is often treated with NO inhibitors, despite animal studies indicating increased mortality with such treatments.

Purpose of the Study:

  • To investigate the potential beneficial effects of an NO donor, linsidomine, in maintaining liver blood flow during early endotoxemia.
  • To evaluate the impact of linsidomine on systemic and hepatic hemodynamics and metabolic acidosis in a rabbit model of endotoxic shock.

Main Methods:

  • Anesthetized and mechanically ventilated rabbits received intravenous endotoxin (E. coli, S. minnesota, S. enteritidis).
  • Hemodynamic parameters including mean arterial pressure (MAP) and blood flow velocities in the aorta, hepatic artery, and portal vein were measured using Doppler techniques.

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  • Animals were treated with either saline or linsidomine perfusion and monitored for serum lactate levels.

    • Main Results:

    • Saline-treated rabbits developed hypodynamic shock with decreased MAP, aortic, and portal vein blood flow, and increased serum lactate.
    • Linsidomine perfusion maintained aortic and portal vein blood flow at control levels and prevented the rise in serum lactate.
    • While hepatic artery flow increased with linsidomine, it did not fully compensate for portal vein flow reduction in the saline group, and MAP was not further affected by linsidomine.

    Conclusions:

    • Linsidomine perfusion is beneficial in the early phase of endotoxin shock for maintaining systemic and hepatic perfusion and preventing lactic acidosis, especially without aggressive fluid resuscitation.
    • These findings suggest that endogenous nitric oxide (NO) release is insufficient to maintain adequate liver perfusion during the early stages of endotoxemia.