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Right ventricular overload causes the decrease in cardiac output after nitric oxide synthesis inhibition in

R I Cohen1, Y Shapir, L Chen

  • 1Division of Pulmonary and Critical Care Medicine, The Long Island Jewish Medical Center, New Hyde Park, NY 11040-1433, USA.

Critical Care Medicine
|April 29, 1998
PubMed
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In endotoxemia, inhibiting nitric oxide synthase decreases cardiac output due to increased right ventricular afterload, not left ventricular afterload. This finding is crucial for understanding circulatory dysfunction in sepsis.

Area of Science:

  • Cardiovascular Physiology
  • Sepsis Pathophysiology
  • Hemodynamic Monitoring

Background:

  • Endotoxemia, a model for sepsis, causes significant circulatory changes.
  • Nitric oxide synthase inhibition is a potential therapeutic target in sepsis.
  • The precise mechanisms leading to decreased cardiac output in endotoxemia remain debated.

Purpose of the Study:

  • To differentiate the contributions of left ventricular (LV) and right ventricular (RV) afterload to decreased cardiac output following nitric oxide synthase (NOS) inhibition in endotoxemia.
  • To investigate the hemodynamic consequences of NOS inhibition in a porcine model of endotoxemia.

Main Methods:

  • A prospective, randomized study was conducted in sedated, mechanically ventilated pigs.
  • Endotoxemia was induced, followed by administration of NG-nitro-L-arginine methyl ester (L-NAME) to inhibit NOS or saline.

Related Experiment Videos

  • Echocardiography, pulmonary artery catheterization, and gastric tonometry were used to assess cardiac function, hemodynamics, and tissue oxygenation.

    • Main Results:

    • Endotoxemia increased pulmonary arterial pressure and RV volumes, and decreased gastric mucosal pH.
    • L-NAME administration restored mean arterial pressure but worsened pulmonary hypertension, increased RV volumes, and decreased cardiac output.
    • Increased LV afterload, induced by aortic occlusion, did not decrease cardiac output, indicating it was not the primary cause of circulatory collapse.

    Conclusions:

    • The reduction in cardiac output after NOS inhibition in endotoxemia is primarily attributed to increased right ventricular afterload.
    • Left ventricular afterload does not appear to be the main determinant of decreased cardiac output in this model.
    • These findings highlight the critical role of RV function in maintaining cardiac output during sepsis-induced hemodynamic compromise.