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Aprotinin is associated with a decrease in nitric oxide production during cardiopulmonary bypass

G E Hill1, D R Springall, R A Robbins

  • 1Department of Anesthesiology, University of Nebraska Medical Center, Omaha 68198-4455, USA.

Surgery
|April 1, 1997
PubMed
Summary
This summary is machine-generated.

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Aprotinin administration during cardiopulmonary bypass (CPB) significantly reduced airway nitric oxide (NO) production in patients. This serine protease inhibitor also decreased cytokine-induced inducible nitric oxide synthase (iNOS) expression in vitro.

Area of Science:

  • Cardiovascular Surgery
  • Pulmonary Medicine
  • Pharmacology

Background:

  • Cardiopulmonary bypass (CPB) increases airway nitric oxide (NO) and inflammatory cytokines like TNF-alpha and IL-1 beta.
  • Cytokine induction of inducible nitric oxide synthase (iNOS) is linked to organ injury.
  • Serine protease inhibitors, such as aprotinin, possess anti-inflammatory properties and can reduce iNOS expression.

Purpose of the Study:

  • To investigate the effect of aprotinin on endogenous airway NO production during CPB.
  • To determine if aprotinin can reduce cytokine-induced iNOS expression in vitro.

Main Methods:

  • Airway NO levels were measured in 10 patients receiving aprotinin during CPB and compared to 10 control subjects.
  • In vitro experiments involved stimulating a murine lung epithelial cell line with cytomix (TNF, IL-1, interferon-gamma) with and without aprotinin.

Related Experiment Videos

Main Results:

  • In control subjects, airway NO increased significantly after 50 minutes of CPB, but this increase was not observed in the aprotinin group.
  • Aprotinin significantly reduced nitrite concentrations in cell culture supernatants.
  • Immunohistochemistry and Northern blot analysis revealed reduced cytokine-induced iNOS expression and mRNA levels in the presence of aprotinin.

Conclusions:

  • Aprotinin effectively reduces nitric oxide production in vivo during cardiopulmonary bypass.
  • Aprotinin demonstrates inhibitory effects on cytokine-induced iNOS expression in vitro.