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Endotoxin-induced pulmonary dysfunction is prevented by C1-esterase inhibitor

R Guerrero1, F Velasco, M Rodriguez

  • 1Unidad de Investigación, Hospital Universitario Reina Sofía, Spain.

The Journal of Clinical Investigation
|June 1, 1993
PubMed
Summary

C1-esterase inhibitor (C1-INH) mitigated cardiovascular and respiratory dysfunction in endotoxic shock by inhibiting the blood coagulation contact system. This intervention prevented hypoxemia and pulmonary dysfunction in dogs.

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Area of Science:

  • Physiology
  • Immunology
  • Pharmacology

Background:

  • Septic shock involves hypotension, disseminated intravascular coagulation, and neutrophil activation linked to the blood coagulation contact system.
  • The blood coagulation contact system plays a critical role in the pathophysiology of endotoxic shock.

Purpose of the Study:

  • To evaluate the effect of C1-esterase inhibitor (C1-INH) on cardiovascular and respiratory dysfunction in canine endotoxic shock.
  • To investigate the role of the blood coagulation contact system in endotoxic shock-induced pulmonary dysfunction.

Main Methods:

  • Endotoxemic shock was induced in dogs using Escherichia coli endotoxin.
  • Two groups were studied: controls receiving endotoxin and a C1-INH group receiving C1-INH infusion prior to endotoxin.
  • Cardiovascular parameters (systolic index, ventricular systolic work indexes) and respiratory parameters (arterial O2 partial pressure, alveolo-arterial O2 difference, intrapulmonary shunt) were measured.

Main Results:

  • Endotoxin induced hypodynamic shock in both groups, but the C1-INH group showed less severe decreases in systolic index and ventricular systolic work.
  • Controls experienced significant hypoxemia (30% decrease in arterial O2 partial pressure) and increased alveolo-arterial O2 difference (625%), which were prevented by C1-INH.
  • C1-INH administration prevented endotoxin-induced hypoxemia, increased intrapulmonary shunt, and decreased blood coagulation contact factors.

Conclusions:

  • Pulmonary dysfunction in canine endotoxic shock is associated with activation of the blood coagulation contact system.
  • Inhibition of the blood coagulation contact system with C1-INH effectively prevented endotoxin-induced hypoxemia and pulmonary dysfunction.
  • C1-INH demonstrates a protective role against the detrimental effects of endotoxic shock on the cardiovascular and respiratory systems.