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Angiotensin-converting enzyme (ACE) in sepsis.

C L Rice, J P Kohler, L Casey

    Circulatory Shock
    |January 1, 1983
    PubMed
    Summary

    Sepsis significantly depletes serum angiotensin-converting enzyme (ACE) activity in baboons, correlating with decreased blood pressure. This suggests sepsis-induced endothelial dysfunction may impair bradykinin inactivation.

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    Area of Science:

    • Physiology
    • Biochemistry

    Background:

    • Angiotensin-converting enzyme (ACE) is crucial for blood pressure regulation and peptide inactivation.
    • Sepsis can lead to endothelial cell dysfunction.
    • Previous studies indicated reduced serum ACE in septic patients with Adult Respiratory Distress Syndrome (ARDS).

    Purpose of the Study:

    • To investigate the effect of induced sepsis on serum ACE activity in a baboon model.
    • To explore the relationship between serum ACE levels and hemodynamic changes during sepsis.

    Main Methods:

    • Seven baboons were induced into sepsis using live E. coli infusion.
    • Serum ACE activity was measured over time.
    • Mean arterial pressure and PaO2 were monitored.

    Main Results:

    • Serum ACE activity significantly declined from a control value of 41.5 +/- 4.2 to 25.8 +/- 2.2 U/L at 8 hours post-sepsis induction (P < 0.05).
    • The decrease in serum ACE correlated with a 65 +/- 11 torr decline in mean arterial pressure.
    • No significant change in PaO2 was observed.

    Conclusions:

    • Sepsis causes a marked depletion of serum ACE activity.
    • This depletion correlates with decreased mean arterial pressure in septic baboons.
    • Reduced serum ACE may indicate impaired bradykinin inactivation due to endothelial dysfunction in sepsis.

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